Fibromyalgia Thiab Irritable Bowel Syndrome Interaction: Ib Lub Luag Haujlwm Ua Tau Rau Gut Microbiota Thiab Gut-Brain Axis Ⅱ

2. Tib neeg Microbiota thiab Gut-Brain Axis hauv Kev Noj Qab Haus Huv thiab Kab Mob

Tib neeg lub plab microbiota muaj ib qho nyuaj, dynamic, thiab heterogeneous ecosystem nyob los ntawm ntau tshaj ib trillion microorganisms nrog rau cov kab mob, archaea, fungi, kab mob, protozoa, thiab helminths interacting nrog ib leeg thiab nrog tus tswv [39–41]. Cov kab mob hauv tib neeg lub plab microbiota suav nrog xya phyla: Bacteroidetes, Firmicutes, Actinobacteria, Fusobacteria, Proteobacteria, Verrucomicrobia, thiab Cyanobacteria, nrog Bacteroidetes thiab Firmicutes sawv cev ntau dua 90% ntawm tag nrho cov kab mob [42]. Qhov sib piv ntawm Firmicutes thiab Bacteroidetes yog suav tias yog ib qho tseem ceeb ntawm kev coj mus rau hauv tus account rau kev kho mob plab hnyuv [43]. Lub Bacteroidetesphylum suav nrog Bacteroides thiab Prevotella genera, Firmicutes phylum suav nrog Clostridium, Eubacterium, thiab Ruminococcus genera [44].

Nyem rau sai ua laxative

Tseem, cov txheeb ze nplua nuj ntawm cov kab mob phyla mayvary heev ntawm cov tib neeg [44]. Kev sib raug zoo ntawm tib neeg tus tswv tsev thiab gutmicrobiota yog ob qho tib si commensal thiab mutualistic: thaum tus tswv tsev muab ib qho ecological niche rau tag nrho cov Cheebtsam ntawm lub plab microbiota, ib co ntawm lawv pab txhawb rau host txoj kev loj hlob, qoj, thiab metabolism. Ua ntej ntawm tag nrho cov, los ntawm kev nyob thiab replicating. Nyob rau ntawm txoj hnyuv, plab microbiota generatesa ruaj khov system uas tiv thaiv kev cuam tshuam ntawm cov kab mob pathogenic. Tsis tas li ntawd, gutmicrobes synthesizes ntau chav kawm ntawm cov as-ham xws li branched-chain amino acids, amines, phenols, indoles, phenylacetic acid, thiab vitamins [41,45-47]. Tshwj xeeb, Bacteroides koom nrog hauv kev sib txuas ntawm biotin, riboflavin, pantothenate, thiab ascorbate, thaum Prevotella koom nrog hauv thiamine thiab folate synthesis [44].

Lub plab microbiota txhawb nqa cov synthesis ntawm cov kua tsib acids, thiab cov roj (cholesterol) nrog rau kev nqus ntawm calcium, magnesium, thiab hlau [46,48] . Ntxiv rau, nyob rau hauv kev ntxhov siab, nws txhim kho qhov nqus ntawm cov as-ham los ntawm kev ua kom ntev ntawm plab hnyuv villi thiab microvilli. .Gut microbiota yog suav hais tias yog tus thawj tswj hwm ntawm cov metabolism ntawm indigestiblecarbohydrates, xws li cellulose, pectin, thiab oligosaccharides, rau hauv luv-chain fatty acids (SCFAs) (acetate, propionate, thiab butyrate), uas yog tsim los ntawm Firmicutes, Bacteroidetes thiab Qee cov kab mob hauv plab anaerobic [49]

