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PART1: Suav Herbal Tshuaj Kho Mob Epilepsy

Mar 02, 2022

Hu rau: Audrey Hu Whatsapp / hp: 0086 13880143964 Email:audrey.hu@wecistanche.com

Taw qhia

Epilepsy yog ib yam kab mob uas tshwm sim thiab mob ntev. Cov etiologies ntawm qaug dab peg yog txhais raws li cov qauv, noob caj noob ces, kis kab mob, metabolic, tiv thaiv kab mob, thiab tsis paub, uas yog npaj los ntawm International League tawm tsam Epilepsy kev faib tawm system nyob rau hauv 2017 (Scheffer li al., 2017). Qhov tshwm sim thiab qhov muaj feem ntau ntawm cov neeg mob qaug dab peg yog siab dua hauv cov tebchaws tau nyiaj tsawg thiab nruab nrab dua li hauv cov tebchaws tau nyiaj ntau, nrog kwv yees li 80 feem pua ​​​​ntawm cov neeg mob qaug dab peg nyob hauv cov tebchaws tau nyiaj tsawg thiab nruab nrab (Meyer et al., 2010; Beghi, 2020 ). Lub nra ntawm tus kab mob tuaj yeem raug txo los ntawm kev txhim kho kev nkag mus rau kev kho mob zoo (Beghi, 2020).

Lub pathogenesis ntawm qaug dab peg yog txawv txav hluav taws xob tawm los ntawm lub hlwb xws li hippocampal, neocortical, cortico-thalamic, thiab basal ganglia tes hauj lwm (Moshe li al., 2015). Txawm hais tias qhov ua rau mob qaug dab peg tsis meej meej, qee qhov ua tau ntawm kev qaug dab peg tau raug npaj hauv ntau cov kev tshawb fawb. Neurotransmitters, synapses, receptors, ion channels, inflammatory cytokines, lub cev tsis muaj zog, glial hlwb, oxidative kev nyuaj siab, apoptosis, mitochondrial dysfunction, noob hloov, glycogen, thiab glucocorticoids metabolism yog koom nrog hauv pathogenesis ntawm qaug dab peg (Nws 20 thiab 20). Gamma-aminobutyric acid (GABA) yog ib qho inhibitory neurotransmitter, thiab glutamate yog ib qho excitatory ib. Ntawm peb hom GABA receptors, GABAa receptors tswj cov tshuaj chloride ion influx, thiab GABAB receptors nce cov poov tshuaj tawm tam sim no thiab txo cov calcium nkag.

Kev ua kom ntawm GABA receptors ua rau muaj kev cuam tshuam rau cov kab mob neuronal membrane. Glutamate ua rau alpha-amino- 3-hydroxy-5-methyl-4-isoxazole-propionate (AMPA) receptors, kainite receptors, thiab N-methyl-D-aspartate (NMDA) receptors. Kev nce ntxiv ntawm NMDA receptors ua rau Ca2 ntxiv rau kev nkag mus. Kev qaug dab peg thiab kev puas tsuaj neuronal tuaj yeem tshwm sim thaum qhov tsis txaus ntseeg ntawm inhibitory thiab excitatory neural kev ua haujlwm. Nicotine acetyl cholinergic (nACh) receptors thiab 5-Hydroxytryptamine (5- HT) receptors kuj tswj cov neuronal excitability thiab koom nrog qaug dab peg (Iha li al., 2017; Zhao et al., 2018). SCN1A, SCN2A, SCN3A, thiab SCN8A cov noob uas ib tus zuj zus encode voltage gated sodium channels, uas yog NaV1.1, NaV1.2, NaV1.3, thiab Nav1.6, muaj feem xyuam rau qhov pib mob vwm (Brunklaus li al., 2020) . Lwm qhov kev hloov pauv hauv ion channel, xws li KCNMA1, KCNQ2, KCNT1, KCNQ3, CACNA1A, CLCN2, thiab HCN1- 4, cuam tshuam rau kev thauj mus los ntawm cov poov tshuaj, calcium, chloride, thiab cyclic nucleotide (He et al., 2021). Kev mob yog qhov ua rau thiab qhov tshwm sim ntawm qaug dab peg, dhau los ua ib lub voj voog vicious thiab ua rau qaug dab peg los txhim kho thiab tsis zoo (Vezzani et al., 2011). Ob qho tib si kis kab mob thiab tsis kis kab mob cov lus teb sib koom ua ke ntawm kev tiv thaiv kab mob ces ua rau muaj mob vwm (Vezzani li al., 2016). Oxidative stress thiab mitochondrial dysfunction kuj tuaj yeem yog qhov ua rau thiab cov txiaj ntsig ntawm caj ces thiab kis mob vwm los ntawm kev puas tsuaj rau cov proteins, lipids, DNA, enzymes, thiab hloov cov neuronal excitability (Pearson- Smith thiab Patel, 2017). Oxidative stress thiab mitochondrial dysfunction induce apoptosis ces coj mus rau neuronal tuag (Mendez-Armenta li al., 2014).

Kev kho mob qaug dab peg muaj cov tshuaj tiv thaiv kab mob vwm, kev phais mob, thiab kev phais kev ua haujlwm, thiab tshuaj kho mob yog qhov kho mob loj. Tam sim no pom zoo tshuaj tiv thaiv kab mob vwm feem ntau yog tsom rau cov kab hluav taws xob-gated ion xws li sodium, potassium, thiab calcium channels, los hloov kho hluav taws xob tua hluav taws xob ntawm cov neuron. Rau cov piv txwv ntawm cov tshuaj no yog phenytoin, carbamazepine, valproate, retigabine, ethosuximide, zonisamide, thiab lwm yam. Qee cov tshuaj xws li benzodiazepines, barbiturates, thiab tiagabine ua rau GABA transporters thiab GABA receptors los txhim kho cov synaptic inhibition. Vigabatrin inhibit GABA transaminase kom txo cov metabolism ntawm GABA. Qee cov tshuaj ua rau ionotropic glutamate receptors, xws li perampanel thiab topiramate ua ntawm AMPA glutamate receptors lossis kainate receptors, thiab felbamate inhibit NMDA receptors, txhawm rau txhawm rau ua kom muaj zog synaptic. Levetiracetam thiab brivaracetam khi rau synaptic vesicle glycoprotein 2A (SV2A) los tiv thaiv kev tso tawm ntawm glutamate (Wang thiab Chen, 2019).

