Paraoxonase Lub luag haujlwm hauv Tib Neeg Cov Kab Mob Neurodegenerative Part 3

Cov pawg ntawm PON noob yog polymorphic heev, muaj peev xwm nthuav dav qhov sib txawv thiab sib txawv ntawm cov haiv neeg, nrog rau cov kab mob sib txawv. Q192Rpolymorphism yog qhov kev ntxub ntxaug ntawm AD thiab VD; Txawm li cas los xij, tsis muaj qhov sib txawv ntawm genotypic distributions ntawm pawg [199].

Kev sib raug zoo ntawm PON gene pawg thiab kev nco tau yog qhov tseem ceeb ntawm kev tshawb fawb tshawb fawb. Kev tshawb fawb qhia tau hais tias muaj qhov sib txuas tsis sib xws ntawm PON gene pawg thiab nco. PON gene pawg yog ib pawg ntawm cov noob uas muaj cov haujlwm biochemical zoo sib xws uas tuaj yeem cuam tshuam rau lub cev thiab cov txheej txheem biochemical ntawm tib neeg lub cev, suav nrog cov metabolism, antioxidants, tiv thaiv kab mob, thiab neuroprotection.

Ib txoj kev tshawb fawb tsis ntev los no tau pom tias ib tus tswv cuab ntawm PON gene pawg, PON1 gene, txuas nrog rau kev nco. Txoj kev tshawb no ua pov thawj tias PON1 protein tsis xws luag tshwm sim los ntawm PON1 noob kev hloov pauv yuav txo tau lub hlwb kev siv cov pa oxygen, yog li ua rau poob ntawm kev txawj ntse. Lwm cov kev tshawb fawb tseem pom tau tias PON2 noob muaj feem xyuam rau lub hlwb kev txawj ntse thiab qib kev txawj ntse.

Cov kev tshawb pom los ntawm cov kev tshawb fawb no ua rau peb nkag siab tob ntxiv tias peb yuav tsum tsis tsuas yog tsom rau kev noj qab haus huv ntawm peb lub cev tab sis kuj yog kev noj qab haus huv ntawm peb lub hlwb. Kev tswj hwm kev noj qab haus huv PON gene pawg ua haujlwm yog ib qho tseem ceeb hauv kev tswj xyuas kev noj qab haus huv ntawm peb lub cev thiab lub hlwb. Los ntawm kev tswj hwm txoj kev noj qab haus huv, xws li noj zaub mov kom zoo, qoj ib ce tsis tu ncua, pw tsaug zog txaus, thiab txo kev ntxhov siab, peb tuaj yeem pab peb pawg PON gene pawg tswj hwm kev ua haujlwm zoo, yog li txhim kho kev nco thiab kev txawj ntse. Tsis tas li ntawd, peb tuaj yeem siv peb lub hlwb thiab txhim kho kev nco thiab kev txawj ntse los ntawm kev ua ub no xws li kev cob qhia kev txawj ntse, kawm txuj ci tshiab, thiab kev nyeem ntawv.

Ua ke, qhov sib txuas ntawm PON gene pawg thiab nco qhia txog kev sib raug zoo ntawm lub cev thiab lub hlwb. Los ntawm kev tswj hwm txoj kev noj qab haus huv thiab siv zog ua haujlwm ntawm peb lub hlwb, peb tuaj yeem txhim kho peb lub cim xeeb thiab kev txawj ntse, ua rau muaj kev noj qab haus huv thiab ua tiav lub neej. Nws tuaj yeem pom tias peb yuav tsum txhim kho kev nco, thiab Cistanche deserticola tuaj yeem txhim kho kev nco, vim Cistanche deserticola tseem tuaj yeem tswj hwm qhov sib npaug ntawm cov neurotransmitters, xws li nce qib ntawm acetylcholine thiab kev loj hlob. Cov khoom no tseem ceeb heev rau kev nco thiab kev kawm. Tsis tas li ntawd, Cistanche deserticola kuj tseem tuaj yeem txhim kho cov ntshav khiav thiab txhawb nqa cov pa oxygen, uas tuaj yeem ua kom lub hlwb tau txais cov as-ham txaus thiab lub zog, yog li txhim kho lub hlwb tseem ceeb thiab kev ua siab ntev.

