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ƆL DI ATIKUL ƐN PRODƆKT INFƆMƐSHƆN WE DƐN GI NA DIS WƐBSAYT NA FƆ ƆL FƆ DI INFƆMƐSHƆN ƐN FƆ EDYUKESHƆN.
Di prɔdak dɛn we dɛn gi na dis wɛbsayt na fɔ in vitro risach nɔmɔ. in vitro risach (Latin: *in glas*, we min insay glas) dεn de du am ausayd mכtalman bכdi. Dɛn prɔdak ya nɔto mɛrɛsin, dɛn nɔ gɛt di aprɔval frɔm di US Food and Drug Administration (FDA), ɛn dɛn nɔ fɔ yuz dɛn fɔ protɛkt, trit, ɔ mɛn ɛni mɛrɛsin, sik, ɔ sik. Di lɔ nɔ gri fɔ mek dɛn put dɛn tin ya insay mɔtalman ɔ animal bɔdi ɛni we.
Insay di fild fɔ layf sayɛns, ol ol tɛm na wan big risach tɔpik. as risεch pan di mεkanism dεm fכ ol de kכntinyu fכ dip, di rol we nikotinamid adenine dinucleotide (NAD+) de ple fכ di anti-aging prכsεs dεn gεt mכr atεnshכn. as kכεnzym we involv insay plεnti kכl fysiolojikal prכsεs dεm insay sεl dεm, dεn fכnshכn se NAD+ de kכlכs fכ di ol prכsεs.
Figure 1 Bayolojikal fכnshכn dεm fכ NAD. NAD de rεgεl εnεji bεlε, strεs rεspכns, εn sεlyul homכstasis tru sirtuin dεm, PARP dεm, εn difrεn rεdכks εnzym dεm.
Ovaviu fכ di Fisiolojikal Fכnshכn dεm fכ NAD+
NAD+ na kכεnzym we de bכku bכku wan insay sεl dεm, we de tek pat pan difrεn ki fysiolojikal prכsεs dεm. i de fכs fכm insay tu fכm dεm insay sεl dεm: di כksidayz fכm (NAD+) εn di ridyus fכm (NADH), we kin intakכnvכlt. dis dinamik bכlεns implεnt fכ mεnten nכmal sεlyul mεtabolism εn fכnshכn.
1. εnεji mεtabolism: NAD+ de ple sεntri rol insay sεlyul rεspireshכn. insay enεji mεtabolism path dεm lεk glycolysis, di tricarboxylic acid saykl, εn oksidativ fכsfכrayleshכn, NAD+ de akt lεk εlektrכn aksepta, we de rεsεp εlektrכn dεm we de rilis di tεm we di mεtabolik sabstεt dεm de כksidεshכn fכ fכm NADH. afta dat, NADH de tכn εlektrכn dεm to di maytochכndrial rεspiretכri chen, usay כksidεtiv fכsfכrayleshכn de jεnarεt adenosin trifכsfεt (ATP), we de gi enεji fכ di sεl. dis prכsεs de mek sכh se di sεl dεm kin kכntinyu fכ gεt inof enεji fכ mεnten dεn nכmal fysiolojikal aktiviti dεm lεk di sεl dεm we de gro, divεlכpmεnt, εn ripa.
di tεm we di glycolysis de, 3-fכsfoglisεrayt de tכn di haydrojεn atכm dεm to NAD+ כnda di akshכn fכ 3-fכsfoglisεrayt dεhaydrojenεz, we de jεnarεt NADH εn 1,3-difosfoglisεrayt. afta dat, NADH de transfכm εlektrכn dεm to כksijεn tru di rεspiretכri chen na di maytochכndria, we kin te fכ prodyuz wata εn kכpl ATP sεntesis. dis de sho se NAD+ na wan indispεns kכmכpכnt fכ sεlyul εnεji mεtabolism, εn chenj dεm na in kכnsantreshכn de afekt di efyushכn fכ enεji prodakshכn dεn wan dεm.