Lawv tau sai absorbed los ntawm epithelial hlwb los ntawm passive diffusion los yog active thauj los ntawm G protein-coupledreceptors xws li GPR41, GPR43, thiab GPR109A [50]. SCFAs, tshwj xeeb tshaj yog butyric acid, thiabbutyrate, paub tias yog ib qho tseem ceeb rau kev saib xyuas cov hnyuv hauv plab vim lawv lub peev xwm los txhawb kev qhia ntawm mucins, antimicrobial peptides, thiab tightjunction proteins [41,45,51,52].SCFAs kuj tau ua. pom tau hais tias muaj anti-inflammatory teebmeem. Hauv particular, los ntawm kev khi rau GPR43, butyrate induces zus tau tej cov anti-inflammatorycytokines xws li TGF thiab IL-10 raws li zoo raws li upregulation ntawm FoxP3, tus tswv transcription yam tseem ceeb ntawm kev tswj T hlwb (Tregs) [50]. Butyrate kuj inhibits histone deacetylaseactivity thiab downregulates lub nuclear factor-κ, ib tug ntawm cov tseem ceeb mediators ntawm inflammatory teb [50]. Tsis tas li ntawd, kev sib xyaw ua ke ntawm propionate thiab butyrateinhibits lipopolysaccharide (LPS)-induced o los ntawm activating Tregs thiab txo cov zus tau tej cov inflammatory cytokines xws li IL-6 thiab IL{19}} [53].

Cov pov thawj preclinical kuj qhia tau hais tias lub plab microbiota thiab nws cov metabolites koom nrog hauv kev hloov pauv tus cwj pwm thiab cov txheej txheem hauv hlwb, suav nrog kev ntxhov siab, kev coj cwj pwm, thiab kev kho mob [54]. Lub plab microbiota tau raug tshaj tawm tias muaj peev xwm tossynthesize ntau yam neurotransmitters thiab neurotrophic yam, xws li dopamine, noradrenaline, serotonin, gamma amino butyric acid (GABA), acetylcholine, thiab histamine, uas tuaj yeem cuam tshuam rau hauv nruab nrab lub paj hlwb thiab peripheral enteric systems [40, 55] ib. Kev taw qhia los ntawm entericmicrobiota mus rau lub hlwb yog kho los ntawm cov hlwb epithelial, receptor-mediated signaling, thiab ncaj qha stimulation ntawm lamina propria hlwb [4]. Ntawm qhov tod tes, lub hlwb actson enteric microbiota ntawm kev hloov hauv plab hnyuv motility, permeability, thiab tso tawm.kev taw qhia cov molecules hauv plab lumen.

Qhov kev sib txuas no, hu ua lub plab-hlwb axis, yog qhov tseem ceeb heev rau kev tswj lub plab zom mov homeostasis.Lub plab-hlwb axis tseem koom nrog hauv kev tswj cov neuronal, endocrine, thiab immunepathways [38,40,56]. Yog li ntawd, ib qho microbiota ruaj khov yog qhov tseem ceeb rau kev saib xyuas ntawm normalgut physiology thiab kev xa mus raws lub plab-hlwb axis. Ntawm qhov tsis sib xws, dysbiosis, piv txwv li, qhov tsis txaus ntseeg hauv cov plab hnyuv microbial, cuam tshuam tsis zoo rau cov kab mob guthomeostasis thiab yuav ua rau muaj kev ua tsis zoo ntawm lub plab-hlwb axis [43,57], nrog rau kev puas tsuaj ntawm kev ua haujlwm hauv nruab nrab ntawm kev nkag siab [57,58] ]. Ntau yam kev pheej hmoo tau raug pom zoo los cuam tshuam nrog qhov pib ntawm lub plab dysbiosis: raug tshuaj tua kab mob thiab xenobiotics, xws li cov hlau hnyav thiab tshuaj tua kab, rog rog, rog thiab qab zib ntau ntau, cov noob caj noob ces, hnub nyoog, thiab hom yug [40, 51].Dysbiosis tau txuam nrog cov pathogenesis ntawm ntau cov kab mob inflammatory [17,25,51]. Ntxiv mus, kev hloov pauv hauv cov kab mob plab microbiota tau tshaj tawm tsis ntev los no hauv FM [59,60].