Nyem Paub txhawm rau txhim kho lub cim xeeb luv luv

Ntawm qhov tod tes, lub koom haum nruab nrab ntawm Q192R, Alzheimer's disease, thiab kab mob coronary artery (CAD) yog controversial.Scacchi li al. [200] tau pom qhov tsawg zaus ntawm R allele hauv cov tib neeg nrog AD; qhov kev hloov kho rau hnub nyoog, poj niam txiv neej, thiab polymorphism ntawm Apo-Eε4 tau hais tias qhov genotype PON1 RR yog qhov kev tiv thaiv rau AD, hos, rau cov tub ntxhais hluas nrog CAD, qhov genotype no tau cuam tshuam nrog kev pheej hmoo [200].

Cov txiaj ntsig zoo sib xws rau R allelehav tau tshaj tawm hauv cov pej xeem Suav. Lub xub ntiag ntawm R allele qhia tias muaj kev tiv thaiv tiv thaiv kev txhim kho ntawm AD [201]. Txawm li cas los xij, hauv cov neeg laus SingaporeanChinese, R allele tau cuam tshuam nrog kev ua haujlwm tsis zoo, muaj cov tsos mob neuropsychiatric, thiab mob hnyav heev hauv cov neeg mob uas muaj kev sib xyaw ua ke [202].

Controversially, nyob rau hauv ib tug Fabkis cov pej xeem, tus R allele zoo li yuav muaj kev pheej hmoo fordementia, ua ke nrog cov T allele (C-107T), ntawm nws tus kheej ntawm Apo-Eε4 allele [203].Txawm li cas los xij, SNP Q192R ntawm PON1 noob tsis tau cuam tshuam nrog kev pheej hmoo ntawm AD hauv Italian thiab Polish pejxeem [204,205].PON1 yog ib qho exogenous acetylcholinesterase inhibitor (ChEI) [206].

Kev cuam tshuam ntawm SNP Q192R hauv kev teb rau kev kho mob nrog ChEIs tau raug soj ntsuam hauv ib pawg me me ntawm cov neeg mob nrog AD [207]. Cov tib neeg nrog AD thiab R allele muaj cov lus teb zoo dua rau kev kho mob piv rau homozygous QQ cov tib neeg [207]. Cov kws sau ntawv tau taw qhia tias allele yog txuam nrog lub peev xwm ntau dua rau hydrolysis ntawm enzyme; Vim li no, tej zaum yuav muaj kev sib koom ua ke hauv cov metabolism hauv cov tshuaj xws li donepezil, galantamine, thiab rivastigmine, uas tuaj yeem txhim kho lawv cov txiaj ntsig [207].

Ntawm qhov tod tes, lwm txoj kev tshawb fawb nrog peb PON1 SNPs (Q192R, L55M, thiab A-162G) tsis pom muaj kev hloov pauv rau kev kho mob nrog acetylcholinesterase inhibitors hauv cov neeg mob AD [208]. Ntau yam tuaj yeem hloov kho cov lus teb rau acetylcholinesterase inhibitors. Txawm li cas los xij, kev tshawb fawb txog kev sib koom tes ntawm PON1 enzymatic kev ua si thiab polymorphisms nrog ib puag ncig, kev noj zaub mov, cov caj ces ntawm kev raug rau AD, thiab cov tshuaj metabolism-txuas nrog polymorphism, tsis muaj [209-211].