2. DNA ripa: NAD+ na sabstεrayt fכ di poly(ADP-ribose) polimεrayz (PARP) famili. afta PARP dכn no εn biεn di DNA sayt dεm we dεn dכn pwεl, i de yuz NAD+ as sabstεrayt fכ transfכm ADP-ribose grup dεm to insεf כ כda protin dεm, we de fכm poly(ADP-ribose) (PAR) chen dεm. dis PAR chen dεm kin rikrut εn aktibכt wan siriכs protin dεm we de involv fכ DNA ripa, lεk DNA ligase εn DNA polimεrayz, we de mek dεn bigin di DNA ripa prכsεs. we di sεl dεm de εkspos to DNA dεm we dεn kכz fכ tin dεm lεk כltra vayolet rεdyushכn כ kεmikכl, di PARP-NAD+ sistεm de rεspכnd kwik kwik wan fכ ripa di DNA we dεn dכn pwεl εn mεnten di jεnomik stεbiliti. if di NAD+ lεvεl dεm nכ infεkt, di PARP aktiviti de inhεbit, we de mek di DNA ripa kapasiti dεm dכn rεdכks, di jεnomik instεbiliti de inkrεs, εn aksεlεrat sεl dεm we de ol εn di sik bigin.
3. post-transleshכnal modifyushכn fכ di protin dεm: NAD+ de tek pat bak pan di katalytik riakshכn dεm fכ di sirtuin famili protin dεm. Sirtuins na wan klas fכ NAD+-dipεndεnt deacetylases we kin pul asetyl modifyushכn frכm laysin rεsidεns pan protin dεm. dis deacetylation modifyushכn de rεgεl di aktvכti, stεbiliti, εn sכbsεlyul lכkalεyzeshn fכ plεnti protin dεm, we de infכlכw sεlyul mεtabolism, strεs rispכns, ol, εn כda fysiolכjik prכsεs dεm. fכ egzampl, SIRT1 kin rεgεl di aktvכti fכ transkripshכn fכktכ dεm lεk p53 εn FOXO tru deacetylation modifyushכn, we de infכlכw sεl saykl, apoptosis, εn antioksidant strεs prכsεs dεm. we sεl dεm de כnda strεs, SIRT1 de dεasetεlayt p53 bay we i de it NAD+, we de inhεbit p53 in transkripshכnal aktiviti, ridyus di כkכrεshכn fכ apoptosis, εn εnhans di sεl sכvayv kapasiti.
Chenj dεm na di NAD+ lεvεl dεm we yu de ol
stכdi dεn sho se wit di ej, di NAD+ lεvεl dεm de dכn sכmtεm na di mכtalman tisu dεm εn sεl dεm na di bכdi. dis dכn dכn si insay difrεn spεshal, inklud mami dεm, nematod, εn frut flay, we sho se di ridyus NAD+ lεvεl kin bi wan kכnsyuv fεnomen insay di ol prכsεs.
1. di chenj dεm we de apin to di tisu dεm: di εkstenshכn εn di mεkanism dεm we di NAD+ lεvεl de dכn wit di ej kin difrεn akɔdin to difrεn tisu dεm. insay di skel mכsul, di ol we de kכmכt wit di dכn pan di aktvכti fכ di kכl εnzym dεm na di NAD+ bayosεntetik path, we de mek di NAD+ sεntesis de ridyus. di εksprεshכn εn aktvכti fכ NAD+ kכnsכm εnzym dεm lεk CD38 de inkrεs, aksεlεrayt NAD+ dεgradashכn εn ultimately rizulta in signifyant dεkrεshכn pan NAD+ lεvεl dεm na skel mכsul. insay di liva, apat frכm di כltεrayshכn dεm we wi bin dכn tכk bכt pan di sεntesis εn dεgradashכn path dεm, ol kin afekt NAD+ transpכt prכsεs dεm bak, we kin mek i nכ balans insay intasεlulyar NAD+ distribushכn εn i kin ridyus in ifektiv kכnsantreshכn mכr.
2. Asosieshɔn wit sik dɛm we gɛt fɔ du wit di ej: Di NAD+ lɛvɛl we de dɔŋ kin gɛt fɔ du wit di biginin ɛn prɔgrɛs fɔ difrɛn sik dɛm we gɛt fɔ du wit di ej. insay di sik dεm we de kכmכt na di at, di dכn we di mayokardia sεl NAD+ lεvεl dεm de kכz fכ ol de mek di enεji mεtabolism dizכrd, inkrεs כksidεtiv strεs, εn mayokardial sεl apoptosis, we de mek di kadyak disfכnkshכn bכku. insay nyurodijεnεraytiv sik dεm lεk Alzaima sik εn Pakinsin sik, di rεdukshכn pan nyuronal NAD+ lεvεl de afekt DNA ripa εn protin homכstasis, we de protεkt di agregεshכn fכ nyurotoksik protin dεm εn nyuronal dεd. mεtabolik sik dεm lεk dayabεtis de sho bak wit di dכn we di NAD+ lεvεl dεn de dכn, biכs we NAD+ de dכn de mek di insulin sekreshכn εn insulin sεnsitiviti de pwεl, we de mek di bכdi glukכs rεgulεshכn abnכmal.
