Kev Tshawb Fawb Txog Kev Tshawb Fawb Txog Pharmacological Mechanism Ntawm Tsob Ntoo Suav Tshuaj Saponins hauv Kev Kho Mob Parkinson's Disease

AbstractTus kab mob Parkinson(PD) yog cov kab mob neurodegenerative tshwm sim los ntawm ntau yam, uas ua rau tib neeg lub neej zoo, thiab tseem tsis muaj cov tshuaj kho tau zoo. Cov kev tshawb fawb pharmacological niaj hnub tau pom tiassaponinsrho tawm los ntawmSuav tshuaj ntsuabmuaj cov teebmeem tseem ceeb ntawm covkev kho mob ntawm PD, thiab lawv cov mechanisms suav nroginhibiting kev ua kom ntau dhau ntawm microglia,tswj cov neurotransmitters, anti-apoptosis, thiabanti-oxidative kev nyuaj siab. Ntawm lawv, ntau yam saponins hauv cistanche tuaj yeem kho thiab tswj ntau yam receptors thiab txoj hauv kev, thiab ua si los tiv thaiv PD los ntawm ntau txoj hauv kev thiab ntau lub hom phiaj, uas muaj kev tshawb fawb zoo. Tam sim no, kev tshawb fawb ntawm anti-PD mechanism ntawm saponins tsuas yog tsom rau cov tsiaj sim, thiab tseem tsis muaj kev tshawb fawb soj ntsuam zoo thiab cov ntaub ntawv tshawb fawb txog tshuaj pharmacokinetic, thiab tsis muaj kev tshawb fawb txog cov tshuaj muaj txiaj ntsig zoo, receptor. molecules, thiab signaling txoj kev muaj feem xyuam rau pharmacological teebmeem. Raws li kev txheeb cais, cov kauj ruam tom ntej yog pib tshawb fawb los ntawm cov ntsiab lus saum toj no, txhawm rau muab cov tswv yim thiab cov lus qhia rau kev soj ntsuam kev tshawb fawb thiab kev tsim tshuaj.

Cov lus tseem ceebSuav tshuaj saponins; Tus kab mob Parkinson; oxidative kev nyuaj siab; apoptosis; tshuaj xyuas

Nyem rau Cistanche bioflavonoids ntsiav tshuaj thiab cistanche rau Parkinson tus kab mob

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Tus kab mob Parkinson(PD) yog ib qho kab mob neurodegenerative mob ntev uas tshwm sim nyob rau hauv cov neeg laus, uas tshwm sim los ntawm tshee, nqaij tawv, hypokinesia, thiab dementia [1]. PD cuam tshuam rau 6.1 lab tus tib neeg thoob ntiaj teb, thiab ntau dua 1 feem pua ​​​​ntawm cov neeg muaj hnub nyoog 65 xyoos raug kev txom nyem los ntawm tus kab mob no, thiab qhov kev sib kis tau nce zuj zus txhua xyoo [2]. Cov ntaub ntawv cuam tshuam qhia tau tias qhov kev nthuav dav ntawm PD yuav ob npaug los ntawm 2030 [2]. Lub ntsiab kev kuaj mob ntawm PD yog qhov deterioration ntawm dopaminergic (DArgic) neurons thiab tsub zuj zuj ntawm cov protein -synuclein (-Syn) nyob rau hauv lub cytoplasm, thiab cov pathogenesis muaj feem xyuam rau apoptosis, oxidative kev nyuaj siab, neuroinflammation, thiab mitochondrial dysfunction. , neurotransmitter secretion disorders thiab lwm yam xwm txheej [3], tam sim no kev kho mob ntawm PD feem ntau siv qhov ncauj levodopa npaj thiab lwm yam dopamine receptor agonists. Cov tshuaj xws li levodopa muaj txiaj ntsig zoo rau cov neeg mob PD thaum ntxov thiab tuaj yeem ua tiav lub hom phiaj ntawm kev txhim kho kev ua ub no txhua hnub [4]. Txawm li cas los xij, raws li cov ntaub ntawv txuas ntxiv, kev siv cov levodopa mus sij hawm ntev thiab lwm yam kev npaj yuav ua rau muaj kev cuam tshuam tsis zoo [4], suav nrog kev hloov pauv ntawm lub cev muaj zog, dyskinesia, thiab cov teeb meem neuropsychiatric, thiab cov tshuaj siv tau nce zuj zus.