Hauv cov neeg mob Alzheimer's tus kab mob, homozygous TT genotype (PON1 C-107T) tau cuam tshuam nrog kev hloov pauv hauv kev faib cov lipoprotein cholesterol nrog ntau dua ntawm qhov me me thiab denser LDL [212]. Nws kuj tau cuam tshuam nrog kev nce hauv plasma oxidized LDL qib [212]. Oxidative stress in Alzheimer's disease contributes to lipoprotein oxidation, nce neuroinflammation, neuronal poob, thiab endothelialdamage [213,214].

Txawm li cas los xij, cov no yog cov txheej txheem multifactorial uas tsis tuaj yeem raug ntaus nqi vim muaj ib qho polymorphism. Tsis tas li ntawd, nyob rau hauv kev tshawb fawb Italian rooj plaub, tsis muaj kev koom tes ntawm T allele (C-107T) thiab kev loj hlob ntawm AD. Tseeb tiag, tsis muaj Apo-Eε4 genotype koom haum tau pom [215]. Lwm polymorphism inpromoter cheeb tsam gene PON-1, SNP C-108T, tau cuam tshuam nrog kev txhim kho AD.

T allele tau nquag nquag hauv cov neeg mob AD, thiab homozygous genotype (TT) tau cuam tshuam nrog kev ua haujlwm qis arylesterase ntawm PON1 [216,217]. Txawm li cas los xij, kev sib raug zoo ntawm AD thiab SNP PON1 C-107T thiab C-108T tseem yuav tsum tau qhia meej.Erlich li al. [58] genotyped 29 SNPs nyob rau hauv cheeb tsam PON noob nyob rau hauv ib pawg loj uas tsim los ntawm Afro- xeeb leej xeeb ntxwv thiab Caucasians nrog AD.

Nws tau pom tias qhov chaw ntawm kev sib raug zoo rau kev txhim kho AD tau pom nyob rau hauv cov cheeb tsam sib txawv hauv PON genein ob haiv neeg. Sliding qhov rais haplotype tsom xam pom tias SNP C-161T tau koom nrog AD; Txawm li cas los xij, SNP C-161T tsis cuam tshuam nrog AD hauv Fab Kis ADpopulation [218].

Tsis tas li ntawd, cov kws sau ntawv tau tsim ib lub koom haum qauv uas muaj T allele muaj cov nyhuv deleterious, ntawm nws tus kheej los yog koom nrog lwm cov genotypes [58]. Ntxiv mus, hauv txoj kev tshawb no, nws tau pom tias cov SNPs, A-107G, Q192R, L55M hauv PON1 thiab C311S hauv PON2, ua ntej cuam tshuam nrog AD kev pheej hmoo yuav tsis ua rau nws tus kheej, tab sis qhov sib txuas tsis sib xws nrog lwm cov polymorphisms uas cuam tshuam. nrog rau pathophysiology ntawm AD.

Cov txiaj ntsig no tuaj yeem piav qhia qee qhov tsis sib xws ntawm cov kev tshawb fawb uas tshawb xyuas PON1 Q192R thiab L55M polymorphismsas cuam tshuam nrog kev txhim kho Alzheimer's kab mob.Nyob rau hauv cov ntaub so ntswg ntawm cov neeg mob AD, muaj ntau zaus ntawm homozygous genotypeMM PON1 L55M tau pom [219]. Tsis tas li ntawd, cov neeg mob uas muaj homozygous MM muaj a2. Ntxiv mus, AD cov neeg mob nrog R allele (Q192R) muaj qhov qis dua A 42 / A 40 piv rau Q192Q homozygous ADpatients [219].

Tsis tas li ntawd, cov tib neeg uas muaj M allele (L55M PON1) tau pom qhov txo qis ntawm tag nrho cov nicotinic receptor thiab choline acetyltransferase (CHAT) kev ua haujlwm hauv lub sijhawm cortex [219]. Ib pawg loj ntawm cov kws kho mob tau lees paub qhov kev tshawb fawb no los ntawm AD autopsy(n=1.066) [220]. M allele ntawm L55M SNP tau cuam tshuam nrog kev pheej hmoo ntawm kev tsim cov txiv neej ADin. Cov txiv neej thiab cov poj niam uas muaj MM-QQ genotype muaj kev ciaj sia ntau dua (kwv yees li 2.5 xyoo) thiab tom qab hnub nyoog ntawm tus kab mob pib (kwv yees li 1.5 xyoo).