di mεkanism dεm we di NAD+ lεvεl dεm we dεn dכn dכn de mek dεn ol
1. **Enεji mεtabolism dizכrd**: NAD+ de ple wan kכl rol insay sεlyul εnεji mεtabolism. as di ej de inkrεs, di rεdכks NAD+ lεvεl dεm de mek di εnεji mεtabolism path dεm de impεri εn di ATP prodakshכn de ridyus. dis nכ de כnli afekt nכmal sεlyul fysiolojikal fכnshכn dεm bכt i de trigεr wan siriכs kכmpεnsatri rεspכns dεm, lεk we di maytochכndrial proliferashכn pasmak εn fכnshכnal abnכmaliti dεm. di maytochכndria dεm na di sεl pawa dεm; we NAD+ nכ inof, di maytochכndrial rεspiretכri chen fכnshכn de impεri, we de rεsult in inkrεs prodakshכn fכ riaktiv כksijεn spεs (ROS) dεm we di εlektrכn transpכt de. di ROS we pasmak kin atak di maytochכndrial DNA, protin dεm, εn lipid dεm, we de disrupt di maytochכndrial strכkchכ εn fכnshכn mכr, we de mek wan bad bad saykl we de mek di sεl dεm ol kwik kwik wan.
Figure 2 di mεkanism dεm we dεn prכpos fכ aw ol de afekt NAD mεtabolism. di ol we dεn de ol de disrupt di bεlε bitwin NAD sεntesis εn dεgradashכn, we de mek di NAD lεvεl dεm na difrεn tisu dεm dכn dכn.
2. Akyumyuleshכn fכ DNA dεmεj: As sabstεrayt fכ PARP, ridyus NAD+ lεvεl dεm de wik DNA ripa kapasiti. we dεn nכ kin ebul fכ rεpεr di DNA dεm fayn fayn wan insay di tεm, i kin mek di jεnomik instεbiliti, we kin kכmכt bכku mכtεshכn dεm εn di kromozom abnכmaliti dεm. dis jεnεtik dεmεj dεm de intafεr wit nכmal sεlyul fysiolojikal fכnshכn dεm, we de afekt sεl proliferashכn, difrεns, εn apoptosis, we de mek sεl dεm ol. di DNA dεm we dεn dכn pwεl de aktibכt bak di signal path dεm we de rilet to di ol we de insay di sεl dεm, lεk di p53-p21 εn p16INK4a-Rb path dεm, we de mek di sεl dεm we de ol mכr.
3. Disrεgulεshכn fכ di senesεns-rεlatεd signal path dεm: NAD+-dipεndεnt sirtuin famili protin dεm de ple imכtant rol fכ rεgεl di senesεns-rεlatεd signal path dεm. as di NAD+ lεvεl dεn de dכn, di sirtuin aktvכti de inhεbit, we de mek dεn ridyus di deacetylation modifyushכn dεm fכ di dכwnstrim tכgεt protin dεm. di ridyus SIRT1 aktvכti de rizulta in p53 de insay wan hεli asetylet stet, we de εnhans p53 in transkripshכnal aktvכti, we de lid to sεl saykl arεst εn apoptosis; di sem tεm, wik diasetyleshכn fכ di FOXO transkripshכn fכktכ bay SIRT1 de afekt di sεl in antioksidant strεs rεsistεns εn mεtabolik rεguleshכn. apat frכm dat, כltεrayshכn dεm na di aktvכti fכ כda sirtuin famili mεmba dεm lεk SIRT3 εn SIRT6 de impכkt bak di maytochכndrial fכnshכn, jεnomik stεbiliti, εn inflammatory rεspכns dεm, we kכlektif wan de drεb di prכgreshכn fכ sεlyul sεnesεns.
Anti-aging strateji fɔ inkrisayz NAD+ lɛvɛl
giv di klos rilayshכn bitwin ridyus NAD+ lεvεl εn ol, stratεji fכ delay ol bay we dεn inkrεs NAD+ lεvεl dεn bi wan risach hotspot.
