Urolithin Ib Powder

Urolithin Ahmoov yog ib tug natural polyphenolic compound, tshuaj hu ua 3,8-dihydroxy-6H-dibenzo[B,D]pyran-6-ib, tsim los ntawm cov metabolism ntawm ellagic acid los ntawm txoj hnyuv flora. Nws zoo nkaus li cov hmoov dawb mus rau daj daj crystalline hmoov thiab muaj ntau yam kev ua haujlwm lom neeg, nrog rau cov tshuaj tua kab mob antioxidant, tiv thaiv kab mob, tiv thaiv proliferative, thiab mitophagy-activating teebmeem.

Cov kev tshawb fawb tau pom tias urolithin A yog ib qho ntawm ob peb lub ntuj molecules uas muaj peev xwm ua rau muaj kev xaiv tshem tawm ntawm kev puas tsuaj mitochondria ntawm autophagy thaum ib txhij txhawb kev biosynthesis ntawm kev noj qab haus huv mitochondria. Nws tuaj yeem hla cov ntshav- lub paj hlwb teeb meem thiab siv cov teebmeem neuroprotective, qhia meej cov peev txheej hauv kev cuam tshuam kev laus, kev tiv thaiv kab mob neurodegenerative, thiab kev cuam tshuam ntxiv rau sarcopenia.

YTBIO yog cov chaw muag khoom thiab chaw tsim khoom ntawm Urolithin, feem ntau muabUrolithin A thiab Urolithin B nrog cov lus qhia ntawm 98%. Tag nrho cov khoom uas peb muab tau raug sim thiab txhawb nqa thib peb -kev xeem. Hauv kaum xyoo ntawm txoj kev loj hlob hauv kev lag luam, peb tau sau cov neeg siv khoom thoob ntiaj teb thiab tau txais kev lees paub los ntawm cov neeg siv khoom. Yog tias koj xav tau ib tus neeg muag khoom nrog qee lub zog, kuv xav tias YTBIO yog qhov kev xaiv zoo.

1. Urolithin A txhim kho mitochondrial thiab cov leeg nqaij ua haujlwm, txhim kho cov leeg nqaij thiab kev ua siab ntev thaum laus.
Urolithin A alleviates cov leeg nqaij atrophy hauv cov neeg laus. Qhov kev sim no qhia tau hais tias urolithin A supplementation tuaj yeem txhim kho cov nqaij ntshiv ntawm cov leeg pob txha, nrog kev txhim kho tseem ceeb hauv tes thiab ob txhais ceg ntawm cov kev kawm.

2. Tsis tsuas yog nws tuaj yeem tiv thaiv cov leeg, kev tshawb fawb tshiab tau pom tias urolithin A tuaj yeem cuam tshuam rau cellular lipid metabolism thiab rog ntau lawm. Nws txo qis triglyceride tsub zuj zuj thiab fatty acid oxidation, nrog rau kev qhia ntawm cov noob koom nrog hauv lipogenesis.

3. Kev tiv thaiv cov leeg nqaij yog qhov kev tshawb pom tsis ntev los no, thiab kev tshawb fawb yav dhau los ntawm nws tau tsom mus rau mitochondria, tshwj xeeb tshaj yog mitophagy. (Mitophagy yog hais txog kev xaiv tshem tawm ntawm mitochondria puas los ntawm autophagosomes)
UA tuaj yeem qhib mitophagy hauv ntau txoj hauv kev, xws li ua kom cov enzymes uas txhawb nqa mitophagy, lossis tswj txoj hauv kev mitophagy, thiab txhawb kev tsim cov autophagosomes.

4. Ntawm tag nrho cov qauv kev kho mob ntawm UA, muaj ib qho kev tshwm sim, uas yog qhov tsis muaj zog ntawm inflammatory teb.

Cov nyhuv no tau pom thawj zaug thaum ob qho tib si mRNA thiab cov protein ntau ntawm cov kab mob inflammatory cyclooxygenase 2 tau txo qis hauv kev sim plab hnyuv hauv cov nas.

Nrog rau kev tshawb fawb ntxiv, nws tau pom tias lwm cov cim inflammatory, xws li pro- cov kab mob inflammatory, kuj txo qis mus rau qhov sib txawv.
Cov tshuaj tiv thaiv -cov nyhuv ntawm UA yog ntau-faceted. Ua ntej ntawm tag nrho cov, nws muaj nyob rau hauv ntau ntau nyob rau hauv txoj hnyuv, yog li qhov zoo tshaj plaws yog inflammatory plob tsis so tswj kab mob. Xws li mob enteritis, ulcerative colitis.

Qhov thib ob, UA tsis tsuas yog tiv thaiv kab mob hauv plab, vim tias nws txo qis tag nrho cov ntshav hauv cov ntshav. Hauv txoj kev xav, UA tuaj yeem ua haujlwm ntawm cov kab mob tshwm sim los ntawm kev mob.

Thaum UA tawm los tiv thaiv- cov teebmeem hauv lub hlwb, nws tuaj yeem txhim kho ntau yam kab mob neurodegenerative, suav nrog Alzheimer's disease (AD), nco tsis taus thiab mob stroke.

5. Qhov tseeb, cov tshuaj tiv thaiv - mob thiab mitophagy activation ntawm urolithin A tuaj yeem ua rau qeeb cov tsos mob ntawm cov kab mob metabolic. Tab sis nws kuj muaj cov txiaj ntsig zoo, uas yog txhawm rau txhim kho oxidative kev nyuaj siab, tsis tsuas yog txhawm rau tshem tawm cov dawb radicals, tab sis kuj inhibit oxidase enzymes, thiab txhim kho cellular antioxidant / qhov chaw.

Ntau tus kws kho mob ntseeg tias cov khoom muaj txiaj ntsig ntawm UA yog vim muaj peev xwm antioxidant ntawm UA.

Txhawb kev xaiv autophagy ntawm puas mitochondria thiab kho cov mitochondrial dysfunction tshwm sim los ntawm kev laus yog cov txheej txheem tseem ceeb ntawm UA pom nyob rau hauv ntau hom (nematodes, nas, tib neeg, thiab lwm yam). Thaum mitochondria raug rau sab nraud kev nyuaj siab thiab puas, autophagy theoretically pib. UA qhov tseem ceeb ua raws li autophagy inducer thiab feem ntau koom nrog thiab tswj cov txheej txheem mitophagy los ntawm ob txoj hauv kev:

PINK1/Parkin ubiquitin- nyob ntawm txoj kev
Hauv ubiquitin-dependent txoj kev ntawm mitophagy, tom qab PINK1 protein paub lub hom phiaj mitochondria, nws recruits thiab phosphorylates ubiquitin -binding protein Parkin, sib koom ua ke txhawb cov ubiquitination ntawm mitochondrial proteins, amplifying tophacytes, thiab autophagy signals. UA activates cov kev qhia ntawm cov noob caj noob ces, upregulates cov qib PINK1 thiab Parkin proteins, thiab txhawb cov txheej txheem mitochondrial autophagy.

direct receptor activation txoj kev
Ntxiv rau kev tso siab rau PINK1 / Parkin txoj hauv kev, mitochondria kuj tuaj yeem "hloov txoj hauv kev" los siv qee cov protein receptors (xws li BNIP3) kom ncaj qha rau cov txheej txheem autophagy. UA "yuav tsis tso tseg thiab ua haujlwm ruaj khov", txhim kho qib kev qhia ntawm receptor proteins. ua rau nws yooj yim mus khaws cia rau ntawm mitochondrial nto.

UA tuaj yeem qhib mitophagy los ntawm kev tswj hwm txoj kev sib txawv.

Muaj ntau qhov kev sim siab tau lees paub tias UA muaj txiaj ntsig zoo hauv kev txhim kho cov mob ntev, kab mob plawv, cov leeg tsis ua haujlwm, thiab cov kab mob neurodegenerative.

Thaum cov qauv kab mob nematodes tau pub UA ntev ntev (los ntawm qe theem mus rau kev tuag), piv nrog cov pab pawg tswj hwm, UA tau qhib lawv txoj hauv kev AMPK thiab txhawb nqa mitophagy, txuas ntxiv lub neej ntawm nematodes txog li 45.4%.

UA cuam tshuam txog kev ua neej nyob ntawm C. elegans hauv ib koob -nyob ntawm

Urolithin A ua tau zoo txhim kho endothelial cell ciaj sia nyob rau hauv cov ntshav qabzib siab -induced mob

CCK8 experimental results showed that compared with the normal control group, high glucose significantly reduced cell survival (P < 0.05), and UA (1 μmol ~ 10 μmol) increased the survival of endothelial cells in a dose-dependent manner. There was no significant difference between 10 μmol and 50 μmol (P>0.05 Nws.). UA kev cuam tshuam concentration hauv cov kev sim tom ntej yog 10 μmol.

Urolithin A txhim kho vascular endothelial dysfunction tshwm sim los ntawm ib puag ncig siab qabzib

Los ntawm kev kuaj pom qhov tso tawm ntawm TSIS TAU thiab ET-1 los ntawm cov hlwb endothelial hauv txhua pab pawg, peb tau soj ntsuam cov txiaj ntsig ntawm UA rau vascular endothelial muaj nuj nqi hauv ib puag ncig cov piam thaj ntau. Piv nrog rau pawg tswj hwm ib txwm muaj, cov piam thaj siab tau txo qis qhov tso tawm ntawm NO (P<0.05) and increased the secretion of ET-1 (P<0.05); after adding UA (10 μmol), the secretion of NO increased significantly (P<0.05). 0.05), the secretion of ET-1 decreased (P<0.05). The regulatory effect of UA disappeared after concurrent administration of AMPK inhibitors.

Urolithin A txo cov qabzib siab -induced oxidative stress nyob rau hauv vascular endothelial hlwb

Kev txiav txim los ntawm cov txiaj ntsig ntawm DHE fluorescence staining (kev tshawb pom ntawm ROS tiam), fluorescence quantitative tsom xam thiab SOD kev ua tau zoo, piv nrog rau pawg tswj hwm ib txwm, qhov siab -glucose ib puag ncig tau nce ROS ntau ntxiv thiab txo SOD kev ua hauv vascular endothelial hlwb (P<0.05); UA Incubation significantly reduced ROS levels and increased SOD activity (P<0.05); the above effects were significantly attenuated after simultaneous administration of AMPK inhibitor Compound C (P<0.05)

Urolithin A activates AMPK / eNOS txoj hauv kev los txhim kho endothelial cell puas los ntawm cov piam thaj siab.

Hauv kev tshawb nrhiav ntxiv, peb tau tshawb pom qhov cuam tshuam ntawm UA ntawm AMPK/eNOS teeb liab txoj hauv kev los ntawm Western blotting, thiab cov qib protein phosphorylation sib raug tau cuam tshuam los ntawm p-AMPK/AMPK thiab p-eNOS/eNOS. Cov txiaj ntsig tau pom tias piv nrog cov pab pawg ib txwm muaj, qib phosphorylation ntawm AMPK thiab eNOS hauv cov hlwb endothelial kho nrog cov piam thaj siab tau txo qis (P<0.05); UA can effectively reverse the changes in phosphorylation levels of AMPK and eNOS (P<0.05); but this effect can be Antagonized by AMPK inhibitors (P<0.05). The above results indicate that UA may improve high glucose-induced endothelial cell damage by activating the AMPK/eNOS pathway.

Urolithin A muaj peev xwm siv tau rau hauv thaj chaw ntawm kev laus, cov leeg mob, thiab cov kab mob neurodegenerative.

Nws tau pom tias yuav txo tau cov pob txha ntawm cov protein puas hauv lub hlwb thiab tej zaum yuav muaj peev xwm kho tau cov kab mob xws li Alzheimer's thiab Parkinson's.

Tam sim no dav siv hauv cov khoom noj khoom haus, tshuaj thiab lwm yam khoom

Shaanxi Yuantai Biotechnology Co., Ltd. tau tsim nyob rau xyoo 2014, feem ntau muab cov tshuaj ntsuab rho tawm, cov khoom siv tshuaj pleev ib ce, cov khoom siv organic, thiab lwm yam. Peb muaj peb tus kheej cov chaw tsim khoom, R & D thiab pab pawg soj ntsuam zoo, thiab muaj cov xwm txheej rau kev txhim kho, ntau lawm, thiab kev ruaj ntseg zoo. Tam sim no, peb tau txais ISO9001, ISO22000, HALAL, KOSHER, HACCP, FDA thiab lwm daim ntawv pov thawj. Yog li ntawd, qhov zoo ntawm peb cov khoom yog guaranteed, thiab nws yog peb lub hom phiaj tseem ceeb los coj siab - cov khoom zoo rau cov neeg siv khoom.

Cim npe nrov: Tuam Tshoj urolithin hmoov manufacturers, lwm tus neeg, Hoobkas