Yog li ntawd, nrhiav tau cov tshuaj PD mus sij hawm ntev tau dhau los ua qhov tseem ceeb tshaj plaws. Saponins tau ntev tau suav tias yog cov khoom tseem ceeb ntawm cov tshuaj suav tshuaj, thiab lawv muaj nyob rau hauv ntau hom tshuaj suav tshuaj, xws li cistanche, astragalus, yam, Polygala, Anemarrhena, thiab lwm yam. Saponins yog ib chav kawm ntawm cov khoom lag luam tseem ceeb ntawm cov nroj tsuag nrog kev ua haujlwm lom neeg, uas tuaj yeem muab faib ua triterpene saponins thiab steroidal saponins raws li cov qauv ntawm saponins. Cov ntaub ntawv pov thawj tseem ceeb tau pom tias saponins muaj cov txiaj ntsig tseem ceeb hauv kev tiv thaiv kab mob hauv nruab nrab paj hlwb (CNS) cov kab mob xws li PD, mob stroke, Alzheimer's disease, thiab Huntington's disease. Niaj hnub no botany, pharmacology thiab network pharmacology cov kev tshawb fawb tau pom tias saponins nyob rau hauv cov tshuaj suav tshuaj muaj peev xwm inhibit qhov ua kom ntau dhau ntawm microglial hlwb, tswj cov neurotransmitters, tiv thaiv apoptosis, tiv thaiv oxidative kev nyuaj siab, thiab tswj neurotrophy nyob rau hauv cov txheej txheem ntawm PD lesions. yam, thiab lwm yam. [6-7]. Nyob rau hauv daim ntawv no, kev tshawb fawb ntawm lub pharmacological mechanism ntawm tsoos suav tshuaj saponins nyob rau hauv kev kho mob ntawm PD yog sau tseg raws li nram no.

1 Saponin rau Inhibition ntawm kev ua kom ntau dhau ntawm microglia

Glial hlwb hauv CNS feem ntau muab faib ua microglia, astrocytes, thiab oligodendrocytes, uas ua lub luag haujlwm hauv kev tswj kev mob, metabolism, rov tsim dua tshiab, thiab myelination ntawm neurons. Microglia muaj lub zog tiv thaiv kab mob thiab tso tawm cov cytokines pro-inflammatory, overactivated microglia yuav nce interleukin (IL)-1 , IL-1 , IL-6, qog necrosis factor (TNF)- thiab kev ua haujlwm ntawm lub zais zis. Cov pa oxygen (ROS) txhim kho lub peev xwm phagocytic ntawm microglia thiab infiltration peev xwm ntawm lymphocytes, ua rau cov kab mob neuronal inflammatory teb, ntxiv induces apoptosis ntawm DArgic neurons, thiab thaum kawg ua rau

Rau PD[8,6]. Yog li ntawd, inhibiting qhov ua kom ntau dhau ntawm microglia thiab txo cov lus teb inflammatory yog ib lub tswv yim tseem ceeb rau kev kho mob ntawm PD. Lipopolysaccharide (LPS) yog ib qho ntawm cov txiaj ntsig zoo ntawm macrophages. LPS induces lub teeb liab hloov ntawm tus xov tooj hu-zoo li receptor 4 (TLR4) ua rau inflammatory teb los ntawm activating microglia; Nws tseem tuaj yeem ua kom cov mitogen-activated protein kinase (MAPKs) thiab cov kab mob ntsig txog kev hloov pauv, ua rau muaj kev qhia thiab tso tawm cov tshuaj kho mob, xws li nitric oxide (NO), ROS thiab pro-inflammatory cytokines [9]. Cov kev tshawb fawb tau lees paub tias txo cov phosphorylation ntawm phosphatidylinositol-3 kinase-protein kinase B (PI3K/Akt) tuaj yeem cuam tshuam qhov ua kom muaj zog ntawm nuclear (NF)-κB qhia txoj hauv kev thiab txo cov tiam ntawm ROS, yog li txo qhov kev mob tshwm sim. ntawm BV2 hlwb induced los ntawm LPS; ROS tiam yog inversely correlated nrog heme oxygenase-1 (HO-1), ib qho tseem ceeb nyob rau hauv kev tswj ntawm oxidative kev nyuaj siab thiab inflammatory teb nyob rau hauv lub peripheral thiab central paj hlwb [10-11].

LEE YY li al[12] pom tias ginsenoside Rg5 tuaj yeem tsis tsuas yog inhibit LPS-induced NO ntau lawm thiab tso tawm ntawm pro-inflammatory factor TNF-, tab sis kuj inhibit phosphorylation ntawm PI3K / Akt thiab MAPKs, tiv thaiv kev ua kom NF-κB. kev taw qhia txoj hauv kev, txo qis kev ua kom ntau dhau ntawm microglial hlwb; Nyob rau tib lub sijhawm, ginsenoside Rg5 inhibits kev tsim cov ROS los ntawm kev tswj hwm cov lus qhia ntawm HO-1 hauv LPS-stimulated BV2 hlwb, yog li inhibiting kev ua kom cov microglial hlwb, txo cov inflammatory teb, thiab tiv thaiv DArgic neurons. LID W et al[13] pom tias ginsenoside Rb1 tuaj yeem txo qhov tso tawm ntawm cov kab mob sib kis xws li TNF- thiab IL- los ntawm inhibiting kev ua haujlwm ntawm NF-κB kev taw qhia txoj hauv kev, thiab inhibit qhov ua kom ntau dhau ntawm microglia induced los ntawm LPS. Bisapenosides yog aglycones ntawm steroidal saponins, feem ntau yog muab rho tawm los ntawm disco cog thiab fenugreek noob. LEE SL et al [14] pom tias ob chav saponin pretreatment tuaj yeem tiv thaiv LPS-induced neurite shortening ntawm tyrosine hydroxylase (TH) zoo neurons nyob rau hauv midbrain neuron thiab glial hlwb, yog li txo qhov Qhia ntawm TNF- thiab inducible nitric oxide synthase (iNOS), inhibited LPS-induced activation ntawm extracellular signal-regulated kinase (ERK), thiab alleviated inflammatory teb. Polygala saponin yog cov khoom xyaw nquag muab rho tawm los ntawm Polygala. Yuan Huili et al. [15] ua cov kev tshawb fawb tsiaj thiab pom tau tias Polygala saponin tuaj yeem cuam tshuam LPS-vim cov khoom tsim tawm los ntawm substantia nigra (SN) microglial hlwb thiab txo qhov poob ntawm DArgic neurons hauv SN, yog li txhim kho tus cwj pwm kev puas tsuaj ntawm inflammatory PD qauv nas.

2 Regulating neurotransmitters

Neurotransmitters yog nruab nrab ntawm intercellular signal transduction, nrog rau cov amino acids xws li glutamic acid, aminobutyric acid (GABA), monoamines xws li dopamine (DA), 5-hydroxytryptamine thiab lwm yam neurotransmitters. Neurotransmitter secretion disorders yuav ua rau CNS mob, induced PD thiab lwm yam kab mob neurological [16]. Kev tshawb fawb lees paub tias

Kev nthuav qhia ntawm GABA transmitters tuaj yeem txo cov paj hlwb apoptosis, txo excitotoxicity, inhibit tiv thaiv kab mob, thiab lwm yam, thiab ua lub luag haujlwm neuroprotective [17].

Liu Yan [18] pom tias ginsenoside Rb1 tuaj yeem thaiv glutamate excitotoxicity hauv SN striatum thiab cortical pyramidal system los ntawm kev tswj glutamate transporter GLT-1, thiab txhim kho 1-methyl-4- benzene

Methyl-1,2,3,6-tetrahydropyridine (MPTP)-induced motor deficits nyob rau hauv PD nas, tiv thaiv DArgic neuron tuag, suppresses -synuclein qhia thiab astrogliosis. LIU Y et al [19] kuj tau lees paub tias ginsenoside Rb1 tuaj yeem nce thiab txhawb cov ntsiab lus thiab kev sib kis ntawm GABA hauv prefrontal cortex ntawm cov nas, txhawm rau txo cov kev tsis sib haum xeeb thiab kev txawj ntse hauv cov nas induced los ntawm MPTP. Cov yam ntxwv ntawm PD yog poob ntawm DArgic neurons hauv SN thiab txo qis DA qib hauv striatum. DA yog synthesized nyob rau hauv SN thiab yog ib qho inhibitory neurotransmitter. 1-methyl-4-phenylpyridinium ion (MPP ntxiv rau

) rau hauv DArgic neuron hlwb los ntawm DA transporter, thiab txo cov synthesis ntawm DA los ntawm inhibiting cov kev ua ntawm intracellular tyrosine hydroxylase (TH) [20].

TH yog tus nqi-txheej enzyme hauv DA synthesis thiab tus cim ntawm DArgic neuron ciaj sia taus. Thaum TH yog inhibited, DA qib tau txo qis, thiab PD cov tsos mob tshwm sim. WANG JY li al[21] pom tias American ginsenoside-F11 tuaj yeem ua rau MPP ntxiv rau -induced extracellular DA qib hauv striatum ntawm PD nas.