1. Suplεnt NAD+ Prεkursכr dεm: fכ supliment NAD+ prεkursכr dεm na kכmכn we fכ inkrεs di NAD+ lεvεl dεm. di kכmכn NAD+ prεkursכr dεm inklud nikotinamid (NAM), nikotinamid mכnonyukliotayd (NMN), εn nikotinamid raybosayd (NR). dis prεkursכr dεm kin kכnvכlt to NAD+ tru spεsifi k mεtabolik path dεm insay sεl dεm, we de mek in lεvεl dεm go כp.
Nikotinamid (NAM): NAM na wan fכm fכ vaytam in B3 we dεn kin kכnvכlt to nikotinamid mכnonyukliotayd (NMN) tru di akshכn fכ nikotinamid fכsfכribosyltransfεrayz (NAMPT), we dεn kin yuz fכ sכntez NAD+. di hכy dכz NAM suplimentεshכn kin fכdbכk inhεbit NAMPT aktiviti, we de limited in abiliti fכ inkrεs NAD+ lεvεl dεm. fכ yuz NAM fכ lכng tεm i kin mek sayd ifekt dεm lεk fכ fכlכ di skin, bכt if dεn gi am di rayt doz, NAM kin inkrεs di intasεlulyar NAD+ lεvεl dεm fayn fayn wan, impruv di εnεji mεtabolism, εn εnhans di DNA ripa fכnshכn dεm.
Nikotinamid mononyukliotayd (NMN): NMN na dayrekt prεkursכr insay di NAD+ bayosεntetik path. stכdi dεn sho se di כral NMN de abzכp kwik kwik wan εn kכnvכlt to NAD+, we de ifektiv wan inkrεs di NAD+ lεvεl dεm na difrεn tisu dεm. insay animal εkspεriεns, NMN suplimentεshכn dεn sho sכm improvεmεnt pan εj-rεlatεd mεtabolik dizכrd, kכdivaskyul disfכnkshכn, εn nyurodijεnεraytiv sik dεm. fכ egzampl, insay di ol mays dεm, NMN suplimentεshכn impruv locomotor abiliti, εnhans insulin sεnsitiviti, εliviet εj-rεlatεd patכlayz chenj dεm na di at, εn εnhans kכgnitiv fכnshכn. apat frכm dat, dεn sho se NMN de protεkt di maytochכndrial bayojεnεsis, εnhans di maytochכndrial fכnshכn, εn ridyus כksidεtiv strεs-indyus dεmεj.
Nikotinamid ribosayd (NR): NR na ɔda ifektiv NAD+ prɛkursɔ we kin kɔnvɔyt to NMN tru fכsfכrayleshכn bay nikotinamid ribosayd kinaz (NRK), we dεn kin yuz afta dat fכ sכntez NAD+. sεm lεk NMN, supliment wit NR kin inkrεs di intasεlulyar NAD+ lεvεl, impruv mεtabolik fכnshכn, εn delay εj. insay di ol mays dεm, NR suplimentεshכn kin rimodεl mεtabolik εn strεs rεspכns path dεm, εnhans di kromatin-bכnd kapasiti fכ di sirkadian klok jin BMAL1, rεstכr di maytochכndrial rεspiretכri ritm dεm εn sirkadian aktiviti, εn patli rεstכr di fysiolojikal stet fכ di ol mays dεm to di wan fכ yכng mays dεm.
Fig 3 Mכdel we de sho di NAD+ salvεj path εn nikotinamid ribosayd (NR) kכnvכshכn to NAD+.
2. Rεgulεshכn fכ NAD+ mεtabolik εnzym dεm:
aktibכshכn fכ NAD+ sεntez: NAMPT na di rεt-limit εnzym insay di NAD+ bayosεntetik path, εn inkrεs aktvכti kin protεkt NAD+ sεntez. sכm nεchכral kכmpawnd dεm, lεk rεsvεratrol εn apigenin, dεn fכnshכn fכ aktibכt NAMPT, we de mek NAD+ prodakshכn inkrεs. Resveratrol na wan polyphenolic kompound we de insay grep skin, rɛd wayn, ɛn ɔda plant dɛn. i kin indaykt upregulate NAMPT εksprεshכn bay we i de aktibכt di SIRT1-PGC-1α signal path, we de inkrεs di NAD+ lεvεl dεm. rεsvεratrol tritmεnt de impruv εnεji mεtabolism, rεdכks כksidεtiv strεs dεmεj, εn εksεnd layfspan insay ol mays.
inhibit NAD+ kכnsum εnzym dεm: CD38 na mεjכr NAD+ kכnsכm εnzym we in εksprεshכn εn aktvכti de inkrεs wit di ej, we de aksεlεrat NAD+ dεgradashכn. inhibit CD38 aktiviti de ridyus NAD+ kכnsכmshכn εn mεnten intasεlulyar NAD+ lεvεl dεm. sכm sכm sכm sכm mכlikul kכmpawnd dεm, lεk 78c εn apigenin, dεn ripot fכ inhibit CD38 aktiviti. if yu yuz CD38 inhibito dεm i kin inkrεs di NAD+ lεvεl dεm εn impruv di εj-rεlatεd fysiolojikal disfכnkshכn, lεk fכ εnhans di kadyak fכnshכn εn impruv mεtabolik dizכrd dεm.
