{"id":6829,"date":"2024-04-10T01:59:41","date_gmt":"2024-04-10T01:59:41","guid":{"rendered":"https:\/\/longchangchemical.com\/?post_type=product&p=6829"},"modified":"2025-12-17T02:18:24","modified_gmt":"2025-12-17T02:18:24","slug":"beta-nicotinamide-mononucleotide-cas-1094-61-7","status":"publish","type":"product","link":"https:\/\/longchangchemical.com\/hu\/product\/beta-nicotinamide-mononucleotide-cas-1094-61-7\/","title":{"rendered":"b\u00e9ta-nikotinamid-mononukleotid CAS 1094-61-7"},"content":{"rendered":"

B\u00e9ta-nikotinamid mononukleotidgyors r\u00e9szletek<\/strong><\/p>\n

K\u00e9miai n\u00e9v: B\u00e9ta-nikotinamid-mononukleotid<\/p>\n

CAS-sz\u00e1m: 1094-61-7<\/p>\n

Molekul\u00e1ris k\u00e9plet: C11H15N2O8P<\/p>\n

B\u00e9ta-nikotinamid-mononukleotidSzerkezet:\"B\u00e9ta-nikotinamid-mononukleotid<\/p>\n

Molekulat\u00f6meg: 334,22<\/p>\n

Megjelen\u00e9s: Feh\u00e9r por<\/p>\n

Assay:97%~100.0%<\/p>\n

B\u00e9ta-nikotinamid-mononukleotidot\u00edpusos tulajdons\u00e1gok<\/strong><\/p>\n\n\n\n\n\n\n\n\n\n
T\u00e9tel<\/td>\nM\u0171szaki adatok<\/td>\n<\/tr>\n
Megjelen\u00e9s<\/td>\nFeh\u00e9r por<\/td>\n<\/tr>\n
Az oldat megjelen\u00e9se (5% w\/v v\u00edzben)<\/td>\nSz\u00edntelen vagy halv\u00e1nys\u00e1rga \u00e9s tiszta<\/td>\n<\/tr>\n
V\u00edz<\/td>\n\u22646%<\/td>\n<\/tr>\n
Arz\u00e9n<\/td>\n\u22641 ppm<\/td>\n<\/tr>\n
Neh\u00e9zf\u00e9mek<\/td>\n\u226410 ppm<\/td>\n<\/tr>\n
Assay<\/td>\n97%~100.0%<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

B\u00e9ta-nikotinamid-mononukleotidHaszn\u00e1lat<\/strong><\/p>\n

Anti-aging kutat\u00e1s, Anti-aging eg\u00e9szs\u00e9g\u00fcgyi term\u00e9kek nyersanyagok<\/p>\n

B\u00e9ta-nikotinamid-mononukleotidKiszerel\u00e9s \u00e9s sz\u00e1ll\u00edt\u00e1s<\/strong><\/p>\n

Csomagol\u00e1s: 25kg \/ karton v\u00f6d\u00f6r<\/p>\n

Sz\u00e1ll\u00edt\u00e1s: Nem vesz\u00e9lyes rakom\u00e1ny<\/p>\n

B\u00e9ta-nikotinamid-mononukleotid-t\u00e1rol\u00e1s<\/strong><\/p>\n

Sz\u00e1raz, szell\u0151ztetett helyen t\u00e1rolja, hogy elker\u00fclje a k\u00f6zvetlen napf\u00e9nyt.<\/p>\n

L\u00e9pjen kapcsolatba vel\u00fcnk most!<\/b><\/strong><\/h2>\n

Ha \u00e1rra van sz\u00fcks\u00e9ge, k\u00e9rj\u00fck, t\u00f6ltse ki el\u00e9rhet\u0151s\u00e9g\u00e9t az al\u00e1bbi \u0171rlapon, \u00e1ltal\u00e1ban 24 \u00f3r\u00e1n bel\u00fcl felvessz\u00fck \u00d6nnel a kapcsolatot. \u00d6n is k\u00fcldhet nekem e-mailt info@longchangchemical.com<\/span><\/a>\u00a0munkaid\u0151ben ( 8:30-18:00 UTC+8 H.-Szombat ) vagy haszn\u00e1lja a weboldal \u00e9l\u0151 chatj\u00e9t, hogy azonnali v\u00e1laszt kapjon.<\/b><\/strong><\/h4>\n
\n