Tsis tas li ntawd, AD cov tib neeg nrog Rallele tau txo qis hauv ob qho tib si, A 42 qib thiab A 42 / A 40 piv. Hauv hippocampus thiab frontal cortex, cov neeg mob nrog MM genotype pom qhov txo qis hauv lawv qhov A 40 concentration thiab nce hauv A 42 / A 40 piv rau ob qho tib si, LM thiab LL genotypes. Hauv cov txiv neej nrog MM genotype, nws tau pom ntau cov neuritic senile plaques ntau dua li cov LL genotype hauv fusiform gyrus thiab frontal cortex [220].

Ntawm qhov tod tes, hauv kev tshuaj ntsuam themeta, cov tib neeg uas muaj PON1 polymorphisms Q192R thiab L55M tsis raug rau AD [221]. PON1 kev ua haujlwm qis qis hauv ntau hom kev dementia [40,199,222–226].Qhov kev txo qis ntawm PON1 tau cuam tshuam nrog kev nce hauv atherosclerotic processin cov neeg mob nrog AD [227]. Kev txo qis hauv paraoxonase hauv cov neeg mob nrog AD yog txuam nrog Apo-Eε4 isoforms thiab tag nrho cov roj cholesterol thiab nce LDL-cholesterol [228].

Tseeb, qhov piv ntawm PON1 thiab platelet-activating factor acetylhydrolase (PAF-AH) kev ua haujlwm tau cuam tshuam rau qhov nce hauv oxidized LDL [229]. Ntxiv mus, 8-hydroxy-2'-deoxyguanosine (8-}OHdG), cov khoom oxidized tau los ntawm deoxyguanosine, tsim los ntawm cov txheej txheem oxidation hauv DNA, tau cuam tshuam tsis zoo nrog PON1 kev ua hauv cov neeg mob [230 ].

Txawm li cas los xij, qhov kev faib ua feem ntawm arylesterase PON1 kev ua ub no thiab ApoAI tau qhia txog kev sib raug zoo nrog cov concentration ntawm tag nrho thiab phosphorylatedtau proteins hauv cov neeg mob AD hauv cerebrospinal kua [231].

3.4. Tus kab mob Parkinson

Parkinson's disease (PD) yog qhov tshwj xeeb los ntawm kev txo qis hauv kev tsim cov dopaminein substantia nigra, vim yog degeneration ntawm dopaminergic neurons. Cov txheej txheem no qeeb; thaum xub thawj, muaj kev puas tsuaj ntawm lub cev muaj zog, thiab nyob rau hauv cov ntaub ntawv siab dua tsis yog cov tsos mob tshwm sim. Tam sim no, kwv yees li 1% ntawm cov neeg hauv ntiaj teb hnub nyoog tshaj 60 xyoo tsim PD.

Clinically, cov neeg mob qhia cov kev hloov hauv lub cev muaj zog, xws li bradykinesia, so tremor, thiab txhav, cov tsos mob hu ua parkinsonism [232]. Txawm li cas los xij, cov neeg mob hnyav tau hloov pauv tsis yog lub cev muaj zog, suav nrog anosmia, cem quav, mob, ntxhov siab vim, kev nyuaj siab, thiab kev puas siab puas ntsws. Thaum pib, kev paub tsis meej yog me me, hloov mus rau nruab nrab, thiab tom qab ntawd mus rau dementia [233].