Ntau yam tshuaj ntsuab, xws li Ginkgo biloba thiab Huperzia serrata, tau raug tshaj tawm tias muaj cov tshuaj tiv thaiv kab mob los yog ua rau muaj kev cuam tshuam (Saxena thiab Nadkarni, 2011; Sahranavard et al., 2014; Ekstein, 2015; Kakooza-Mwesige; 10, 2015; thiab al., 2015; Cai, 2017; Wei et al., 2017; Manchishi, 2018). Thawj cov tshuaj tiv thaiv kab mob vwm uas tau txais los ntawm cov nroj tsuag yog cannabidiol, uas tau pom zoo los ntawm United States Food and Drug Administration hauv 2018 rau kev kho Dravet syndrome thiab Lennox-Gastaut syndrome (Samanta, 2019). Cannabidiol yog tus neeg sawv cev tsis muaj hlwb ntawm cannabis uas tau kawm dav thiab ua pov thawj rau nws cov txiaj ntsig thiab kev nyab xeeb. Txawm hais tias cov txheej txheem ntawm nws cov nyhuv antiepileptic tsis paub meej, ntau qhov kev sim tshuaj tau qhia nws lub peev xwm rau kev siv kho mob (Silvestro li al., 2019). Tab sis cov tshuaj tiv thaiv kab mob vwm tshiab no kim heev thiab siv tsis tau hauv ntau lub tebchaws vim tias cannabis raug cai thiab kev kho mob cannabis tseem muaj teeb meem.

Cov tshuaj tiv thaiv kab mob vwm muaj qee qhov tsis zoo rau cov neeg mob lub neej zoo. Tsab ntawv tshuaj ntsuam xyuas zaum kawg tau nthuav dav plaub qhov kev sib tw ntawm cov tshuaj tiv thaiv kab mob vwm, suav nrog cov kev mob tshwm sim dav dav, kev nyuaj siab puas siab ntsws, kev sib raug zoo, thiab kev sib tw nyiaj txiag (Mutanana li al., 2020). Cov teebmeem tsis zoo ntawm cov tshuaj tiv thaiv kab mob muaj xws li kev puas siab puas ntsws loj, kev txawj ntse, kev coj tus cwj pwm, endocrine, thiab kab mob dermatological thiab ua haujlwm tsis zoo (Ekstein, 2015; Cai, 2017; Chen B. et al., 2017). Cov tshuaj yuav cuam tshuam rau kev ua haujlwm ntawm cov neeg mob hauv tsev kawm ntawv, kev ua haujlwm, kev ua haujlwm, thiab tuaj yeem cuam tshuam lawv txoj kev sib yuav, thiab kev sib raug zoo ntawm tus kheej. Kev nyuaj siab thiab kev xav tua tus kheej muaj feem cuam tshuam rau kev nce koob tshuaj tiv thaiv kab mob vwm (Wen li al., 2010). Rau cov neeg uas xav tau kev kho mob ntev ntev ntawm kev qaug dab peg, qee tus ntawm lawv muab cov tshuaj tiv thaiv kab mob vwm uas tsis muaj peev xwm thiab siv tsis tau. Cov kev cov nyom no ua rau cov neeg mob dim ntawm kev kho mob nrog Western tshuaj, tshwj xeeb tshaj yog pom nyob rau hauv cov teb chaws tsim. Tsis tas li ntawd, txawm tias muaj ntau cov tshuaj tiv thaiv kab mob vwm tau tsim nyob rau hauv 20 xyoo tsis ntev los no, kwv yees li ib feem peb ntawm cov neeg mob tsis muaj kev tswj xyuas qaug dab peg vim yog cov tshuaj pharmacoresistance (Wang thiab Chen, 2019). Tam sim no, kev tiv thaiv kab mob vwm thiab kho comorbidities ntawm qaug dab peg uas tsis yog kev tswj cov tsos mob ntawm qaug dab peg yog cov teeb meem tseem ceeb (Kobow li al., 2012; Terrone et al., 2016).

Cov tshuaj ntuj pom tau tias muaj kev phiv tsawg dua thiab muaj txiaj ntsig zoo hauv kev kho mob vwm. Cov txheej txheem ntawm cov tshuaj ntuj tau raug tshaj tawm, suav nrog kev tswj hwm ntawm synapses, receptors, thiab ion channels, inhibition ntawm o, thiab kev tswj hwm ntawm lub cev. Cov tshuaj ntuj kuj tuaj yeem kho cov hlwb glial, txhim kho mitochondrial dysfunction thiab oxidative stress, thiab tswj apoptosis (Nws li al., 2021). Suav tshuaj ntsuab tshuaj ntsuab (CHM) tau dhau los ua ib qho tshuaj ntxiv thiab lwm yam tshuaj. Qhov sib txawv ntawm kev nrhiav tshuaj suav tshuaj rau kev kho mob yog tshwm sim los ntawm cov neeg mob ntshai ntawm kev mob tshwm sim ntawm kev phais lossis tshuaj Western (Ekstein, 2015; Kakooza-Mwesige, 2015). Cov tshuaj ntsuab tshuaj ntsuab tseem pheej yig dua li kev kho mob tseem ceeb thiab tuaj yeem siv tau rau cov neeg mob.

Suav tshuaj ntsuab tau siv los kho mob qaug dab peg thiab qaug dab peg rau ntau txhiab xyoo. Cov tshuaj suav tshuaj yog ua raws li txoj kev xav tias cov tshuaj thiab zaub mov los ntawm tib qhov chaw. Yog li ntawd, tib neeg tuaj yeem noj tshuaj ntsuab hauv lawv cov khoom noj txhua hnub. Qhov kev xyaum no yog hu ua kev kho mob noj zaub mov. Kev kho mob kev noj haus yog lub tswv yim ntawm kev sib txuas cov khoom noj khoom haus thiab tshuaj kho kab mob los ntawm kev noj mov (Wu and Liang, 2018).

Kev ua tau zoo ntawm CHMs kuj tau pom nyob rau hauv cov kev tshawb fawb tsis ntev los no. CHM yog tus kheej cov tshuaj kws kho mob raws li kev cai lij choj txoj kev xav ntawm Suav tshuaj los tswj kev noj qab haus huv thiab kho cov kab mob (Li et al., 2019). Yog li ntawd, cov tib neeg tuaj yeem tau txais kev kho tshuaj ntsuab sib txawv rau tib qhov kev kuaj mob.

Lub hom phiaj ntawm qhov kev tshuaj xyuas no yog los piav qhia txog kev siv tshuaj kho mob thiab cov txheej txheem ntawm antiepileptic CHM thiab muab pov thawj rau kev ua tau zoo ntawm kev kho mob noj haus, uas lav kev tshawb nrhiav ntxiv.

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Tsoos tshuaj rauEpilepsy:Cistanche

Cov khoom siv thiab cov txheej txheem

Cov chaw kho mob feem ntau siv CHMs rau kev kho mob qaug dab peg thiab qaug dab peg tau tshawb nrhiav thiab tshuaj xyuas hauv PubMed thiab Cochrane Library. Kev sib xyaw ua ke ntawm cov ntsiab lus tseem ceeb suav nrog cov ntsiab lus qaug dab peg, qaug dab peg, antiepileptic, anticonvulsive,Suavtshuaj ntsuabtshuaj kho mob" "Suav tshuaj ntsuab"thiab txhua lub npe Latin, cov npe Askiv, thiab cov npe tshawb fawb ntawmtshuaj ntsuab. Cov txheej txheem tshawb nrhiav tau nthuav tawm hauv daim duab 1. Cov peev txheej ntawm cov tshuaj tiv thaiv kab mob no tau sau tseg hauv Table 1 raws li Taiwan tus kws tshuaj tshuaj ntsuab, tsab thib peb (TaiwanTshuaj ntsuabPharmacopeia 3rd Edition Committee, 2019).