Yog li, dysbiosis tuaj yeem sawv cev rau qhov tsis zoo rau kev txhim kho FM. Ua ke nrog dysbiosis, SIBO (cov kab mob hauv plab me me) sawv cev rau lwm hom kev hloov pauv ntawm lub plab microbiota uas cuam tshuam rau kev sib txuas lus hauv hlwb [61]. Nyob rau hauv ib txwm muaj, cov kab mob Gram-zoo nrog 103 kab mob / mL feem ntau colonize sab sauv ntawm cov hnyuv. Ntawm qhov tsis sib xws, thaum lub sij hawm SIBO, cov kab mob hauv cov kab mob tau nce siab tshaj 105-106 kab mob / mL [62]. Tib neeg tus tswv tswj xyuas kev loj hlob ntawm cov kab mob enteric los ntawm ntau lub tshuab. Tseeb tiag, gastric acids tshem tawm cov kab mob, peristalsis cheb cov kab mob mus rau hauv txoj hnyuv thiab lawv txoj kev nkag tau raug tiv thaiv ua tsaug rau cov kev sib tshuam nruj ntawm cov epithelialcells.

Tsis tas li ntawd, ntau cov khoom siv tshuaj tua kab mob ua rau kom txwv tsis pub cov kab mob overgrowth [63,64]. Ib qho kev puas tsuaj hauv ib lossis ntau dua ntawm cov kev tiv thaiv homeostatic nrog rau qee yam kev txawv txav ntawm lub cev ua rau SIBO txoj kev loj hlob. Feem ntau, cov neeg mob uas muaj SIBO tam sim no cov tsos mob tsis tshwj xeeb, xws li tsam plab, mob plab, mob lossis tsis xis nyob, raws plab, qaug zog, ntxhov siab / kev nyuaj siab, thiab tsis muaj zog [4]. Qhov tseeb, qhov sib xws ntawm cov tsos mob ntawm FM thiab SIBO tau pom, qhia txog lub luag haujlwm ntawm SIBO hauv FM [65,66].

3. Microbiota Composition nyob rau hauv FM Cov Neeg Mob: Zoo sib xws thiab sib txawv nrog IBS

Raws li tau hais dhau los, kev hloov pauv hauv plab microbiota tuaj yeem cuam tshuam rau lub plab-brainaxis [43,67]. Yog li, nws zoo li tias dysbiosis tuaj yeem ua lub luag haujlwm hauv FM pathogenesis los ntawm kev hloov pauv kev nkag siab thiab kev ua haujlwm ntawm qhov mob stimuli [2,68]. Raws li, kev soj ntsuam ntawm gut microbiota hauv FM cov neeg mob tau pom tias muaj kev hloov pauv [59,60].

Tshwj xeeb, cov kab mob uas yog cov tsev neeg ntawm Lachnospiraceae thiab Ruminococcaceae nrog rau Eubacterium thiab Bifidobacterium genera pom muaj qis dua nyob rau hauv lub plab microbiotaof FM cov neeg mob, thaum Rikenellaceae tsev neeg thiab ntau hom ntawm Clostridiaclass tau overrepresented [59,60]. Ntau yam ntawm cov tsiaj uas nws cov nplua nuj hloov pauv hauv cov neeg mob FM tau koom nrog hauv SCFA metabolism. Tseeb, Lachnospiraceae koom nrog hauv kev sib txuas ntawm butyric acid, thaum Eubacterium hom thiab Faecalibacterium prausnitzii, belongs rau Ruminoccaceae, tsim butyrate [53]. Yog li, lawv cov depletion yuav pom tias muaj kev puas tsuaj ntawm SCFAs, uas nyob rau hauv lem yuav cuam tshuam rau lub plab permeability.Vim qhov tseem ceeb ntawm cov kab mob plab yog Gram-negative-species shedding LPS, ib tug leaky gutbarrier yuav ua rau nws systemic tso tawm. Nyob rau hauv lub periphery, LPS tuaj yeem txhim kho qhov mob pom los ntawm kev cuam tshuam ncaj qha nrog peripheral neurons lossis los ntawm kev ua kom dav dav ntawm lub cev tiv thaiv kab mob, uas ua rau secretes inflammatory mediators sensitizing nociceptorneurons [69].

Tsis tas li ntawd, SCFAs hloov kho qhov permeability ntawm cov ntshav-hlwb thaiv kev cuam tshuam los ntawm kev koom tes rau lub koom haum raug ntawm cov kev sib tshuam nruj [70]. Yog li ntawd, nyob rau hauv cov ntaub ntawv ntawm SCFA depletion, LPS kuj tseem tuaj yeem ncav cuag lub hauv paus paj hlwb (CNS) thiab ua haujlwm ntawm theem nrab. Qhov kawg tab sis tsis kawg, SCFAs tawm dag zog los tiv thaiv kev ua haujlwm los ntawm kev txo cov leukocytes 'chemotaxis, adhesion, thiab secretion ntawm pro-inflammatory yam, yog li tiv thaiv cov teebmeem ntawm LPS [71]. Txawm li cas los xij, cov txiaj ntsig zoo no yog tshuaj-nyob ntawm seb, txij li thaumhigh concentrations ntawm butyrate tau pom tias yuav txhawb apoptosis ntawm plab hnyuv hlwb, yog li cuam tshuam cov hnyuv barrier [72].

Hauv cov neeg mob FM, ntau SCFAs-ua cov kab mob ntawm Clostridia chav kawm tau nthuav dav [60]. Nyob rau hauv txoj kab nrog qhov kev soj ntsuam no, cov concentration ntawm butyric acid tau nce nyob rau hauv cov ntshav thiab cov zis ntawm cov kev kawm no [60,68] txhawb nqa lub tswv yim ntawm dysregulated SCFA ntau lawm hauv FM cov neeg mob ntau dua li qhov tsis muaj peev xwm. Ntawm qhov tod tes, cov kab mob los ntawm Bifidobacterium. genus koom nrog hauv neurotransmitter metabolism los ntawm synthesizing GABA los ntawm glutamate [73]. GABA yog qhov tseem ceeb tshaj plaws inhibitory neurotransmitter nyob rau hauv CNS thiab ua los ntawm inducing neuron hyperpolarization thiab nce lub excitability pib, yog li tiv thaiv qhov mob xaav thiab kis los ntawm nociceptive neurons. Conversely, glutamate ua oppositely thiab yog li sawv cev rau lub loj excitatory neurotransmitter koom nyob rau hauv mob rhiab heev [74].

Raws li qhov tshwm sim, qhov txo qis ntawm cov kab mob tuaj yeem tsim GABA, xws li Bifidobacterium, yuav hloov GABA / glutamate tshuav nyiaj li cas rau qhov kawg. Raws li, peripherallevels ntawm glutamate tau pom tias tau nce hauv FM cov neeg mob [59]. Zuag qhia tag nrho, cov ntaub ntawv pov thawj no qhia tias qhov kev txhim kho thiab nthuav qhov mob rhiab heev tau pom hauv FM cov neeg mob tuaj yeem cuam tshuam lub peev xwm ntawm plab microbiota los tsim GABA uas, nrog rau kev nce permeability ntawm txoj hnyuv, yuav ua rau muaj kev sib txuam ntawm glutamate thiab nthuav dav neurons. Cov kab mob ntawm cov kab mob Clostridia kuj tseem cuam tshuam nrog cov tsos mob hnyav, suav nrog kev mob hnyav, mob hnyav, qaug zog, thiab hloov pauv pw tsaug zog [60]. Ntawm Clostridia cov tswv cuab, Clostridium cinders tau raug npaj los txhim kho qhov mob rhiab heev vim lawv lub luag haujlwm hauv kev tsim cov kua tsib acids. C. scindens yog ib hom tsiaj muaj peev xwm ua tau 7a-dehydroxylation uas xav tau rau kev hloov pauv los ntawm cov kua tsib theem nrab hauv cov kua tsib acids [75], uas tau thov kom koom nrog nociception [38].