Az iszk\u00e9mi\u00e1s agyi \u00e9rbetegs\u00e9g k\u00e9t t\u00edpusa a tranziens agyi iszk\u00e9mia \u00e9s az agyi infarktus. K\u00f6z\u00fcl\u00fck az agyi infarktust a k\u00ednai orvosl\u00e1s diagnosztik\u00e1j\u00e1ban iszk\u00e9mi\u00e1s stroke-nak (IS) nevezik, amely az agysz\u00f6veti ter\u00fcletek helyi v\u00e9rell\u00e1t\u00e1si akad\u00e1lyainak k\u00fcl\u00f6nb\u00f6z\u0151 okai miatt fell\u00e9p\u0151 neurol\u00f3giai m\u0171k\u00f6d\u00e9si zavarok sorozata, ami az agysz\u00f6vet iszk\u00e9mi\u00e1s \u00e9s hipoxi\u00e1s nekr\u00f3zis\u00e1t eredm\u00e9nyezi. A hal\u00e1loz\u00e1si \u00e9s rokkants\u00e1gi ar\u00e1ny magas, a k\u00f3ros mechanizmus \u00f6sszetett, \u00e9s \u00e9vente nagy gazdas\u00e1gi terhet r\u00f3 a vil\u00e1gra. Az oxig\u00e9n-gl\u00fck\u00f3zmegvon\u00e1s (OGD) az IS leggyakrabban haszn\u00e1lt in vitro modellje, \u00e9s sz\u00e9les k\u00f6rben haszn\u00e1lj\u00e1k az alap- \u00e9s preklinikai stroke-kutat\u00e1sban.<\/p>\n

A sejtek autof\u00e1gi\u00e1ja (autof\u00e1gia) sz\u00e9les k\u00f6rben jelen van az eukari\u00f3ta sejtekben, \u00e9s fontos szerepet j\u00e1tszik a sejtek t\u00fal\u00e9l\u00e9s\u00e9nek \u00e9s hal\u00e1l\u00e1nak szab\u00e1lyoz\u00e1s\u00e1ban. Sz\u00e1mos tanulm\u00e1ny arra utal, hogy az autof\u00e1gia szorosan \u00f6sszef\u00fcgg az IS el\u0151fordul\u00e1s\u00e1val \u00e9s kialakul\u00e1s\u00e1val. Egyes tanulm\u00e1nyok kimutatt\u00e1k, hogy a neuron\u00e1lis autof\u00e1gia enyh\u00edti az ischaemi\u00e1s agyk\u00e1rosod\u00e1st, m\u00edg m\u00e1sok arr\u00f3l sz\u00e1moltak be, hogy a neuron\u00e1lis autof\u00e1gia s\u00falyosb\u00edtja az ischaemi\u00e1s agyk\u00e1rosod\u00e1st, de a specifikus mechanizmus nem egy\u00e9rtelm\u0171.
\nA \u03b2-nikotinamid-mononukleotid (NMN) sz\u00e1mos \u00e9lelmiszerben megtal\u00e1lhat\u00f3, \u00e9s n\u00e9lk\u00fcl\u00f6zhetetlen a sejtek \u00f6reged\u00e9s\u00e9nek szab\u00e1lyoz\u00e1s\u00e1hoz \u00e9s a szervezet norm\u00e1lis m\u0171k\u00f6d\u00e9s\u00e9nek fenntart\u00e1s\u00e1hoz, valamint sz\u00e1mos fontos intracellul\u00e1ris jel\u00e1tviteli \u00fatvonal \u00e1tvitel\u00e9ben vesz r\u00e9szt. Arr\u00f3l sz\u00e1moltak be, hogy az NMN in vitro adagol\u00e1sa gyorsan \u00e1talak\u00edtja a NAD+-ot NAD+ -v\u00e1, \u00e9s szab\u00e1lyozza a sejtek \u00f6reged\u00e9s\u00e9t \u00e9s fenntartja a szervezet norm\u00e1lis funkci\u00f3it. az NMN kompenz\u00e1lhatja az IS \u00e1ltal okozott NAD+ cs\u00f6kken\u00e9st, \u00e9s jav\u00edthatja az agyi iszk\u00e9mi\u00e1s neuronok k\u00e1rosod\u00e1s\u00e1t. Ez arra utal, hogy az NMN szerepet j\u00e1tszik az IS-ben. Egyes tanulm\u00e1nyok kimutatt\u00e1k, hogy az NMN el\u0151seg\u00edtheti a neurovaszkul\u00e1ris regener\u00e1ci\u00f3t, jav\u00edthatja az agyi mikrovaszkul\u00e1ris endot\u00e9lfunkci\u00f3t, a gyullad\u00e1scs\u00f6kkent\u00e9st \u00e9s az anti-apopt\u00f3zist. N\u00e9h\u00e1ny tanulm\u00e1ny arra is utal, hogy az autof\u00e1gia szab\u00e1lyoz\u00e1s\u00e1val iszk\u00e9mi\u00e1s agyk\u00e1rosod\u00e1s elleni szerepet j\u00e1tszhat, azonban nem vil\u00e1gos az a specifikus mechanizmus, amellyel az NMN szab\u00e1lyozza az autof\u00e1gi\u00e1t az IS ellen.<\/p>\n