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Nroj tsuag

Gastrodia elata

Gastrodia elata yog ib hom tshuaj suav siv dav siv los kho cov kab mob neurological, xws li mob taub hau, insomnia, thiab qaug dab peg (Zhan li al., 2016; Liu et al., 2018). G. elata muaj anticonvulsive, anti-inflammatory, neuroprotective, antiapoptosis, thiab antioxidative teebmeem (Hsieh li al., 2001; Zhan li al., 2016; Liu et al., 2018). Hauv cov qauv nas ntawm ferric-chloride-induced epileptic qaug dab peg, Vanillyl cawv, ib feem ntawm G. elata, suppressed qaug dab peg thiab lipid peroxidation. Kev kho ua ntej nrog 200 mg / kg lossis 100 mg / kg Vanillyl cawv txo qis tus dev ntub dej. Vanillyl cawv 200 mg / kg pawg muaj qhov cuam tshuam loj dua ntawm lipid peroxidation dua li Vanillyl cawv 100 mg / kg pawg thiab phenytoin 10 mg / kg pawg (Hsieh li al., 2000). Hauv cov qauv nas ntawm kainic acid-induced qaug dab peg, G. elata tuaj yeem tiv thaiv kab mob vwm los ntawm kev tswj hwm c-Jun N-terminal kinases (JNK) teeb liab txoj kev thiab activator protein 1 (AP{18}}) qhia. Ob leeg ua ntej thiab tom qab kev kho mob nrog G. elata modulated phosphorylated JNK thiab c-Jun protein. Txawm li cas los xij, piv rau kev kho ua ntej thiab tom qab kev kho mob nrog G. elata, tsuas yog pretreatment nrog G. elata hloov cov qib ntawm c-Fos protein, JNK protein, phosphorylated extracellular signal-regulated kinase, thiab p38 proteins (Hsieh li al., 2007. ).

Ib feem ntawm G. elata, gastrodin, tsis ua rau ionotropic glutamate receptors rau inhibit N-methyl-D- aspartate (NMDA) receptor-facilitated qaug dab peg tab sis tau ua tiav cov teebmeem neuroprotective los ntawm kev tiv thaiv NMDA excitotoxicity uas tau soj ntsuam ntawm nas hippocampal daim (Wong et al., 2016). Liu et al. tshuaj xyuas cov teebmeem ntawm Gastrodin, thiab tau sau cov txheej txheem ntawm Gastrodin suav nrog kev hloov pauv ntawm cov neurotransmitters, tshuaj tiv thaiv oxidative, tiv thaiv kab mob, inhibition ntawm microglial activation, tswj mitochondrial muaj nuj nqi, thiab nce-regulating neurotrophins. Gastrodin muaj peev xwm sib npaug cov kev ua ntawm gamma-aminobutyric acid thiab glutamate (Liu li al., 2018). Gastrodin kuj tau hloov kho mitogen-activated protein kinase (MAPK)-kev cuam tshuam cov lus teb inflammatory thiab inhibited Nav1.6 sodium tam sim no, yog li txo qhov mob qaug dab peg uas tau ua pov thawj los ntawm pentylenetetrazole (PTZ)-vim qaug dab peg nas qauv (Chen L. et al., 2017; Shao et al., 2017). Ib txoj kev tshawb nrhiav thiab muab piv cov tshuaj pharmacokinetics ntawm dawb gastrodin, parisin, thiab G. elata extract hauv nas. Parishin thiab G. elata extract tau ntev t] / 2 piv nrog dawb gastrodin hauv nas ntshav, uas yog 3.09 土 0.05 h, 7.52 土 1.28 h thiab 1.13 土 0.06 h feem, qhia tias Parish hauv thiab G. ntev tshaj li pub dawb gastrodin (Tang li al., 2015). Matias et al. (2016) tau tshuaj xyuas ntau yam ntawm G. elata ntsig txog kev ua haujlwm ntawm cov tshuaj tiv thaiv kab mob, suav nrog G. elata rhizome extracts, gastrodin, 4-Hydroxybenzyl cawv, 4-Hydroxybenzaldehyde thiab analogues, vanillin, thiab vanillyl cawv.

Kev tshawb fawb xyoo 2020 qhia txog kev sib cuam tshuam tshuaj ntsuab ntawm G. elata thiab carbamazepine (CBZ). G. elata txo qhov autoinduction ntawm CBZ thiab nce plasma CBZ concentration (Yip li al., 2020). Cov kev tshawb fawb no qhia txog qhov tseem ceeb ntawm G. elata raws li kev siv tshuaj tiv thaiv kab mob lossis kev kho mob ntxiv. Txawm li cas los xij, cov kws kho mob yuav tsum ua tib zoo xav txog cov tshuaj noj thiab cov kev mob tshwm sim, xws li khaus khaus, thiab qab los noj mov tsis zoo, tshwm sim los ntawm kev sib cuam tshuam ntawm tshuaj ntsuab (Yip li al., 2020).