Yog li, cov kua tsib theem ob tau pom tias muaj kev hloov pauv loj hauv cov ntshav los ntawm cov neeg mobFM thiab muaj feem cuam tshuam nrog kev nce ntxiv ntawm C. cinders thiab kev hloov pauv dav dav hauv cov txheeb ze ntawm cov kab mob uas muaj nyob rau hauv cov kua tsib acid hauv plab. Tshwj xeeb, qhov txo qis hauv -muricholic acid tau tshaj tawm, uas paub tias yuav ua kom puas los ntawm C. scindens. Ntxiv mus, -muricholic acid serum concentration tsis zoo cuam tshuam nrog FM cov tsos mob, tsis ncaj qha txhawb nqa lub luag haujlwm pathogenetic ntawm C. cinders thiab bile acid alterations raws li ib tug downstream mechanism nyob rau hauv FM [76,77]. Ntawm qhov tod tes, cov kua tsib kua qaub yog tshuaj lom rau cov kab mob Gram-zoo thiab ua rau muaj kev nthuav dav ntawm Clostridia, depleting cov txiaj ntsig zoo tib lub sijhawm [78].

Yog li, dhau los ntawm cov lus pom zoo, cov kua qaub yuav ntxiv dag zog rau lub plab dysbiosis pom hauv FM.Interestingly, cov kev hloov pauv hauv plab microbiota muaj nyob hauv FM kuj tau tshaj tawm hauv IBS (Table 1). Tsev neeg Ruminococcaceae, suav nrog F. prausnitzii, thiab Bifidobacterium genus raug txo qis hauv cov neeg mob IBS [52,79–81]. F. prausnitziiabundance cuam tshuam tsis zoo nrog cov tsos mob 'qhov hnyav hauv IBS [82], nyob rau hauv txoj kab nrog nws lub luag haujlwm hauv kev tiv thaiv plab hnyuv los ntawm SCFA ntau lawm. Interestingly, nyob rau hauv ib tug non-inflammatory IBS-zoo li nas qauv, cov tsos mob ntawm tus kab mob thiab F. prausnitzii depletion tau pom nyob rau hauv cov tsiaj muaj kev ntxhov siab nyob rau hauv thaum ntxov lub neej [83], ntxiv dag zog rau lub tswv yim hais tias neurotransmission yuav modulate plab microbiota muaj pes tsawg leeg los ntawm lub plab-hlwb axis, uas nyob rau hauv lem. cuam ​​tshuam qhov pib ntawm qhov mob stimuli. Ntawm qhov tod tes, cov kab mob los ntawm Bifidobacterium genus tau pom tias tau siv ntau yam kev tiv thaiv rau cov kab mob guthomeostasis, xws li upregulation ntawm nruj hlws ris proteins nrog rau downregulation ntawm inflammatory mediators 'kev tsim tawm los ntawm cov hnyuv thiab lub cev tiv thaiv kab mob [84–{9}} ].Yog li ntawd, qhov depletion ntawm Bifidobacterium genus tuaj yeem ua rau muaj kev mob plab hnyuv hauv IBS thiab FM.

Txawm li cas los xij, vim nws muaj peev xwm txo qis qhov mob ntawm lub cev [86] thiab tsim GABA [73], Bifidobacterium genus kuj tseem yuav cuam tshuam rau CNS.Bifidobacterium genus abundance tau pom tias tsis zoo cuam tshuam nrog kev nyuaj siab hauv IBS cov neeg mob. [87,88].Ntau cov pov thawj tsis sib haum xeeb tau tshaj tawm txog Lachnospiraceae. Ib qho enrichmentin cov kab mob no tau pom tshwj xeeb hauv cov neeg mob IBS uas mob raws plab [89–91].