3. Layf stayl intavɛnshɔn: Layf stayl factor dɛm bak kin rili inflɔws di NAD+ lɛvɛl dɛm.
εksεsayz: rεgulεr εksεsayz de mek di NAD+ bayosεntetik path εn i de inkrεs di NAD+ lεvεl. כl tu di aerobik εksεsayz εn strכng trenin kin inkrεs di εksprεshכn εn aktvכti fכ NAMPT insay skel mכsul, we de protεkt NAD+ sεntesis. εksεsayz kin rεgεl bak di εksprεshכn fכ di NAD+ mεtabolism-rεlatεd jin dεm, impruv di maytochכndrial fכnshכn, εn εnhans sεlyul antioksidant kapasiti. pan di ol pipul dεm, mכdarεt εksεsayz kin εfεktiv fכ inkrεs di NAD+ kכntεnt na di mכsul dεm, impruv di mכsul dεm trεnk εn mכtal fכnshכn, εn slo dכn di ol prכsεs.
Fɔ stɔp fɔ it: Bɔku pipul dɛn no se fɔ stɔp fɔ it, lɛk fɔ stɔp fɔ it kalori (CR) ɛn fɔ fast wan wan tɛm (IF), as fayn we fɔ mek pɔsin nɔ ol. dis it pat dεm de εksyεrt dεn anti-aging ifekt dεm bay we dεn de rεgεl NAD+ mεtabolism. CR εn IF de aktibכt sirtuin famili protin dεm lεk SIRT1, we de promuot NAD+ sεntez εn yutilizeshכn. If yu nɔ it di it kin ridyus di ɔksidativ strɛs bak, i kin mek di mɛtabolik wok fayn, ɛn i kin ridyus di risk fɔ gɛt sik dɛn we gɛt fɔ du wit di ej. insay animal εkspεriεns, lכng tεm kalori rεstrikshכn kin sכmtεm inkrεs di NAD+ lεvεl εn εksεnd di layfspan fכ mכltipכl spεshal.
Anti-aging Efεkt dεm we di NAD+ Lεvεl dεm de Inkrεs
1. Anti-aging ifekt dεm na animal εkspεriεns: כl di animal εkspεriεns dεn dכn kכnfכm se we di NAD+ lεvεl dεm de inkrεs i kin sכmtεm slo dכn di ej prכsεs εn impruv di ej-rεlatεd fysiolojikal disfכnkshכn.
Impruv Mεtabolik Fכnshכn: Insay di ol mays dεm, supliment wit NMN כ NR kin εnhans insulin sεnsitiviti, rεgεl di blכd glukכs lεvεl, εn impruv di lipid mεtabolism dizכrd. NAD+ prεkursכr supliment kin inkrεs fεt asid כksidεshכn insay adipos tisu, ridyus fεt akyumyuleshכn, εn lכs di risk fכ sik dεm we de fכ fat. we di NAD+ lεvεl dεm de inkrεs i kin mek di liva mεtabolik fכnshכn fayn bak, i kin mek di liva in dεtכksifikεshכn kεpasiti fכ drog εn tכxin dεm, εn i kin mεnten di nכmal liva fysiolojikal fכnshכn.
di kכdivaskyul fכnshכn protεkshכn: we di kכdivaskyul sistεm de ol, di kכdivaskyul sistεm de gεt strכkchכral εn fכnshכnal chenj dεm, lεk di mayokardial haypatrכfi εn di vaskulεr εlastik we de ridyus. supliment wit NAD+ prεkursכr kin impruv di kadyak kכntrikshכn εn rilaks fכnshכn, ridyus mayokardial fכbrosis, εn mitigate כksidεtiv strεs dεmεj. insay animal mכdel, supliment wit NMN כ NR kin lכs bכdi prεshכn, impruv di vaskulεr εndoteyl fכnshכn, εn ridyus di risk fכ kכdivaskyul sik. insay mayokardial infarkshכn mכdel dεm, we di NAD+ lεvεl dεm de inkrεs kin mek di mayokardial sεl dεm sכvayv εn rεpa, ridyus infarkshכn saiz, εn impruv di kadyak fכnshכn.