Uncaria rhynchophylla

Uncaria rhynchophylla (UR) thiab G. elata feem ntau yog siv ua ke los kho tus mob convulsive (Hsieh li al., 1999). Lawv suav hais tias yog tshuaj ntsuab khub. Hauv kainic acid-kho nas qauv, UR muaj cov tshuaj tiv thaiv kab mob thiab cov dawb radical scavenging thiab tej zaum yuav muaj kev sib koom ua ke thaum ua ke nrog G. elata uas ncua qhov pib ntawm cov dev ntub dej, uas yog 63 min piv nrog 27 min hauv pawg tswj hwm. , thaum 40 feeb hauv pawg G. elata (Hsieh li al., 1999). Rhynchophylline yog ib feem ntawm UR uas tuaj yeem kho qhov tsis txaus ntseeg ntawm macrophage migration inhibitory factor (MIF) thiab cyclophilin A nyob rau hauv lub frontal cortex thiab hippocampus hauv kainic acid-induced epilepsy nas. Nws pom tias UR pab pawg tau nce 3.1-fold MIF thiab 2.08-fold cyclophilin A thaum rhynchophylline pawg nce 2.75-fold MIF thiab 1.83-fold cyclophilin A hauv lub frontal cortex; UR pab pawg nce 1.57-fold MIF thiab 1.35-fold cyclophilin A thaum rhynchophylline pawg nce 1.69-fold MIF thiab 1.26-fold cyclophilin A hauv hippocampus , uas tau muab piv rau pawg tswj hwm (Lo et al., 2010). Cov kev tshawb fawb tau tshaj tawm tias rhynchophylline tuaj yeem txo qis qaug dab peg, ib qho kainic acid-induced qaug dab peg nas qauv qhia pom rhynchophylline tuaj yeem pib c-Jun aminoterminal kinase phosphorylation (JNKp) hauv MAPK signaling pathways (Hsu et al., 2013 as wellcarpine as well. -induced raws li txoj cai epilepticus nas qauv ntawm lub cev nqaij daim tawv mob hlwb qhia tau tias nws muaj peev xwm inhibit Nav1.6 persistent sodium tam sim no (INaP) thiab NMDA receptor tam sim no (Shao li al., 2016). Hauv kainic acid-induced epileptic qaug dab peg nas, UR muaj cov teebmeem neuroprotective los ntawm kev txo qis glial fibrillary acidic protein thiab S100B protein qhia thiab inhibiting receptors rau qib siab glycation kawg cov khoom, tsis suav nrog GABAA thiab transient receptor tej zaum vanilloid subtype 1 (TRPV1) receptors. UR kuj tau pom zoo kom txo qis mossy fiber ntau sprouting thiab astrocyte proliferation thiab tiv thaiv hippocampal neuron tuag, tshwj xeeb tshaj yog nyob rau hauv CA1 thiab CA3 cheeb tsam (Lin thiab Hsieh, 2011; Liu li al., 2012; Tang li al., 2017). Tsis tas li ntawd, UR tswj hwm tus xov tooj zoo li receptor thiab neurotrophin signaling txoj hauv kev thiab inhibits cov kab lus ntawm interleukin.

Acori tatarinowii

Acori tatarinowii yog hom nroj tsuag dej uas feem ntau siv los kho cov kab mob neurological, hlab plawv, ua pa, thiab kab mob plab. A. tatarinowii decoction thiab nws cov roj volatile tau pom tias txo qhov qaug dab peg hauv cov qauv maximal electroshock (MES). Lub decoction ntawm A. tatarinowii txo qis convulsive tus nqi nyob rau hauv PTZ-induced qaug dab peg nas los ntawm 100 feem pua ​​(ib txwm saline tswj pab pawg) mus rau 67 feem pua ​​(dose 10 g / kg ntawm decoction) thaum 33 feem pua ​​ntawm cov sodium valproate pawg. Cov roj tsis hloov pauv ntawm A. tatarinowii tsis tuaj yeem txo qis qis tab sis tuaj yeem txo cov neeg tuag ntawm pentylenetetrazol-induced qaug dab peg los ntawm 92 feem pua ​​(cov pab pawg tswj hwm saline) mus rau 40 feem pua ​​(tswj nrog koob tshuaj 1.25 g / kg ntawm cov roj tsis haum) (Liao thiab ib., 2005). Cov khoom xyaw tseem ceeb ntawm A. tatarinowii, a-asarone, modulates GABAA receptors, txhim kho tonic GABAergic inhibition, thiab suppresses lub excitability ntawm CA1 hippocampal pyramidal neurons hauv PTZ thiab kainate nas qauv (Huang li al., 2013). a-asarone thiab p-asarone nce qhov kev qhia ntawm neurotrophic yam, nrog rau cov paj hlwb loj hlob (NGF), BDNF, thiab glial-derived neurotrophic factor (GDNF), hauv kab lis kev cai nas astrocytes. Cov lus qhia yog ib feem ua haujlwm los ntawm kev ua rau cAMP dependent protein kinase (PKA) txoj kev taw qhia (Lam li al., 2019). Hauv kev sim MES thiab PTZ-vim qaug dab peg hauv cov qauv nas, eudesmin muab rho tawm los ntawm A. tatarinowii tuaj yeem nce GABA thaum txo qis glutamate. Tsis tas li ntawd, eudesmin upregulates qhov kev qhia ntawm GABAA thiab glutamate decarboxylase 65 (GAD65) thiab modulates Caspase -3 thiab Bcl-2, ob qho tib si muaj feem xyuam rau neuron apoptosis (Liu li al., 2015).

Paeonia lactiflora

Paeonia lactiflora tuaj yeem cuam tshuam qhov nce ntawm c-Fos protein thiab nce transthyretin thiab phosphoglycerate mutase 1 qhia hauv cobalt-kho nas cerebrum, yog li ua rau muaj kev tiv thaiv neuroprotective ntawm cerebral neurons (Kajiwara li al., 2008). Paeoniflorin yog lub luag haujlwm tseem ceeb ntawm P. lactiflora. Nyob rau hauv hyperthermia-induced qaug dab peg ntawm cov nas tsis paub qab hau 'tus qauv, paeniflorin suppresses qhov nce ntawm glutamate-induced intracellular Ca2 ntxiv, uas cuam tshuam rau metabotropic glutamate receptor 5 (mGluR5) ua kom. Cov nyhuv anticonvulsive ntawm paeoniflorin tsis cuam tshuam nrog kev tso tawm GABA, kev tswj hwm ntawm a-amino-3-hydroxy-5-methyl-4-isoxazolpropionic acid (AMPA), lossis kev tswj hwm ntawm NMDA receptors. Nws yuav yog qhov ua tautshuaj ntsuabtshuaj kho mob febrile qaug dab peg hauv menyuam yaus (Hino li al., 2012). Shosaiko-to-go-keishika-shyakuyaku-to yog Japanese Kampo tshuaj, thiab tsuas yog Paeoniae radix, lub ntsiab lus ntawm cov mis, muaj ib qho tseem ceeb inhibition nyhuv ntawm PTZ-induced EEG zog spectrum hloov (Sugaya li al., 1988)

