Cov khoom

Niacin (nicotinic acid) raws li kev kho mob monotherapy tuaj yeem txo qis kev pheej hmoo ntawm cov kab mob vascular, tab sis nws cov txheej txheem ntawm kev txiav txim tseem muaj teeb meem, thiab tej zaum yuav tsis yog nyob ntawm kev hloov kho lipid.Niacin tsis ntev los no tau pom tias txhim kho endothelial muaj nuj nqi thiab vascular regeneration, ywj siab ntawm kev kho dyslipidemia, nyob rau hauv nas qauv ntawm vascular raug mob thiab kab mob metabolic.Raws li qhov muaj peev xwm biosynthetic precursor rau NAD(+), niacin tuaj yeem cuam tshuam cov txiaj ntsig vascular los ntawm NAD(+)-dependent, sirtuin (SIRT) kho cov lus teb.Xwb, niacin tuaj yeem ua los ntawm nws cov receptor, GPR109A, los txhawb kev ua haujlwm ntawm endothelial, txawm hais tias cov hlwb endothelial tsis paub qhia cov receptor no.Peb xav tias niacin ncaj qha txhim kho endothelial cell muaj nuj nqi thaum lub sij hawm raug rau lipotoxic tej yam kev mob thiab nrhiav los txiav txim lub peev xwm mechanism (s) koom nrog.Angiogenic muaj nuj nqi nyob rau hauv ntau tshaj palmitate raug soj ntsuam los ntawm tube tsim tom qab kev kho mob ntawm tib neeg microvascular endothelial hlwb (HMVE C) nrog ib tug. kuj tsis tshua muaj concentration ntawm niacin (10 μM), los yog nicotinamide mononucleotide (NMN) (1 μM), ib tug ncaj NAD (+) precursor.Txawm hais tias ob qho tib si niacin thiab NMN txhim kho HMVEC raj tsim thaum lub sij hawm palmitate overload, tsuas yog NMN nce cellular NAD (+) thiab SIRT1 kev ua.Peb tau soj ntsuam ntxiv tias HMVEC nthuav qhia GRP109A.Ua kom cov receptor no nrog acifran lossis MK-1903 recapitulated niacin-induced txhim kho hauv HMVEC tube tsim, thaum GPR109A siRNA txo qis cov nyhuv ntawm niacin.Niacin, ntawm qhov tsis tshua muaj siab, txhim kho HMVEC angiogenic muaj nuj nqi nyob rau hauv lipotoxic tej yam kev mob, yuav ywj siab ntawm NAD ( +) biosynthesis thiab SIRT1 ua kom, tab sis theej los ntawm niacin receptor activation.