Txawm li cas los xij, thaum lub plab microbiota nyob rau hauv cov neeg mob IBS yog tus cwj pwm tsis hais txog kev mob plab hnyuv, ib qho kev depletion ntawm Lachnospiraceae tau tshaj tawm [92-94].

Tej zaum, qhov tsis sib xws no yuav yog vim muaj kev nplua nuj / txo qis ntawm cov tsiaj tshwj xeeb hauv tsev neeg no, uas tsis tau qhia meej meej hauv cov kev tshawb fawb no. Ntawm cov ntawv ceeb toom, cov qib qis ntawm Lachnospiraceae tau tshaj tawm hauv cov neeg mob IBS uas qhia txog kev ntxhov siab thiab kev nyuaj siab [93,95,96], uas yog cov tsos mob tshwm sim hauv FM [25], qhia tias Lachnospiraceae tej zaum yuav muaj kev cuam tshuam tshwj xeeb hauv qhov pib ntawm kev puas siab puas ntsws pom nyob rau hauv ob kab mob. .

Txawm hais tias muaj cov ntaub ntawv me me txog qhov ntau ntxiv ntawm C. cinders hauv IBS [97], lub luag haujlwm ntawm cov kua tsib acids hauv tus kab mob yog qhov pom zoo. Kev nce qib ntawm fecal bile acids tau tshaj tawm hauv cov neeg mob IBS, tshwj xeeb yog cov tsos mob raws plab. Tseeb tiag, cov kua tsib kua qaub tau koom nrog ntau qhov tshwm sim cuam tshuam nrog kev mob raws plab, xws li nce plab hnyuv permeability, plab motility, thiab mob plab [98]. Raws li, C. scindens nthuav dav tau qhia tshwj xeeb hauv cov neeg mob raws plab IBS [99].

Nyob rau hauv sib piv rau FM (Table 1), qhov ntau ntawm Eubacterium genus hauv IBS cov neeg mob tau pom tsis ntev los no tau nce hauv IBS thiab cuam tshuam nrog cov tsos mob hnyav, zoo ib yam li Lachnospiraceae [89,99]. Ntawm qhov tod tes, Rikenellaceae, uas tau nthuav dav hauv FM, feem ntau yog depleted hauv IBS [90,91], txawm hais tias qee tus kws sau ntawv cuam tshuam txog lawv cov kev nplua nuj nrog cov tsos mob ntawm lub hlwb [95].Quantitative alterations nyob rau hauv plab microbiota kuj tau tshaj tawm hauv FM. Qhov tseeb, feem ntau ntawm cov neeg mob FM tau pom tias kuaj tau zoo rau SIBO, raws li kev soj ntsuam los ntawm lactulose hydrogen breath test [65,66]. SIBO qhov xwm txheej tau siab dua hauv FM piv rau cov neeg mob IBS thiab cuam tshuam nrog qhov mob hnyav [66], thaum siv cov tshuaj tua kab mob txo cov tsos mob hauv plab hauv FM thiab IBS [65,100].

Nws tau raug pom zoo tias cov kab mob nthuav dav tuaj yeem ua rau muaj kev hloov pauv loj ntawm cov kab mob endotoxins dhau los ntawm cov kab mob plab hnyuv puas tsuaj, ua rau muaj kev mob ntxiv thiab hyperalgesia sib koom los ntawm FM thiab IBS [39]. Txawm li cas los xij, FM cov neeg mob nyiam tsim cov hydrogenthan IBS ntau dua [66], tawm tswv yim tias, nrog rau cov kab mob dav dav, qhov nthuav dav ntawm qee hom kev cuam tshuam rau qhov mob rhiab heev yuav tshwm sim hauv FM.Tshaj tag nrho, cov pov thawj no qhia tias plab dysbiosis tej zaum yuav tshwm sim. ua rau qhov pib ntawm FM thiab IBS. Dysbiosis ua ke nrog SIBO koom nrog hauv pathogenesis ntawm FM thiab IBS thiab qhov zoo sib xws hauv kev hloov pauv hauv plab microbiota tuaj yeem piav qhia ob kab mob sib tshooj.

Ntuj Herbal Tshuaj Rau Relieving cem quav-Cistanche

Cistanche yog ib tug genus ntawm parasitic nroj tsuag uas belongs rau tsev neeg Orobanchaceae. Cov nroj tsuag no paub txog lawv cov khoom siv tshuaj thiab tau siv hauv Cov Tshuaj Suav Tshuaj (TCM) rau ntau pua xyoo. Cov hom Cistanche feem ntau pom muaj nyob hauv thaj av qhuav thiab suab puam ntawm Tuam Tshoj, Mongolia, thiab lwm qhov chaw ntawm Central Asia. Cistanche nroj tsuag yog tus cwj pwm los ntawm lawv cov nqaij tawv, yellowish stems thiab muaj nuj nqis heev rau lawv cov txiaj ntsig kev noj qab haus huv. Hauv TCM, Cistanche ntseeg tau tias muaj cov khoom siv tonic thiab feem ntau yog siv los kho lub raum, txhim kho qhov tseem ceeb, thiab txhawb kev ua haujlwm ntawm kev sib deev. Nws kuj yog siv los daws cov teeb meem ntsig txog kev laus, qaug zog, thiab kev noj qab haus huv tag nrho. Thaum Cistanche muaj keeb kwm ntev ntawm kev siv tshuaj ib txwm siv, kev tshawb fawb tshawb fawb txog nws txoj kev ua tau zoo thiab kev nyab xeeb yog tsis tu ncua thiab txwv. Txawm li cas los xij, nws paub tias muaj ntau yam bioactive tebchaw xws li phenylethanoid glycosides, iridoids, lignans, thiab polysaccharides, uas tuaj yeem ua rau nws cov teebmeem tshuaj.

Wecistanche covcistanche hmoov, cistanche ntsiav tshuaj, cistanche capsules, thiab lwm yam khoom tsim los sivsuab puamcistancheraws li cov khoom siv raw, txhua yam muaj txiaj ntsig zoo rau kev tshem tawm cem quav. Cov txheej txheem tshwj xeeb yog raws li hauv qab no: Cistanche ntseeg tau tias muaj cov txiaj ntsig zoo rau kev tshem tawm cem quav raws li nws cov kev siv ib txwm siv thiab qee cov tshuaj uas nws muaj. Txawm hais tias kev tshawb fawb tshawb fawb ntawm Cistanche qhov cuam tshuam rau cem quav yog txwv, nws xav tias muaj ntau lub tswv yim uas tuaj yeem pab txhawb rau nws lub peev xwm los daws cem quav. Laxative nyhuv:Cistanchetau ntev tau siv nyob rau hauv tsoos suav tshuaj raws li ib tug tshuaj rau cem quav. Nws ntseeg tau tias muaj cov nyhuv laxative me me, uas tuaj yeem pab txhawb kev zom zaub mov thiab ua rau cem quav. Cov nyhuv no tuaj yeem raug ntaus nqi rau ntau lub tebchaw nyob hauv Cistanche, xws li phenylethanoid glycosides thiab polysaccharides. Moistening cov hnyuv: Raws li kev siv ib txwm siv, Cistanche suav hais tias muaj cov khoom siv moisturizing, tshwj xeeb yog tsom rau cov hnyuv. Txhawb nqa dej thiab lubrication ntawm cov hnyuv yuav pab tau cov cuab yeej soften thiab yooj yim dua, yog li no relieving cem quav. Anti-inflammatory Effect: cem quav tej zaum yuav txuam nrog o nyob rau hauv lub plab zom mov. Cistanche muaj qee qhov sib txuas, suav nrog phenylethanoid glycosides thiab lignans, uas ntseeg tau tias muaj cov tshuaj tiv thaiv kab mob. Txo qhov mob hauv cov hnyuv tuaj yeem pab txhim kho kev zom zaub mov kom zoo thiab txo qhov cem quav.