Bupleurum Suav

Bupleurum chinense muaj ntau yam haujlwm, suav nrog hepatoprotective, antitumor, antioxidant, antidepressant, anti-inflammatory, thiab anticonvulsant teebmeem (Jiang li al., 2020). Saikosaponin ib qho kev cais tawm los ntawm B. chinense tau pom cov tshuaj tiv thaiv kab mob thiab cov tshuaj tiv thaiv neuroprotective los ntawm inhibiting NMDA receptor tam sim no, INap, thiab lub hom phiaj mammalian ntawm rapamycin (mTOR) kev taw qhia txoj hauv kev thiab nce Kv4.2-kev kho A-hom voltage-gated potassium tam sim no ( Kv4. Saikosaponin tuaj yeem txo qhov mob hnyav thiab ntev ntawm kev qaug dab peg, thiab ua kom ntev lub latency ntawm qaug dab peg hauv PTZ-induced nas (Ye et al., 2016). Qee cov tshuaj suav suav muaj B. chinense, xws li "Saiko-Keishi-To (Chai-Hu-Gui-Zhi-Tang)" thiab hloov kho mis ntawm "Chaihu-Longu-Muli-Tang" tau tshaj tawm tias muaj tshuaj tiv thaiv thiab Cov teebmeem antioxidant (Sugaya et al., 1985, 1988; Wu et al., 2002). Kev saib xyuas ntawm calcium tis thiab calcium binding xeev tau pom nyob rau hauv PTZ-rhiab heev snail neurons incubated nyob rau hauv Saiko-keishi-to, thiab nws qhia tau hais tias Saiko-keishi-to muaj ib tug inhibitory nyhuv ntawm calcium hloov thiab khi lub xeev hloov (Sugaya li al. Ib., 1985). Ib qho kev tshawb nrhiav ntxiv tau hloov kho cov mis ntawm Chaihu-Longu-Muli-Tang rau 20 refractory qaug dab peg thiab 20 tus neeg mob qaug dab peg 4 lub hlis, thiab cov mis txo qis qaug dab peg hauv refractory epileptics los ntawm 13.4 土 3.4 mus rau 10.7 5 土 ib hlis twg. -tus nqi yog 0.084) uas tej zaum yuav raug ntaus nqi rau cov teebmeem antioxidant nrog txo cov ntshav malondialdehyde thiab tooj liab-zinc superoxide dismutase (p <0.05) thaum="" tsis="" muaj="" kev="" hloov="" pauv="" tseem="" ceeb="" hauv="" cov="" neeg="" mob="" qaug="" dab="" peg,="" uas="" yog="" vim="" tias="" tsuas="" yog="" pab="" pawg="" neeg="" mob="" qaug="" dab="" peg="" muaj="" qhov="" hloov="" pauv="" loj.="" ntawm="" lipid="" peroxidation="" piv="" rau="" hnub="" nyoog-matched="" noj="" qab="" haus="" huv="" pab="" pawg="" neeg="" (wu="" li="" al.,="">

Ziziphus jujuba

Ziziphus jujuba feem ntau yog siv los kho insomnia hauv cov tshuaj suav tshuaj. Ib txoj kev tshawb fawb tsim los nrog MES qauv thiab PTZ qauv ntawm nas qhia tias Z. jujuba ua tiav cov teebmeem anticonvulsant los ntawm kev nce acetylcholinesterase (AChE) thiab butyrylcholinesterase (BChE) kev ua thiab latency ntawm myoclonic jerks, yog li tiv thaiv qaug dab peg (Pahuja et al., 2011). Kev siv ntxiv ntawm hydroalcoholic extract ntawm Z. jujuba tuaj yeem txhim kho cov nyhuv anticonvulsant ntawm phenytoin thiab phenobarbitone tab sis tsis yog carbamazepine uas tau soj ntsuam hauv MES-induced qaug dab peg nas (Pahuja li al., 2012).

PinelHa ternata

Pineilia ternata feem ntau yog siv los kho cov kab mob ntawm lub ntsws thiab plab hnyuv. Ib feem ntawm P. ternate, pinellia tag nrho alkaloids, yog koom nrog hauv kev hloov kho ntawm GABAergic systems los ntawm nws qhov nce ntawm GABA thiab GAD65 qhia, txo cov GABA transporter-1 (GAT-1) thiab GABA transaminase (GABA). -T) kev qhia, thiab kev tswj hwm ntawm GABAa receptor a5, 8, a4, thiab y2 subunits hauv hippocampal tsim. Kev tshawb fawb xyoo 2020 tau qhia tias pinellia tag nrho cov alkaloids (PTA) tuaj yeem siv cov tshuaj tiv thaiv kab mob uas txo qhov tshwm sim ntawm qhov tshwm sim tshwm sim tshwm sim hauv pilocarpine-induced epileptic nas, thiab PTA 800 mg / kg pawg muaj qhov tsawg tshaj plaws ntawm spontaneous securrent piv rau spontaneous 40 P. /kg pawg thiab Topiramate 60 mg / kg pawg (Deng li al., 2020).

Paeonia suffruticosa

Paeonol yog muab rho tawm los ntawm cov cag ntoo ntawm peony ntoo thiab feem ntau yog siv los ua kom cov ntshav ncig. Ib txoj kev tshawb fawb hauv 2019 tau tsim nrog tsib pawg ntawm PTZ-vim cov nas qaug dab peg, uas yog pawg tswj hwm ib txwm muaj, pab pawg neeg qaug dab peg, pab pawg tsis tshua muaj paeonol- kho, pab pawg nruab nrab-dose paeonol-kho, thiab cov tshuaj paeonol-kho siab pab pawg uas xub tshawb pom cov nyhuv anticonvulsant ntawm paeonol (Liu li al., 2019). Paeonol tau txiav txim siab los txo qhov hnyav thiab lub sijhawm ntawm kev qaug dab peg thiab ua rau kom muaj kev qaug dab peg. Tsis tas li ntawd, nws tiv thaiv hippocampal neurons los ntawm kev puas tsuaj los ntawm kev txo qis oxidative kev nyuaj siab thiab inhibiting apoptosis nyob rau hauv CA1 cheeb tsam thaum inhibiting kev qhia ntawm proapoptotic yam cleaved caspase {{10}}. Kev qaug dab peg tau qhab nia raws li theem 0, tsis muaj lus teb; theem 1, lub ntsej muag txav thiab pob ntseg thiab whisker twitching; theem 2, myoclonic convulsions tsis tu ncua; theem 3, myoclonic convulsions nrog rearing; theem 4, tonic-clonic convulsions; theem 5, generalized tonic-clonic qaug dab peg nrog poob ntawm postural tswj; thiab theem 6, kev tuag. Cov koob tshuaj paeonol-kho tau siab (60 mg / kg) txo qhov qaug dab peg mus rau 2.17 土 0.41 piv rau PTZ-kindled epilepsy pab pawg 4.67 土 0.52 (Liu li al., 2019).

Stephania tetrandra

Tetrandrine yog ib qho hluav taws xob-gated Ca2 ntxiv rau channel blocker cais los ntawm S. tetrandra. Ib txoj kev tshawb fawb tau tshaj tawm tias tetrandrine tswj apoptosis thiab tiv thaiv cov hlwb hlwb los ntawm kev nce qhov kev qhia ntawm Bcl-2 thiab txo qhov kev qhia ntawm Bax. Thiab tetrandrine tuaj yeem txo cov tsos mob tshem tawm xws li poob phaus los ntawm phenobarbital-dependency uas ua pov thawj los ntawm phenobarbital- rho tawm nas qauv (Han li al., 2015).