Cov yam ntxwv ntawm pathophysiological ntawm PD suav nrog kev qeeb thiab nce zuj zus ntawm dopaminergic neurons, depletion ntawm striatal dopamine, ploj ntawm neuromelanin, thiab cov tsos ntawm intracellular Lewy lub cev, muab los ntawm qhov tsis raug folding ntawm -synuclein protein [234,235]. Thaum lub sij hawm kev loj hlob ntawm PD, muaj kev nce hauv lipid (hydro) peroxidation thiab hloov mitochondrial muaj nuj nqi, vim toelectron toelectron, thiab tsim kom muaj cov hydroxyl radical thiab hydrogen peroxide, nrog rau kev qaug zog ntawm lub redox system.

Cov yam no ua ke ua rau muaj zog dopamine oxidation nyob rau hauv lub synaptic cleft thiab neuronal tuag ua rau txoj kev loj hlob ntawm dementia [236–238] .Lub koom haum ntawm Parkinson tus kab mob thiab PON1 enzyme yog vim cov tshuaj lom metabolites xws li dopaminergic neurotoxin, 1-methyl -4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), tau cuam tshuam nrog kev txhim kho ntawm PD.

MPTP muaj cov qauv achemical zoo ib yam li qee cov organophosphates [239,240]. Ntxiv mus, organophosphates yog bioactivated hauv cholinesterase inhibitors tom qab metabolization los ntawm cytochromeP 450 systems, thiab oxon (toxic) daim ntawv yog hydrolyzed los ntawm PON1. Tsis tas li ntawd, Ballele ntawm SNP Q192R PON1 tau cuam tshuam nrog kev txhim kho ntawm PD hauv cov neeg Nyiv Pooj [241].

Txawm li cas los xij, kev koom tes ntawm SNP Q192R tsis cuam tshuam nrog kev loj hlob ntawm PD hauv lwm haiv neeg, xws li Caucasian thiab Suavpopulations [242–244].SNP L55M tau suav tias yog ib qho kev pheej hmoo ywj pheej rau kev loj hlob ntawm PD indifferent pejxeem. Qhov zaus ntawm M allele tau siab dua hauv cov neeg mob Parkinson, thiab qhov kwv yees kwv yees qhov kev pheej hmoo yog kwv yees li ob zaug siab dua thaum piv nrog cov neeg homozygous rau L allele [245,246].

Tsis tas li ntawd, ib puag ncig exposureto diazinon, chlorpyrifos, thiab parathion hauv cov tib neeg uas muaj homozygous genotypes QQand MM (SNPs Q192 thiab L55M, feem), tau cuam tshuam nrog Parkinson txoj kev loj hlob mus txog peb zaug [247].

Tseeb, nquag siv organophosphatechemicals tau txuam nrog PD ntawm lub caij nyoog txog li 71%. Cov tib neeg uas muaj homozygous genotypes MM thiab QQ muaj kwv yees li 6 npaug ntawm kev tsim PD [248]. Lub xub ntiag ntawm cov polymorphisms ua rau "slow metabolization" ntawm organophosphates. Txawm li cas los xij, hauv lwm cov kev tshawb fawb, kev koom tes ntawm PON1 thiab PDpolymorphism tsis tau pom [205,249–251].

Polymorphism hauv PON1 G-832 Ib cheeb tsam txhawb nqa tau cuam tshuam nrog PD. Aallele muaj ntau dua ntawm kev tswj ntau dua li cov neeg mob PD thiab tej zaum yuav muaj kev tiv thaiv zoo [252]. Tsis tas li ntawd, SNP G-832A nyob hauv qhov tsis sib xws nrog PON1 C-909G polymorphism. [252]. Cov polymorphism tam sim no nyob rau hauv PON1- txhawb cheeb tsam, C-909G, tau koom nrog kev nthuav qhia ntawm PON1 noob [253].