A vizsg\u00e1lat c\u00e9lja egy oxig\u00e9ncukor-hi\u00e1nyos PC12 sejtmodell l\u00e9trehoz\u00e1sa, a sejtek t\u00fal\u00e9l\u00e9si ar\u00e1ny\u00e1nak m\u00e9r\u00e9se MTT-vel in vitro, valamint az autofagosz\u00f3m\u00e1k \u00e9s autofagoliszosz\u00f3m\u00e1k kimutat\u00e1sa transzmisszi\u00f3s elektronmikroszk\u00f3pi\u00e1val, az autofagosz\u00f3m\u00e1k fluoreszcencia-intenzit\u00e1s\u00e1nak megfigyel\u00e9se MDC-vel, valamint az LC3-II\/LC3-I, Beclin1, p62 \u00e9s P-mTOR\/mTOR autof\u00e1gi\u00e1val kapcsolatos feh\u00e9rj\u00e9k expresszi\u00f3j\u00e1nak kimutat\u00e1sa Western blot seg\u00edts\u00e9g\u00e9vel, annak \u00e9rdek\u00e9ben, hogy tiszt\u00e1zzuk az NMN hat\u00e1s\u00e1t az OGD \u00e1ltal kiv\u00e1ltott autof\u00e1gia k\u00e1rosod\u00e1s\u00e1ra a PC12 sejtekben.<\/p>\n

A 2017-es Lancet-tanulm\u00e1ny kimutatta, hogy a stroke a leggyakoribb betegs\u00e9g, amely K\u00edn\u00e1ban az \u00e9let\u00e9vek elveszt\u00e9s\u00e9t okozza, gyors lefoly\u00e1s\u00fa, hal\u00e1los kimenetel\u0171 \u00e9s nagyfok\u00fa rokkants\u00e1ggal j\u00e1r. Ezek k\u00f6z\u00fcl az IS az \u00f6sszes stroke 60-70 sz\u00e1zal\u00e9k\u00e1t teszi ki, \u00e9s az IS-t az agy egy ter\u00fclet\u00e9nek v\u00e9rell\u00e1t\u00e1s\u00e1nak cs\u00f6kken\u00e9se okozza egy \u00e9relz\u00e1r\u00f3d\u00e1s miatt. Az agysz\u00f6vet iszk\u00e9mi\u00e1ja \u00e9s hipoxi\u00e1ja patofiziol\u00f3giai v\u00e1laszok sorozat\u00e1t v\u00e1ltja ki, mint p\u00e9ld\u00e1ul a sejtek autof\u00e1gi\u00e1ja, apopt\u00f3zis, oxidat\u00edv stressz, intracellul\u00e1ris kalcium-t\u00falterhel\u00e9s stb. Az IS t\u00fal\u00e9l\u0151inek hossz\u00fa fel\u00e9p\u00fcl\u00e9si ciklusa van, ami n\u00f6veli a glob\u00e1lis gazdas\u00e1gi terheket. Jelenleg sz\u00e1mos ellenjavallat van a piacon az IS ellen alkalmazott gy\u00f3gyszerekre. Ez\u00e9rt folyamatosan fel kell kutatni az IS megel\u0151z\u00e9s\u00e9re \u00e9s kezel\u00e9s\u00e9re szolg\u00e1l\u00f3 gy\u00f3gyszereket. Az OGD klasszikus modell az IS in vitro tanulm\u00e1nyoz\u00e1s\u00e1ra, \u00e9s a PC12 sejtvonal az egyik leggyakrabban haszn\u00e1lt sejtvonal a neuron\u00e1lis k\u00e1rosod\u00e1s tanulm\u00e1nyoz\u00e1s\u00e1ra, amelyet gyakran haszn\u00e1lnak az iszk\u00e9mia-hypoxia k\u00e1rosod\u00e1s tanulm\u00e1nyoz\u00e1s\u00e1ra. Ez\u00e9rt ebben a k\u00eds\u00e9rletben az OGD PC12 sejtmodellt haszn\u00e1ltuk az in vitro vizsg\u00e1lathoz.<\/p>\n