Lwm cov kev tshawb fawb hauv ntau cov tshuaj tiv thaiv kab mob thiab PTZ-vim qaug dab peg nas qauv qhia tau hais tias tetrandrine tuaj yeem txo cov tshuaj tiv thaiv kab mob ntawm phenytoin thiab valproate los ntawm kev txo cov kev qhia ntawm ntau cov tshuaj tiv thaiv kab mob P-glycoprotein (P-gp) ntawm mRNA thiab protein ntau hauv lub cortex thiab hippocampus, txhim khu kev ua tau zoo ntawm cov tshuaj antiepileptic. Kev qaug dab peg uas raug soj ntsuam los ntawm cov qauv ntawmRacine raws li qib IV thiab V tau txo qis hauv cov nas uas tsis muaj zog uas tau kho nrog tetrandrine (Chen li al., 2015).

Cistanche deserticola

Cistanche deserticolayog hom nroj tsuag suab puam uas loj hlob hauv Suav teb. Echinacoside yog qhov sib xyaw ntawmCistanche deserticola. Pretreated 10 lossis 50 mg / kg echinacoside rau 30 min ntawm kainic acid-induced qaug dab peg nas tuaj yeem txhim kho lawv cov kev muaj sia nyob ntawm lub paj hlwb thiab tiv thaiv kab mob vwm los ntawm inhibiting glutamate excitotoxicity thiab autophagy, suppressing o, thiab activating protein kinase B (Akt) / glycogen synthase kinase (GS) ) 3 & signaling. Yog li ntawd, nws tau nce qaug dab peg latency ntau dua 1 h thiab txo qis qaug dab peg (Lu li al., 2018a). A 4-aminopyridine (4-AP)-induced epileptiform kev ua si nrog rau hauv vitro nas hippocampal neurons 'cov qauv kev tshawb fawb qhia tias echinacoside txo qis glutamate tso tawm, zaus tab sis tsis yog qhov amplitude ntawm spontaneous excitatory postsynaptic tam sim no, qhov kev ncua sij hawm rov ua dua ntawm kev ua haujlwm muaj peev xwm hauv hippocampal CA3 pyramidal neurons (Lu li al., 2018b).

Cistanche deserticola

Cistanche deserticola

Kab mob

Ganoderma lucidum

Nyob rau hauv lus dab neeg, Ganoderma yog suav hais tias yog ib tug paub tsis meej, tej yam yees siv, thiab muaj nuj nqis suav tshuaj. Kev tshuaj xyuas xyoo 2019 tau tshaj tawm tias Ganoderma feem ntau siv yog G. lucidum, G. applanatum, G. sinense, G. tsugae, G. capense, thiab G. boinense (Zhao et al., 2019). Txawm li cas los xij, G. lucidum yog hom kab lig kev cai thiab paub ntau tshaj plaws ntawm Ganoderma.

Ib txoj kev tshawb fawb tau sau thiab cog qoob loo thawj hippocampal neurons los ntawm nas, tom qab ntawd tsim cov kab mob epileptiform tawm hippocampal neuron qauv. Txoj kev tshawb no tau qhia tias G. lucidum polysaccharides tuaj yeem cuam tshuam cov Ca2 ntxiv rau hauv hippocampal neurons thiab txhawb nqa Ca2 plus /calmodulin-dependent protein kinase II a (CaMK II a) kev qhia, yog li txo qis neuronal excitability (Wang li al., 2014). Nyob rau hauv ib qho epileptiform tawm hippocampal neuron qauv, G. lucidum spores inhibit qhov kev qhia ntawm N-cadherin, uas muaj feem xyuam rau mossy fiber ntau sprouting thiab synaptic reconstruction, yog li suppressing neural circuits tsim los ntawm mossy fiber sprouting. N-cadherin kuj txhawb neurotrophin (NT) - 4 qhia, uas yog txuam nrog neuron ciaj sia taus, inhibition ntawm apoptosis, thiab synaptic plasticity, thiab yog li tiv thaiv hippocampal neurons (Wang li al., 2013). Ganoderic acid yog qhov tseem ceeb ntawm G. lucidum spores. Hauv lwm cov kab mob epileptiform tso tawm hippocampal neuron qauv, Ganoderic acid tiv thaiv cov apoptosis ntawm hippocampal neurons thiab txhim kho cov kev qhia ntawm BDNF thiab transient receptor muaj peev xwm canonical 3 (TRPC3), uas koom nrog hauv neuron plasticity thiab synaptic reconstruction, inhibits mosy fiber sprouting, thiab pab nyob rau hauv kev rov qab los ntawm cov neurons puas (Yang li al., 2016).

Kev tshawb nrhiav rov qab rau xyoo 2018 suav nrog 18 tus neeg mob qaug dab peg uas tau kho nrog G. lucidum spore hmoov kho peb zaug hauv ib hnub rau 8 lub lis piam. Txoj kev tshawb no tau qhia tias cov hmoov txo qis qhov qaug dab peg txhua lub lim tiam thiab qhov hnyav ntawm txhua qhov qaug dab peg (Wang li al., 2018). Cov kev tshawb fawb ntxiv yuav tsum tau ua kom paub meej tias nws cov txiaj ntsig zoo hauv kev kho tib neeg mob qaug dab peg.

Tsiaj txhu

Buthus martensii

Txawm hais tias scorpions muaj ntau theem ntawm toxicity, lawv yog ib qho tseem ceeb ntawm cov khoom noj Esxias txoj kev thiab cov tshuaj yeeb dej caw los ntawm lub sijhawm qub. Scorpions feem ntau yog siv los kho cov kab mob neurological thiab musculoskeletal, xws li mob stroke, mob taub hau, qaug dab peg, thiab mob pob qij txha. B. martensii yog hom kab mob Asian scorpion uas muaj ntau tshaj plaws thiab tau siv dav hauv Suav tshuaj txij li Song dynasty ntawm Tuam Tshoj. Antiepilepsy peptides (AEPs) yog bioactive polypeptides muab rho tawm los ntawm lawv cov venom. AEP tuaj yeem yooj yim hla cov ntshav-hlwb teeb meem vim nws qhov hnyav molecular (8.3 kDa), thiab nws muaj cov tshuaj tiv thaiv kab mob los ntawm kev khi nrog synaptosomal-associated protein (SNAP)-25 thiab NMDA (Wang li al., 2009) . Ib txoj kev tshawb fawb pom tau tias AEP tuaj yeem tswj tau cov neuronal excitability los ntawm kev xaiv hloov voltage gated sodium channels hauv thawj cortical neurons cultured los ntawm nas. AEP tshwj xeeb tshaj yog inhibits Navl.6 tam sim no nyob rau hauv tib neeg lub raum embryonic (HEK)-293 hlwb, yog li suppressing tej yam muaj peev xwm nyob rau hauv neurons

Bombyx mas

Silkworms thiab lawv cov chrysalis yog noj tau thiab muaj protein ntau. Kab mob B. mori silkworms nrog fungus Beauveria bassiana tua thiab dries lub cev ntawm silkworms. Cov kab mob kab mob no yog siv los ua tshuaj suav tshuaj suav nrog kev tshaj tawm tshuaj tiv thaiv kab mob, tshuaj tiv thaiv kab mob, tshuaj tiv thaiv kab mob, tshuaj tua kab mob, tshuaj tua kab mob, tshuaj tua kab mob, tshuaj tua kab mob, tshuaj tiv thaiv kab mob, hypoglycemic, thiab cov tshuaj tiv thaiv kab mob (Hu li al., 2017, 2019). Cov tshuaj anticonvulsant, hypnotic, thiab neurotrophic los ntawm qee cov tshuaj molecule me me, xws li beauvericin thiab ammonium oxalate, tau tshawb nrhiav (Hu li al., 2017). Ntau qhov kev tshawb fawb uas muaj cov qauv tsiaj tau tshawb xyuas cov macromolecular compounds ntawm B. Mori, uas tsis tau tshawb xyuas yav dhau los. Cov protein-nplua nuj rho tawm los ntawm B. mori tau txiav txim siab los ua feem ntau ntawm thaj av hippocampus CA1 thiab txo qis qaug dab peg hauv MES-induced qaug dab peg nas thiab nce qaug dab peg thiab tuag latency hauv PTZ-induced qaug dab peg nas (Hu li al., 2019). Cov extracts tiv thaiv neurons los ntawm oxidative puas thiab cell apoptosis los ntawm kev tswj cov phosphoinositide 3- kinase (PI3K)/Akt signaling pathways nyob rau hauv H2O2-stimulated PC12 hlwb (rat pheochromocytoma hlwb) nyob rau hauv vitro (Hu et al., 2019). Cov extracts kuj ua tiav cov teebmeem neuroprotective los ntawm kev txo cov IL-1g, IL-4, thiab qog necrosis factor (TNF)-a, nce 5-HT thiab GABA, thiab txo qis intracellular Ca2 ntxiv rau qib, tiv thaiv neuronal signaling, uas tau tshawb xyuas ntawm NGF-induced PC12 hlwb raug mob los ntawm glutamate (Nws li al., 2020).

Cryptotympana atrata

Cryptotympana atrata, cicada exuviae, yog ib hom tshuaj suav siv tshuaj ntsuab hauv dermatological, ophthalmological, otorhinolaryngological, thiab cov kab mob neurological. C. atrata tuaj yeem ua siav ua porridge thiab kua zaub los yog ua rau hauv tshuaj yej rau kev kho mob noj haus. Hauv kev tshawb fawb txog tshuaj (PTZ, picrotoxin, lossis strychnine)-vim cov tsos mob ntawm tus kab mob nas, cov extracts ntawm C. atrata muaj cov tshuaj tiv thaiv kab mob, sedative, thiab hypothermic teebmeem; dej rho tawm tau zoo dua li ethanol rho tawm (Hsieh li al., 1991).

Yog li ntawd, Suav tshuaj ntsuab (nroj tsuag, fungi, thiab tsiaj txhu) siv tshuaj tua kab mob, antioxidant, thiab neuroprotectant los ntawm kev ua ntawm GABA, NMDA, thiab sodium channels, thiab lwm yam. Cov txheej txheem ua tau zoo tau nthuav tawm nyob rau hauv Table 1. Cov teebmeem no muaj txiaj ntsig zoo rau kev kho mob qaug dab peg. Txawm li cas los xij, randomized, ob qhov muag tsis pom kev soj ntsuam kuaj xyuas kom paub meej tias cov teebmeem antiepileptic thiab qhov ua tau zoo hauv kev kho mob qaug dab peg tsis muaj.

Cistanche deserticola

Cistanche deserticola khoEpilepsy

Cov ntaub ntawv pov thawj-raws li tib neeg

Txhawm rau tshawb nrhiav cov pov thawj thiab kev ntseeg siab ntawm cov ntawv thov tshuaj suav rau tib neeg, peb sau thiab tshuaj xyuas tib neeg kev sim tshuaj. Muaj plaub qhov kev tshawb fawb tib neeg kho mob qaug dab peg nrog cov tshuaj Suav uas tau luam tawm. Peb ntawm cov kev tshawb fawb tau tshawb xyuas cov tebchaw ntawm Suav tshuaj, thiab ib qho ntawm cov kev tshawb fawb tsom mus rau cov tshuaj ntsuab tshwj xeeb. Table 2 piav qhia cov ntsiab lus ntawm cov kev tshawb fawb no.

Saiko-ka-ryukotsu-borei-to (Chaihu-Longu-Muli-Tang) ua ke nrog Gastrodia elata thiab Uncaria rhynchophylla muaj cov tshuaj tiv thaiv antioxidant txo qhov qaug dab peg hauv cov neeg mob ntshav qab zib refractory los ntawm 13.4 土 3.4 txog 10.7 土 txhua hli (Wu. Ib., 2002). Ib hom tshuaj tiv thaiv kab mob vwm, muaj xws li Acorus tatarinowii, ArisaemA cum Bile, Gastrodia elata, Pseudostellaria heterophylla, Poria cocos, Citrus reticulata, Pinellia ternata, Aquilaria Sinensis, thiab Citrus aurantium, pab txhim kho lub hlwb thiab lub hlwb. Cov tsos mob ntawm tus kab mob epileptic hluav taws xob tawm los ntawm electroencephalography. Nws txo qis qhov qaug dab peg ntau zaus thiab lub sijhawm ntawm kev tawm tsam rau ntau hom mob vwm, nrog rau cov me nyuam mos spasm, autonomic, complex ib feem, holotonic-clonic, tsis muaj, localized Rolandic, psychomotor, myoclonus, thiab indefinite hom. Tag nrho cov txiaj ntsig zoo thiab kev rov qab los ntawm pab pawg kev cuam tshuam yog 83.33 thiab 54.3 feem pua, nqe 51.88 thiab 38.4 feem pua ​​​​hauv pawg tswj hwm, raws li (Ma et al., 2003). Dianxianning Pian yog tsim los ntawm Tuam Tshoj tshuaj Hoobkas ntawm Tuam Tshoj. Cov tshuaj muaj Valeriana jatamansi, Acorus tatarinowii, Uncaria rhynchophylla, Pharbitis nil, Euphorbia lathyris, Valeriana officinalis, thiab Nardostachys Chinensis, thiab tuaj yeem tswj tau qhov zaus thiab qhov hnyav ntawm refractory epilepsy raws li kev kho mob ntxiv. Qhov nruab nrab qaug dab peg txo qis 37.84 feem pua ​​​​hauv pab pawg kev cuam tshuam thaum tab sis 13.18 feem pua ​​​​hauv pawg tswj hwm, thiab cov neeg mob qaug dab peg maj mam txo nrog lub sijhawm kho (Nws li al., 2011).