Hauv cov neeg mob uas muaj PD nyob hauv ib cheeb tsam nyob deb nroog raug tshuaj tua kab, cov dej ua haujlwm ntawm acetylcholinesterase (AChE) thiab PON1 raug txo. Ib qho kev sib txuas tsis sib xws tau pom ntawm PON1 thiab AChE locus. Lub polymorphism ntawm PON1 C108T txhawb nqa cheeb tsam thiab AChE deletion (∆AChwasere cuam tshuam nrog Parkinson'sdevelopment kwv yees li ob zaug [254]. Cov kws sau ntawv qhia tias kev sib cuam tshuam ntawm cov kab mob ntawm AChE thiab PON1 locus tuaj yeem ua rau muaj kab mob insecticide-induced [Parkinson's [254]. .

Tsis tas li ntawd, ntshav ferritin concentration yog inverselycorrelated nrog PON1 kev ua [255]. Kev sib koom ua ke ntawm ferritin thiab PON1 tuaj yeem sib txuas ntawm qhov mob thiab cov kab mob antioxidant enzymatic [43]. Kev txo qis hauv serumparaoxonase kev ua haujlwm hauv PD cov neeg mob tau cuam tshuam nrog nce oxidative kev nyuaj siab, lipid peroxidation, thiab kev hloov pauv ntawm cov hlau metabolism hauv cov cim [256-258].

4. Cov lus xaus

PON1 kev ua haujlwm thiab polymorphisms tau cuam tshuam nrog cov kab mob neurodegenerative. Txawm li cas los xij, kev txiav txim siab tias PON1 tuaj yeem muaj cov haujlwm plasma uas tsis cuam tshuam txog kev ua haujlwm enzyme hauv lub hauv paus paj hlwb, tsis tshua paub txog hnub tim txog lub luag haujlwm tiag tiag ntawm PONs hauv lub hauv paus paj hlwb lossis lawv cov txheej txheem ntawm kev ua haujlwm.

Cov ntaub ntawv tau qhia tias Q192R thiab L55M intronic polymorphisms yog qhov txaus ntshai rau kev txhim kho cov kab mob neurodegenerative. Txawm li cas los xij, ob peb lwm yam kev tshawb fawb piav qhia txog cov txiaj ntsig tsis sib xws.Txawm hais tias lub luag haujlwm ntawm PONs tau piav qhia tias yog hydrolase enzymes hauv ntau cov kab mob, cov kev tshawb fawb muaj zog tseem tsis tau qhia meej txog kev sib koom ua ke ntawm polymorphisms ntawm PONs gene pawg, suav nrog PON2 thiab PON3, thiab cov haujlwm enzymatic hauv cov txheej txheem neurodegeneration. .

Kev tshawb fawb ntawm qib cellular yog tsim nyog kom nkag siab txog kev ua haujlwm ntawm lub cev ntawm PONs hauv macro thiab microglia hlwb thiab neurons. Qhov sib txawv ntawm qhov kev faib tawm thiab qhov tshwj xeeb ntawm PONs hauv tib neeg lub cev qhia tias tej zaum yuav muaj cov ntaub so ntswg tshwj xeeb rau txhua qhov enzyme.

Txawm li cas los xij, noj tag nrho cov kev tshawb fawb ua ke, paraoxonase zoo li muaj lub luag haujlwm hauv kev txo qis thiab / lossis kev tiv thaiv ntawm cov txheej txheem neurodegeneration cuam tshuam nrog qhov tsis txaus ntawm cov kab mob redox. Cov kev tshawb fawb ntxiv hauv qhov kev taw qhia no tuaj yeem muab cov ntaub ntawv txaus uas yuav ua rau muaj kev cuam tshuam rau kev kho mob-pharmacological tshiab.

Sau Kev Pabcuam: Sau-tsim daim ntawv npaj, COR, DL, thiab SPB; sau-reviewand editing, COR, DL thiab SPB; Kev nrhiav nyiaj txiag, SPB Txhua tus kws sau ntawv tau nyeem thiab pom zoo rau cov ntawv luam tawm ntawm cov ntawv sau.