Ua kom lub cev muaj zog ntawm TH hauv SN, txhim kho qhov degeneration ntawm DArgic neurons hauv SN thiab DA depletion hauv striatum, yog li tiv thaiv kev ua haujlwm ntawm lub paj hlwb ntawm cov neeg mob PD.

3 Anti-apoptosis

Apoptosis yog cov txheej txheem pathological nyob rau hauv uas muaj ntau yam stimulating yam ua rau cell tuag los ntawm kev ua kom lub cell tuag cov kev pab cuam. Apoptosis ntawm DA paj hlwb nyob rau hauv midbrain SN thiab striatum yog ib qho ntawm cov laj thawj tseem ceeb rau lub pathogenesis ntawm PD. Thaum lub sij hawm pathogenesis ntawm PD, vim muaj kev hloov nyob rau hauv lub sab hauv thiab sab nraud ib puag ncig ntawm DArgic neurons, ib co apoptosis hais txog cov noob xws li cysteine ​​protease -3 (caspase-3), B lymphocyte qog-2 protein (Bcl-2) thiab Bcl-2 Related X protein (Bax) induces DArgic neuron tuag los ntawm regulating cell tuag signaling pathway [22]. Ntawm lawv, kev hloov pauv ntawm Bcl-2/Bax thiab kev qhia ntawm caspase yog qhov tseem ceeb ntawm PD

Ib qho cim tseem ceeb ntawm apoptosis hauv cov hlwb neuron, Bcl -2 yog cov tshuaj tiv thaiv apoptotic uas ncaj qha lossis ncaj qha tiv thaiv kev ncaj ncees ntawm cov mitochondrial membrane sab nrauv, tiv thaiv cell c tso thiab mitochondria-mediated cell puas, thiab pro-apoptotic. protein Bax Nws txhawb kev tso tawm ntawm c los ntawm mitochondrial hlwb [23]. Cov kev tshawb fawb tau pom tias MPTP-induced

Hauv PD nas, qhov kev qhia ntawm Bax protein ntau ntxiv thiab kev qhia ntawm Bcl -2 poob qis, uas ua rau qhov tsis txaus ntawm Bcl-2/Bax, Bax translocation mus rau mitochondria, ua rau muaj kev nce ntawm mitochondrial colloid. osmotic siab, ua raws li los ntawm o, txheej membrane rupture, tso cell c, thiab activation ntawm caspase qhia, induce neuronal apoptosis [24].

Diosgenin, a steroidal saponin, attenuates MPP plus -induced neuronal apoptosis los ntawm down-regulating cov lus qhia ntawm activated caspase -3 thiab Bax thiab ua kom cov lus qhia ntawm Bcl -2 [25]. Ginsenoside Rg1 tsis tsuas yog muaj cov nyhuv ntawm nourishing qab haus huv[26], Chen XC li al.[27] Cov kev tshawb fawb tshawb fawb pom tias ginsenoside Rg1 tseem tuaj yeem txo qis DA-induced ROS tiam thiab mitochondrial c tso tawm hauv PC12 hlwb, thiab txo cov qib iNOS thiab TSIS tsim, yog li txo cov neuronal apoptosis. Lwm txoj kev tshawb fawb tau pom tias ginsenoside Rg1 tuaj yeem txo qis apoptosis thiab tiv thaiv DArgic neurons los ntawm inhibiting qhov ua kom ntawm caspase-3 [28].

Asiaticoside, ib qho triterpenoid saponin cais los ntawm Suav tshuaj ntsuab tshuaj ntsuab Centella asiatica, tuaj yeem ua rau qeeb MPTP-vim kev poob qis hauv DA qib hauv striatum, nce Bcl-2 / Bax ratio, thiab inhibit

Nws tuaj yeem nres qhov apoptosis ntawm DA paj hlwb thiab rov qab cov txheej txheem ntawm PD [29]. Aescin yog triterpenoid saponin los ntawm cov noob txiv ntoo txiv ntoo. Cov kev tshawb fawb tau lees paub tias aescin tuaj yeem tiv thaiv cov neurons los ntawm inhibiting caspase ntau lawm, tswj Bax/Bcl-2 tshuav nyiaj li cas, tiv thaiv mitochondrial dysfunction thiab paj hlwb apoptosis Lub luag hauj lwm ntawm cov hlwb [30]. Caspases tsis ua haujlwm raws li ib txwm muaj. Thaum qhib los ua cov nyhuv, caspases tsim cov tshuaj tiv thaiv cascade thiab koom nrog cov txheej txheem ntawm apoptosis [31]. Saikosaponin D yog lub ntsiab active ingredient nyob rau hauv lub extract ntawm Bupleurum chinensis, ib txwm suav tshuaj. Kev sim tau pom tias saikosaponin D tuaj yeem txo MPP ntxiv -induced neuronal apoptosis los ntawm inhibiting caspase-3 kev ua [32].