Ib txoj kev tshawb fawb hauv 2018 tau tshawb nrhiav qhov ua tau zoo ntawm Ganoderma Lucidum spore hmoov rau kev kho cov neeg mob qaug dab peg. Cov tshuaj ntsuab hmoov tuaj yeem txo qhov nruab nrab ntawm qhov qaug dab peg txhua lub lim tiam los ntawm 3.1 土 0.8 mus rau 2.4 土 1.2, tab sis nws tsis tau qhia qhov sib txawv tseem ceeb hauv lub sijhawm ntawm kev qaug dab peg thiab lub neej zoo. Qhov tshwm sim tsis zoo tshaj plaws yog xeev siab, qhov thib ob yog plab tsis xis nyob, tom qab ntawd lwm tus yog ntuav, kiv taub hau, qhov ncauj qhuav, raws plab, mob caj pas, thiab epistaxis nyob rau hauv kev txiav txim (Wang li al., 2018).

HERB-DRUG INTERACTIONS

Kev sib xyaw ua ke ntawm cov tshuaj tiv thaiv kab mob vwm thiab tshuaj ntsuab yog ntau thiab nrov dua thiab siv tau tam sim no. Ib qho nyuaj kom paub meej tias cov tshuaj ntsuab-tshuaj cuam tshuam yog vim muaj cov khoom xyaw complex ntawm ib hom tshuaj ntsuab, los yog muaj ntau yam tshuaj ntsuab nyob rau hauv ib tug formula ntawm Suav tshuaj. Qee cov tshuaj ntsuab cuam tshuam nrog cov tshuaj tiv thaiv kab mob vwm tom qab ntawd txhim kho cov tshuaj tiv thaiv convulsive tau tshaj tawm. Muaj ob peb txoj kev tshawb fawb uas tshawb xyuas cov tshuaj ntsuab sib cuam tshuam thiab cov txheej txheem ua tau (Pearl li al., 2011; He et al., 2021). Hauv PTZ-induced seizure nas qauv, Nobiletin thiab Clonazepam txo qis qaug dab peg los ntawm kev tswj qhov sib npaug ntawm glutamate thiab GABA, modulating GABAa thiab GAD 65, inhibiting apoptosis, inhibiting BDNF-TrkB signaling pathway, thiab activating PI3K/AYktang. et al., 2018). Kev sib xyaw ntawm Naringin thiab Phenytoin hauv PTZ-kindled nas tuaj yeem txo qhov qaug dab peg, nce GABA thiab dopamine, txo glutamate, tiv thaiv oxidation, thiab tiv thaiv cov neurons hauv PTZ-induced qaug dab peg (Phani li al., 2018). Umbelliferone ua ke nrog phenobarbital los yog valproate elevates qhov pib ntawm electroconvulsions thiab txhim khu kev tiv thaiv convulsive efficacy nyob rau hauv MES-induced seizure nas qauv (Zagaja li al., 2015). Hauv qhov ncauj CBZ nas qauv, sinapic acid inhibits hepatic cytochrome P450 3A2, 2C11, thiab plab hnyuv P-glycoprotein ces ua rau kom CBZ nqus tau (Raish li al., 2019).

Cov kev tshawb fawb no tau tshaj tawm cov tshuaj ntuj, feem ntau yog cov nroj tsuag thiab tshuaj ntsuab, tuaj yeem txhim kho cov txiaj ntsig ntawm cov tshuaj tiv thaiv kab mob vwm. Hauv qee qhov kev tshawb fawb, Suav cov tshuaj tau pom cov txiaj ntsig zoo hauv kev kho mob nrog Western tshuaj uas tau hais hauv tsab xov xwm tshuaj xyuas no. Muaj cov kev tshawb fawb tsawg uas tshawb txog qhov tsis zoo ntawm kev kho ua ke. Nws tseem xav tau cov kev tshawb fawb zoo tshaj plaws los tshawb xyuas cov tshuaj ntsuab-tshuaj cuam tshuam ntawm cov tshuaj suav nrog cov tshuaj tiv thaiv kab mob vwm vim muaj pov thawj tsis txaus. Cov neeg mob uas siv tshuaj ntsuab raws li kev kho mob adjuvant yuav tsum qhia rau lawv cov kws kho mob kom tiv thaiv cov kev mob tshwm sim los yog cov teeb meem uas yuav ua rau muaj peev xwm ntawm cov tshuaj ntsuab-tshuaj cuam tshuam.

TXOJ CAI

Peb tau tshuaj xyuas cov tshuaj suav tshuaj uas yog siv rau hauv kev kho mob hauv kev mob vwm, tab sis lwm yam tshuaj ntsuab yuav tsis raug tshuaj xyuas vim muaj kev tshawb fawb tsawg dua. Qee cov tshuaj ntuj suav nrog cov tshuaj suav tsis muaj pov thawj ntau los lees paub cov tshuaj tiv thaiv kab mob vwm. Tsis tas li ntawd, feem ntau cov kev tshawb fawb tau tshawb fawb txog kev ua tau zoo thiab cov txheej txheem ntawm Suav tshuaj hauv kev kho mob qaug dab peg tab sis tsawg dua hais txog nws cov kev mob tshwm sim. Nws tseem tseem tsis muaj cov kws tshawb fawb los mob siab rau lawv cov kev siv tshuaj ntsuab-tshuaj cuam tshuam thiab kev phiv ntawm cov tshuaj suav. Raws li kev tshawb nrhiav cov ntaub ntawv, peb pom muaj ntau feem ntawm cov xov tooj ntawm tes thiab tsiaj cov qauv hauv kev kawm txog cov tshuaj tiv thaiv kab mob vwm ntawm Suav tshuaj, tab sis tib neeg kev sim tshuaj yog qhov tsis txaus. Rau kev nyab xeeb thiab kev ua tau zoo ntawm cov tshuaj suav tshuaj thiab cov tshuaj ntuj hauv cov pov thawj-raws li kev xyaum, txuas ntxiv tsim kom muaj kev sib tw tswj tau zoo yog xav tau tam sim ntawd.

XAIV

Anticonvulsive tshuaj ntsuab siv nyob rau hauv chaw kho mob chaw kho mob qaug dab peg thiab qaug dab peg yog tham nyob rau hauv tsab xov xwm tam sim no thiab lawv muaj peev xwm antiepileptic mechanisms, nrog rau kev tiv thaiv kab mob, antioxidation, GABAergic nyhuv li, NMDA receptor thiab sodium channel modulation, thiab neuroprotection.

benefit of cistanche

Cov txiaj ntsig ntawm cistanche deserticola

REFERENCES

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  5. Suav tshuaj yog holistic thiab tuaj yeem ua tus kheej rau cov neeg mob raws li lawv cov tsos mob. Kev kho mob noj zaub mov kho mob siv tshuaj suav tshuaj suav tau kis thoob ntiaj teb. Cov tshuaj ntsuab yog siv los ua kev kho mob lossis kev kho tseem ceeb hauv qee lub tebchaws, tshwj xeeb tshaj yog nyob rau sab hnub tuaj. Cov lus qhia yav tom ntej ntawm kev siv tshuaj ntsuab

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Koj Tseem Yuav Zoo Li