Nyiaj Txiag: Txoj haujlwm no tau txais kev txhawb nqa los ntawm cov nyiaj pab los ntawm Conselho Nacional de Desenvolvimento Científicoe Tecnológico (CNPq); Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES);Instituto Nacional de Ciência e Tecnologia–Fluidos Complexos (INCT-FCx); Instituto Nacional deCiência e Tecnologia em Medicina Regenerative (INCT-Regenera), tag nrho los ntawm Brazil.

Kev lees paub: Cov duab hauv qhov kev tshaj tawm no tau tsim hauv BioRender.com

Kev tsis sib haum xeeb ntawm kev txaus siab: Cov neeg sau ntawv tshaj tawm tsis muaj teeb meem ntawm kev txaus siab.

Cov ntaub ntawv

1. Lub Koom Haum Ntiaj Teb Kev Noj Qab Haus Huv. Kev pheej hmoo txo ​​qis ntawm kev paub txog kev poob qis thiab kev poob siab: WHO Cov Lus Qhia; LEEJ TWG: Geneva, Switzerland, 2019; ISBN 9789241550543.

2. KOJ. Ntiaj teb no Action Plan on the Public Health Response to Dementia 2017–2025; LEEJ TWG: Geneva, Switzerland, 2017; ISBN 978-92-4-151348-7.

3. Mathieu, C.; Pappu, RV; Paul Taylor, J. Tshaj qhov sib sau ua ke: Pathological theem hloov hauv cov kab mob neurodegenerative. Science 2020, 370, 56–60. [CrossRef]

4. Reichert, CO; de Freitas, FA; Sampaio-Silva, J.; Rokita-Rosa, L.; de Barros, PL; Levy, D.; Bydlowski, SP Ferroptosis mechanismsinvolved nyob rau hauv cov kab mob neurodegenerative. Int. J. Mol. Sci. 2020, 21, 8765. [CrossRef]

5. Singh, A.; Kev, R.; Saib, L.; Kukreti, S. Oxidative stress: Ib qho tseem ceeb modulator hauv cov kab mob neurodegenerative. Molecules 2019, 24, 1583.

6. Lin, MT; Beal, MF Mitochondrial dysfunction thiab oxidative kev nyuaj siab nyob rau hauv cov kab mob neurodegenerative. Xwm Txheej 2006, 443, 787–795 [PubMed]

7. Liguori, I.; Russo, G.; Curcio, F.; Bulli, G.; Aran, L.; Della-Morte, D.; Gargiulo, G.; Tes, G.; Cacciatore, F.; Bonaduce, D.; thiab al.Oxidative kev nyuaj siab, kev laus, thiab kab mob. Clin. Interv. Hnub nyoog 2018, 13, 757. [PubMed]

8. Lev, D.; Reichert, CO; Bydlowski, SP Paraoxonases kev ua ub no thiab polymorphisms nyob rau hauv cov neeg laus thiab cov laus cov kab mob: Ib qho kev piav qhia.Antioxidants 2019, 8, 118. [CrossRef]9. Rosa-Fernandes, L.; Maselli, LMF; Maeda, NY; Palmisano, G.; Bydlowski, SP Sab nraum-hauv, sab hauv-tawm: Proteomic tsom xam ntawm endothelial kev nyuaj siab kho los ntawm 7-ketocholesterol. Chem. Phys. Lipids 2017, 207, 231–238. [CrossRef] [PubMed]

10. Rosa Fernandes, L.; Stern, ACB; Cavaglieri, RDC; Nogueira, FCS; Domont, G.; Palmisano, G.; Bydlowski, SP 7-Ketocholesterol kov yeej cov tshuaj tiv thaiv nyob rau hauv cov kab mob myeloid leukemia cell kab dhau MDR1 mechanism. J. Proteomics 2017, 151, 12–23. [CrossRef]

For more information:1950477648nn@gmail.com