4 Anti-oxidative kev nyuaj siab

Oxidative kev nyuaj siab tshwm sim nyob rau hauv qhov tshwm sim thiab kev loj hlob ntawm ntau yam kab mob, xws li hlav, dementia, PD, thiab lwm yam. Yog vim li cas yog vim li cas muaj coob tus dawb radicals thiab ROS uas tsis raug tshem tawm raws li lub sij hawm ua rau ib qho kev tsis txaus siab nyob rau hauv cov theem ntawm cov dawb radicals. oxides / antioxidants hauv lub cev, yog li ua rau kev puas tsuaj ntawm cov ntaub so ntswg. Yog li ntawd, alleviating oxidative stress yog ib qho tseem ceeb ntsuas los txo cov paj hlwb puas hauv PD kho. Cov kev tshawb fawb tau pom tias cov tshuaj tua kab mob antioxidants thiab lwm txoj hauv kev tswj hwm xws li thioredoxin -1 (Trx-1), catalase, glutathione peroxidase (GPX), glutathione-S-transferase (GST), Janus kinase 2 (JAK2), trans

Cov ntaubntawv povthawj siv activator 3 (STAT3), nuclear factor E2- cuam tshuam txog 2 (Nrf2), thiab HO-1 tuaj yeem txo cov txheej txheem ntawm oxidative kev nyuaj siab thiab kev puas tsuaj, yog li tiv thaiv cov neurons hauv cov neeg mob PD [33] .

Triol saponins (PTS), lub ntsiab lus tseem ceeb hauv cistanche, tau pom tias txo qis mitochondria-mediated apoptosis thiab MPTP los ntawm kev nce qhov kev qhia ntawm Trx-1 thiab inhibiting overexpression ntawm oxidative stress factor cyclooxygenase (COX){{2 }} induced apoptosis hauv substantia nigra pars compacta (SNc) neurons [34]. Rotenone yog cov khoom siv tshuaj tua kab uas muaj nyob hauv cov nroj tsuag, uas tuaj yeem cuam tshuam los ntawm cov ntshav-hlwb thaiv mus rau hauv lub hlwb thiab ua rau cov paj hlwb puas. Rotenone induces neuronal apoptosis hauv vitro thiab hauv vivo sim qauv

thiab PD nta (piv txwv li, levodopa-teb lub cev muaj zog tsis txaus, SN hlau tsub zuj zuj, thiab -Syn tsub zuj zuj), nws cov txheej txheem cuam tshuam nrog nws cov inhibition ntawm mitochondrial complex I, nce ROS, thiab inducing qhov tsis ua hauj lwm ntawm ubiquitin-proteasome system, ua rau neuronal. apoptosis hais txog kev hloov pauv [35]. Cov kev tshawb fawb tau lees paub tias ginsenoside Rd thiab saponin Re

Tag nrho cov ntawm lawv tuaj yeem cuam tshuam qhov nce ntawm intracellular ROS thiab tsub zuj zuj ntawm cov khoom lipid peroxidation tshwm sim los ntawm rotenone, thiab txhim kho kev ua haujlwm ntawm glutathione system. Cov txheej txheem ntawm kev txiav txim yuav cuam tshuam nrog kev ua kom Nrf2 teeb liab txoj hauv kev. transcription factor, uas plays lub luag hauj lwm tseem ceeb hauv inducing lub cev muaj peev xwm antioxidant [36]. Han Yingjie [37] tau ua pov thawj tias tom qab kev tswj hwm intragastric ntawm ginsenoside Rg3 rau rotenone-induced PD nas, tus naj npawb ntawm TH-positive neurons hauv substantia nigra ntawm cov nas, qhov nruab nrab ntom ntawm TH-positive paj fibers, thiab cov ntsiab lus DA hauv lub striatum tag nrho tau nce ntau. Thiab qib ROS hauv SN tau txo qis; Nyob rau tib lub sijhawm, ginsenoside Rg3 tuaj yeem txhim kho lub cev muaj zog ntawm rotenone-induced PD nas los ntawm kev ua haujlwm ntawm glutathione cysteine ​​ligase subunit nrog cov nyhuv antioxidant. Astragaloside Ⅳ tseem hu ua astragaloside IV. Huang Xiaojing et al. [38] tau tshaj tawm tias astragaloside Ⅳ ua lub luag haujlwm tiv thaiv oxidative kev ntxhov siab los ntawm kev tswj hwm JAK2-STAT3 txoj kev taw qhia thiab txo qis MPP ntxiv rau -induced paj hlwb puas tsuaj. liab -1 yog ib tug serine/threonine kinase uas txo oxidative kev nyuaj siab nyob rau hauv mitochondria, thiab pdr-1 yog ib tug E3 enzyme koom nyob rau hauv lub ubiquitin-mediated proteasome txoj kev; kev hloov pauv hauv pdr-1 ua rau endoplasmic reticulum stress Hypersensitivity, tag nrho cov kev txo qis ntawm ubiquitination ua rau cov protein ntau sib sau ua ke; ubc-12 (ubiquitin coupling enzyme), raws li E2 enzyme, khi rau ubiquitin molecules los ntawm thioester bonds, thiab ua kom E3 enzymes rau proteasomal degradation[39-40] . Aspartoside yog steroidal saponin. SMITA SS et al. [41] pom tias aspartoside tuaj yeem tswj hwm PD-txog cov noob pdr-1, ubc-12 thiab liab dawb-1 los ntawm kev siv ubiquitin-mediated proteasome system los txo oxidation Kev nyuaj siab, thiab pom tias aspartoside tuaj yeem txo cov cellular ROS, protein carbonylation ntsig txog oxidative puas. Glycolipidin ginsenosides, ib qho derivative cais los ntawm cistanche, tau pom tias muaj cov teebmeem neuroprotective tiv thaiv ntau yam kab mob hauv lub paj hlwb, thiab cov txheej txheem ntawm kev ua yog cuam tshuam nrog Nrf2/HO-1 txoj hauv kev, uas tswj SN thiab striatum hauv cov nas hauv vivo.

Kev nthuav qhia ntawm inflammatory cytokines, iNOS thiab apoptosis cov cim kom txo tau oxidative kev nyuaj siab kuj tuaj yeem txo qis -Syn txuam nrog hauv SN thiab striatum [42].

5 Kev xaus

Vim muaj coob tus neeg mob thiab qhov nyuaj ntawm kev kho mob, PD tau dhau los ua qhov chaw kub hauv kev tshawb fawb thoob ntiaj teb. Los ntawm induction thiab combing ntawm lub pharmacological mechanism ntawm tsoos suav tshuaj saponins nyob rau hauv kev kho mob ntawm PD, nws pom tau hais tias ntau yam saponins nyob rau hauvcistanchetuaj yeem kho thiab tswj ntau yam receptors thiab txoj hauv kev, thiab tawm tsam PD los ntawm ntau txoj kev thiab ntau lub hom phiaj, uas muaj kev tshawb fawb zoo. Daim ntawv no xaus lus tias cov txheej txheem ntawm ntau cov saponins hauv kev kho mob ntawm PD tseem tsis tau ua tiav cov kev tshawb fawb soj ntsuam zoo, thiab tsuas yog nyob twj ywm ntawm qib tsiaj thiab hauv vitro cell thwmsim. Txawm li cas los xij, kev nqus thiab cov metabolism hauv cov tshuaj hauv tib neeg lub cev nyob rau hauv cov kab mob pathological txawv ntawm cov tsiaj txhu thiab kev sim hauv vitro cell. Pharmacokinetics tseem tsis paub meej thiab tsis muaj pov thawj kev tshawb fawb. Tsis tas li ntawd, saponins yog monomer Cheebtsam ntawmtshuaj suav tshuaj, thiab muaj ntau txoj kev rho tawm. Muaj teeb meem xws li cov qauv sib txawv thiab qhov sib txawv ntawm kev siv tshuaj. Cov tshuab rho tawm thiab cov qauv yuav tsum tau txhim kho ntxiv. Nyob rau hauv lub neej yav tom ntej, kev tshawb fawb soj ntsuam thiab kws tshuaj tuaj yeem ua tiav raws li qhov tsis txaus siab saum toj no, txhawm rau muab kev txhawb nqa theoretical rau kev siv tshuaj kho mob tom ntej thiab kev tsim tshuaj tshiab.