Nyuroprotεktiv ifekt dεm: Insay mכdel dεm fכ nyurodijεnεraytiv sik dεm, we di NAD+ lεvεl dεm de inkrεs de sho sכm nyuroprotεktiv ifekt dεm. stכdi dεn sho se supliment wit NMN כ NR kin impruv di kכgnitiv fכnshכn, ridyus nyuroinflameshכn, εn dכn di agregεshכn fכ nyurotoxik protin dεm. insay di Alzaima sik maws mכdel dεm, supliment wit NAD+ prεkursכr kin ridyus β-amyloid prodakshכn, inhεbit pasmak fכsfכrayleshכn fכ tau protin, protεkt nyuron dεm frכm damej, εn dat kin impruv di lanin εn mεmכri abiliti.
εkstend layfspan: insay difrεn mכdel כganism dεm, dεn sho se we di NAD+ lεvεl dεm de inkrεs de εksεnd layfspan. insay nematod εn frut flay, fכ inkrεs di NAD+ lεvεl tru jεnεtik manipulεshכn כ supliment wit NAD+ prεkursכr kin sכmtεm εksεnd dεn layfspan. insay maws εkspεriεns, lכng tεm suplimentεshכn wit NMN כ NR sho bak wan tεnd tכwεd εkstεnd layfspan, pan כl we dis ifekt kin difrεnt akraos difrεn stכdi dεm. Ɔl togɛda, dɛn tin ya we dɛn fɛn sho di fayn impak we di NAD+ lɛvɛl go ɔp pan layfspan.
Dɔn
as imכtant kכεnzym insay sεl dεm, NAD+ de ple wan indispεnsεbl rol insay di kכl fysiolojikal prכsεs dεm lεk εnεji mεtabolism, DNA ripa, εn pכst-transleshכnal modifyushכn fכ di protin dεm. as di ej de go כp, di dכn we di NAD+ lεvεl dεn de dכn de kכlכsכl wit di ol prכsεs εn di biginin εn prכgreshכn fכ difrεn sik dεm we de kכmכt frכm di ej. Strateji fכ inkrεs di NAD+ lεvεl, lεk fכ supliment NAD+ prεkursכr, rεgul NAD+ mεtabolik εnzym dεm, εn layf stayl intavεnshכn dεm, dεn dכn sho sכm anti-aging ifekt dεm na animal εkspεriεns, inklud impruv mεtabolik fכnshכn, protεkshכn fכ di kכdivaskyul εn nεv sistεm, εn εkstend layfspan.
Sos dɛn we dɛn pul
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[4] Yuan Y, Liang B, Liu X, ɛn ɔda pipul dɛn. Targeting NAD+: na kɔmɔn strateji fɔ delay di at ol?[J]. Sεl Day Diskכvri, 2022,8. https://api.semanticscholar.org/CorpusID:248393418, di wan dɛn we de stɔdi bɔt di Baybul
[5] Levine D. C., Hɔng H., Weidemann B. J., ɛn ɔda pipul dɛn. NAD(+) Kontrol Sirkadian Riprogramin tru PER2 Nyuklia Translokeshɔn to Kɔnta Ɛj[J]. Molikul Sεl, 2020,78(5):835-849.DOI:10.1016/j.molsεl.2020.04.010.
[6] Fang E. F., Hou Y, Lautrup S, ɛn ɔda pipul dɛn. NAD(+) augmεntεshכn de rεstכr maytofagi εn limited aksεlεrayt εj in Werner sεndrכm[J]. Nature Komyunikeshɔn, 2019,10(1):5284.DOI:10.1038/s41467-019-13172-8.
[7] Yaku K, Okabe K, Nakagawa T. NAD mεtabolism: Implεkshכn in ol εn lכng layf[J]. Aging Risach Rivyu, 2018,47:1-17.DOI:10.1016/j.arr.2018.05.006.
[8] Chaturvedi P, Tyagi S C. NAD(+) : Na big pleya in kadyak ɛn skel mɔsul rimɔdelin ɛn ol[J]. J ɔ rnal ov Sεlyul Fysioloji, 2018,233(3):1895-1896.DOI: 10.1002/jcp.26014.
Prodak we de fɔ yuz fɔ risach nɔmɔ:
