Ntu II-Cistanches Herba Txo Qhov Nyuaj Tshaj hauv Kev Noj Qab Haus Huv Zoo Tshaj Plaws-vim cov nas rog rog tuaj yeem dhau los ntawm Mitochondrial Uncoupling
Mar 25, 2022
Hu rau: Audrey Hu Whatsapp / hp: 0086 13880143964 Email:audrey.hu@wecistanche.com
Hoi Shan Wong, Jihang Chen, Pou Kuan Leong, Hoi Yan Leung, Wing Man Chan, Kam Ming Ko
* Division of Life Science, Hong Kong University of Science thiab Technology, Hong Kong, Suav.
4. Kev sib tham
Kev kho HCF1 inhibited HFD-vim lub cev hnyav nce hauv ob tus txiv neej thiab poj niam nas. HCF1-vim poob phaus tau cuam tshuam nrog kev txo qis hauv HFD-vim cov rog rog nce ntxiv, tshwj xeeb hauv cov rog hauv visceral. Visceral rog, uas yog ib tug metabolically active cov ntaub so ntswg, koom nyob rau hauv cov kev cai ntawm ntau yam neuroendocrinal zog (Cefalu li al., 1995; Ibrahim, 2010; Nguyen-Duy, Nichaman, Church, Blair, & Ross, 2003; Wozniak, Gee, Wachtel , & Frezza, 2009; Zhang et al., 2012), uas nyob rau hauv lub secretion ntawm pro-inflammatory cytokines plays ib tug tseem ceeb luag hauj lwm nyob rau hauv eliciting ib tug systemicmobteb (Ibrahim, 2010). Yog li ntawd, lub peev xwm ntawm HCF1 los suppress HFD-induced nce nyob rau hauv cov roj visceral muaj feem cuam tshuam rau kev tiv thaiv kev rog rog cuam tshuam txog metabolic. Kev kho HCF1 mus sij hawm ntev kuj tseem txwv tsis pub HFD-vim cov rog ectopic cev xeeb tub, raws li pom los ntawm qhov txo qis hauv qib siab TG hauv HCF1-cotreated HFD-fed nas. Lub deposition ntawm ectopic rog, uas feem ntau pom nyob rau hauv cov neeg rog rog (Iacobellis, Barbarini, Letizia, & Barbaro, 2013), tshwm sim thaum cov khoom noj khoom haus lipids tshaj lub peev xwm ntawm cov ntaub so ntswg adipose (Bays, Mandarino, & DeFronzo, 2004) Nrog rau qhov tshwm sim ntawm cov lipids hauv cov ntaub so ntswg uas tsis yog-adipose xws li cov leeg pob txha thiabdaim siab(Lettner & Roden, 2008). Cov kev tshawb fawb soj ntsuam tau pom muaj kev sib raug zoo ntawm kev tso tawm ntawm ectopic rog thiab kev loj hlob ntawm hom 2 mob ntshav qab zib. Xws li cov kab mob pathogenic tau pom los ntawm kev sib haum xeeb los ntawm kev sib sau ntawm intermediates ntawm lipid metabolism. Piv txwv li, qhov nruab nrab ntawm qhov tsis tiav -oxidation tuaj yeem ua rau lub cev tsis ua haujlwm ntawm insulin receptors ntawm diacylglycerol signaling (Snel li al., 2012). Yog li, cov kev tshawb pom qhia tias HCF1 tuaj yeem txo qis cov rog ntawm ectopic los ntawm kev txo cov lipids thiab yog li tsim cov txiaj ntsig zoo ntawm insulin rhiab heev.
Cistanche tshuaj ntsuabyog qhov zoo rauhnyavtswj
Chengdu Wecistanche tsuas yog tsim cov khoom Cistanche rau lub neej noj qab haus huv.
Kev nce qib ntawm HFD hauv plasma TG thiab cov piam thaj hauv cov ntshav, qhia txog kev tiv thaiv insulin, yuav yog vim muaj kev cuam tshuam ntawm kev tswj hwm ntawm insulin-mediated TG synthesis thiab qabzib uptake (Koo, 2013; Leto & Saltiel, 2012; Moore, Coate, Winnick, An, & Cherrington, 2012). Qhov nce hauv plasma TG thiab cov piam thaj hauv cov ntshav tuaj yeem raug ntaus nqi los ntawm deregulation ntawm hepatic TG/glucose anabolism kho los ntawm phosphoinositide-3-kinase/protein kinase B txoj hauv kev hauv kev taw qhia insulin (Farese, Sajan, & Standaert, 2005). Lub peev xwm ntawm HCF1 los cuam tshuam qhov nce siab ntawm HFD hauv plasma TG thiab cov piam thaj hauv cov ntshav qhia nws cov txiaj ntsig zoo ntawm insulin rhiab heev. Cov tshuaj insulin-rhiab heev tau txhawb nqa ntxiv los ntawm HCF1- cuam tshuam cov metabolism hauv ob qho tib si ND thiab HFD. Kev kho HCF1 zoo li txhawb nqa glycolysis hauv ND-fed nas, raws li qhia los ntawm kev txhawb nqa ntawm PFK kev ua, qhia txog kev siv cov piam thaj ntau ntxiv los ua cov roj molecules. Ntawm qhov tod tes, kev noj HFD ua rau muaj kev hloov pauv ntawm lub zog metabolism los ntawm cov piam thaj mus rau fatty acid oxidation, qhia txog kev hloov kho cov lus teb rau kev nce qib hauv plasma TG, suav tias yog los ntawm peroxisome proliferation-activated receptor-alpha (PPAR) fatty acid sensing mechanism. (Georgiadi & Kersten, 2012; Poulsen, Siersbak, & Mandrup, 2012). Nyob rau hauv tus txheej txheem, kev khi ntawm fatty acids los yog fatty acid derivatives activates PPAR . Qhov tshwm sim ntawm kev hloov pauv hauv nuclear ntawm PPAR txhawb nqa fatty acid metabolism hauv cov noob caj noob ces, nrog rau kev nce ntxiv hauv fatty acid oxidation (Georgiadi & Kersten, 2012; Poulsen li al., 2012), zoo li cov ntaub ntawv hauv cov nas uas tsis tau noj HFD. . HCF1 inhibited HFD-stimulated fatty acid oxidation, txawm tias kho los ntawm kev txhim kho insulin rhiab heev hauv HFD-fed nas. Ntxiv mus, HFD pub mis rau dyslipidemia, raws li pom los ntawm kev nce siab hauv siab thiab ntshav TC qib, nrog rau kev txo qis ntawm HDL rau LDL (Klop, Elte, & Cabezas, 2013). Muab qhov tseeb tias cov roj cholesterol metabolism yog nyob rau hauv ib feem tswj hwm los ntawm plasma / hepatic TG qib thiab insulin-dependent signaling pathway (Dickson-Humphries, Bottenberg, & Kuntz, 2013; Ruderman, Carling, Prentki, & Cacicedo, 2013), muaj peev xwm. ntawm HCF1 los hloov cov roj cholesterol metabolism muab pov thawj los txhawb ntxiv nws txoj haujlwm muaj txiaj ntsig hauv insulin rhiab heev.
Suab puam Cistanche
Txhawm rau tshawb xyuas cov txheej txheem hauv qab ntawm HCF1- ua rau qhov hnyav txo, qhov cuam tshuam ntawm HCF1 ntawm mitochondrial uncoupling tau kuaj xyuas. Qhov induction ntawm mitochondrial uncoupling nyob rau hauv nas skeletal nqaij, raws li qhia los ntawm kev txo nyob rau hauv mitochondrial RCR thiab lub siab mitochondrial UCP3 qhia, yog txuam nrog cov txo nyob rau hauv lub cev hnyav thiab tag nrho cov rog indices nyob rau hauv HCF1-co-kho HFD-fed. nas. Qhov kev tshawb pom qhia tias muaj kev koom tes ntawm mitochondrial uncoupling hauv kev tsim cov nyhuv txo qhov hnyav hauv cov nas, tshwj xeeb hauv HFD. Thaum HCF1 induced mitochondrial uncoupling nyob rau hauv cov txiv neej thiab poj niam nas nyob rau hauv ob qho tib si ND thiab HFD tej yam kev mob, ib tug loj npaum li cas ntawm HCF 1-induced yuag tau pom nyob rau hauv txiv neej nas. Qhov sib txawv ntawm poj niam txiv neej yog xav tias yog vim qhov loj ntawm pob txha pob txha loj hauv cov txiv neej dua li cov nas poj niam. Qhov sib txawv suppressive nyhuv ntawm HFD-induced nce nyob rau hauv subcutaneous thiab visceral rog los ntawm HCF1 co-kev kho mob kuj lends txhawb rau kev koom tes ntawm mitochondrial uncoupling nyob rau hauv poob phaus. Tsis tas li ntawd, qhov kev tshawb pom tias HCF1 ua rau muaj kev txo qis hauv cov roj visceral muaj feem cuam tshuam nrog cov ntsiab lus mitochondrial siab hauv cov roj visceral thaum piv nrog cov ntaub so ntswg subcutaneous adipose (Krauneoe li al., 2010). Ntawm qhov tod tes, thaum HCF1 tau tsim cov tshuaj noj raws li qhov hnyav ntawm ND-fed thiab HFD-fed nas, nws cov nyhuv ntawm mitochondrial uncoupling tau pom tias nws tus kheej txwv. Kev soj ntsuam tsis sib xws yuav raug ntaus nqi rau lwm yam uas tsis yog qhov induction ntawm mitochondrial uncoupling. Piv txwv li, qhov nce hauv cov leeg nqaij ntshiv tom qab kev kho mob nrog HCF1 tuaj yeem ua rau muaj qhov loj dua ntawm mitochondrial uncoupling-induced zog noj hauv HFD-fed nas. Tsis tas li ntawd, cov txiaj ntsig tau los ntawm kev tshawb fawb sib piv ntawm qhov cuam tshuam ntawm HCF1 thiab CT ntawm HFD vim kev rog rog kuj tsis suav nrog kev cuam tshuam ntawm inhibition ntawm kev noj zaub mov muaj roj hauv HCF1- ua rau poob phaus. Hauv txoj kev tshawb no, ob qho tib si CT thiab HCF1 kev kho mob ua rau txo qis hauv ND-fed thiab HFD-fed nas. Interestingly, CT-mediated yuag txo cov nyhuv cuam tshuam nrog kev txo qis hauv cov ntshav plasma LDL thiab qhov tshwm sim ntawm qhov sib piv ntawm HDL rau LDL, tab sis tsis yog qhov induction ntawm mitochondrial uncoupling hauv cov leeg pob txha. Qhov kev tshawb pom qhia tias qhov kev poob phaus ntawm CT tej zaum yuav muaj feem cuam tshuam nrog nws lub peev xwm hauv sequestering bile acid uas cuam tshuam kev noj zaub mov muaj roj (Chen li al., 2010; Yamato li al., 2012). Tsis tas li ntawd, nyob rau hauv sib piv rau HCF1 uas txhim kho cov glycolytic flux rau lub zog tiam, CT ua tsis tau tejyam ua rau muaj kev cuam tshuam rau lub zog metabolism. Kev txhim kho cov piam thaj thiab lipid metabolism los ntawm CT co-kev kho mob hauv HFD-fed nas yog cov xwm txheej thib ob rau CT-vim txo qis hauv kev noj zaub mov noj rog thiab yog li txo qhov hnyav. Qhov sib txawv ntawm HCF1 thiab CT kev kho mob qhia tau hais tias HCF1-vim qhov hnyav txo qis yuav tsis zoo los ntawm qhov tsis zoo ntawm kev noj zaub mov muaj rog.
cov txiaj ntsig kev noj qab haus huv ntawm cov suab puamcistanche
Raws li kev soj ntsuam los ntawm kev ua haujlwm siab ua kua chromatography (HPLC) thiab kua chromatography-mass spectrometry (LC-MS), kev tshawb pom ua ntej pom tias phytosterols, xws li -sitosterol (BSS), yog cov tshuaj tseem ceeb ntawm HCF1. Peb tau ua pov thawj ntxiv tias HCF1 thiab BSS tau txais txiaj ntsig los ntawm kev ua kom cov mitochondrial uncoupling hauv H9c2 hlwb hauv vitro thiab hauv nas lub siab ex vivo los ntawm ROS-mediated mechanism (Wong, Chen, Leong, & Ko, 2013), tawm tswv yim BSS raws li cov khoom siv. ntawm HCF1. BSS, uas sib koom cov qauv tshuaj zoo sib xws nrog cov roj cholesterol, tau pom tias muaj peev xwm ua kom cov kua dej hauv mitochondrial membrane los ntawm daim nyias nyias perturbation, nrog rau kev nce hauv mitochondrial electron thauj (Shi, Wu, & Xu, 2013). Peb, yog li ntawd, postulate tias phytosterols nyob rau hauv HCF1, tshwj xeeb tshaj yog BSS, yuav ua rau kom mitochondrial membrane fluidity ntawm lub hydrophobic kev sib tshuam ntawm lub pentacyclic skeleton thiab mitochondrial puab membrane. Qhov cuam tshuam ntawm kev thauj mus los ntawm mitochondrial electron, raws li tau pom nyob rau hauv peb cov kev tshawb fawb yav dhau los (Wong et al., 2013; Wong & Ko, 2013) tuaj yeem ua rau muaj kev nce ntxiv hauv mitochondrial ROS ntau lawm, uas tuaj yeem ua rau mitochondrial uncoupling. thiab thaum kawg ua rau poob phaus hauv vivo.
cistanche cov txiaj ntsig kev noj qab haus huv
5. Cov lus xaus
Ua ke, HCF1 kev kho mob tau pom tias ua rau txo qhov hnyav hauv HFD-vim cov nas rog rog, suav tias yog los ntawm kev ua kom lub zog hauv vivo metabolism, tshwj xeeb tshaj yog nyob rau hauv cov leeg pob txha los ntawm induction ntawm mitochondrial uncoupling. Covhnyav txonyhuvkuj tseem cuam tshuam nrog kev txhim kho insulin rhiab heev. Cov kev tshawb fawb ntxiv uas siv 6-keto cholestanol ua ib qho kev sib txuas yuav raug ua kom paub meej tias kev koom tes ntawm HCF1-induced mitochondrial uncoupling hauv kev tsim covhnyavtxonyhuv. Tsis tas li ntawd, kev tshawb fawb txog cov teebmeem ntawm BSS rauhnyav tswjtau lav. Cov kev tshawb pom qhia tias muaj peev xwm siv HCF1 rau kev tiv thaiv kev noj zaub mov vim kev rog rog thiab cuam tshuam nrog cov kab mob metabolic.
Cistanche extract tau txais txiaj ntsig
Tsis sib haum xeeb
Peb tshaj tawm tias peb tsis muaj teeb meem ntawm kev txaus siab.
Siv:
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