Az NMN az emberi szervezetben \u00e9s sz\u00e1mos \u00e9lelmiszerben term\u00e9szetesen el\u0151fordul\u00f3 anyag, molekulat\u00f6mege 334,22. A nikotinamid-foszf\u00e1t riboszil-transzfer\u00e1z reakci\u00f3 term\u00e9ke \u00e9s a NAD+ egyik legfontosabb prekurzora. Egyes tanulm\u00e1nyok szerint az NMN szintj\u00e9nek szab\u00e1lyoz\u00e1s\u00e1val a szervezetben jobb ter\u00e1pi\u00e1s \u00e9s helyre\u00e1ll\u00edt\u00f3 hat\u00e1st fejt ki a sz\u00edv- \u00e9s \u00e9rrendszeri \u00e9s agyi \u00e9rrendszeri betegs\u00e9gekre, a neurodegenerat\u00edv betegs\u00e9gekre \u00e9s az \u00f6reged\u00e9s degenerat\u00edv betegs\u00e9geire. Arr\u00f3l is besz\u00e1moltak, hogy az NMN bead\u00e1sa cs\u00f6kkentheti az infarktus ter\u00fclet\u00e9t \u00e9s a neurol\u00f3giai funkci\u00f3 k\u00e1rosod\u00e1s\u00e1t patk\u00e1ny MCAO modellben. Ebben a k\u00eds\u00e9rletben MTT-vel kimutatt\u00e1k, hogy az OGD cs\u00f6kkentheti a PC12 sejtek t\u00fal\u00e9l\u00e9si ar\u00e1ny\u00e1t, \u00e9s az NMN 400, 800 \u00e9s 1600 \u03bcmol\/L koncentr\u00e1ci\u00f3ban n\u00f6velte az OGD PC12 sejtek t\u00fal\u00e9l\u00e9si ar\u00e1ny\u00e1t, a legmagasabb t\u00fal\u00e9l\u00e9si ar\u00e1ny a 800 \u03bcmol\/L koncentr\u00e1ci\u00f3ban volt; m\u00edg az NMN 200 \u00e9s 3200 \u03bcmol\/L koncentr\u00e1ci\u00f3ban nem volt jelent\u0151s k\u00fcl\u00f6nbs\u00e9g a sejtek t\u00fal\u00e9l\u00e9si ar\u00e1ny\u00e1ban, ami arra utal, hogy az NMN 200 \u03bcmol\/L koncentr\u00e1ci\u00f3ja n\u00f6velheti a PC12 sejtek t\u00fal\u00e9l\u00e9si ar\u00e1ny\u00e1t. Ez arra utal, hogy a 200 \u03bcmol\/L koncentr\u00e1ci\u00f3 m\u00e9g nem hat\u00e9kony koncentr\u00e1ci\u00f3 az OGD-induk\u00e1lt PC12 sejtek t\u00fal\u00e9l\u00e9si ar\u00e1ny\u00e1nak n\u00f6vel\u00e9s\u00e9re, m\u00edg a 3200 \u03bcmol\/L koncentr\u00e1ci\u00f3 t\u00fal magas lehet, \u00e9s k\u00e1ros\u00edthatja magukat a sejteket.<\/p>\n

A sejtes autof\u00e1gia, m\u00e1s n\u00e9ven II. t\u00edpus\u00fa programozott sejthal\u00e1l, egy olyan folyamat, amelyben a sejtek a saj\u00e1t t\u00fal\u00e9l\u00e9s\u00fck, differenci\u00e1l\u00f3d\u00e1suk, n\u00f6veked\u00e9s\u00fck \u00e9s stabilit\u00e1suk fenntart\u00e1sa \u00e9rdek\u00e9ben az autof\u00e1gi\u00e1val kapcsolatos g\u00e9nek szab\u00e1lyoz\u00e1sa mellett a lizosz\u00f3m\u00e1k seg\u00edts\u00e9g\u00e9vel lebontj\u00e1k saj\u00e1t s\u00e9r\u00fclt, denatur\u00e1lt vagy \u00f6reged\u0151 makromolekul\u00e1ikat, valamint organellumaikat. A tanulm\u00e1nyi t\u00e1bl\u00e1zat azt mutatja, hogy az autof\u00e1gia az IS ut\u00e1n induk\u00e1l\u00f3dik, \u00e9s ugyanakkor az autof\u00e1gia az IS patol\u00f3giai folyamat\u00e1nak kialakul\u00e1s\u00e1t is k\u00eds\u00e9ri, k\u00fcl\u00f6nb\u00f6z\u0151 szab\u00e1lyoz\u00f3 szerepet j\u00e1tszva az IS n\u00e9gy f\u00e1zis\u00e1ban, nevezetesen az akut, szubakut, gy\u00f3gyul\u00e1si \u00e9s k\u00f6vetkezm\u00e9nyes f\u00e1zisokban.<\/p>\n

Az mTOR egy atipikus szerin\/treonin feh\u00e9rje kin\u00e1z, amelynek relat\u00edv molekulat\u00f6mege 289 kDa. k\u00fcl\u00f6nb\u00f6z\u0151 feh\u00e9rj\u00e9i 2 k\u00fcl\u00f6nb\u00f6z\u0151 komplexet, az mTORCl \u00e9s az mTORC2 komplexet alkotva k\u00f6t\u0151dnek. az mTORCl \u00e9rz\u00e9keny a rapamicinre, \u00e9s a n\u00f6veked\u00e9si faktorok \u00e9s t\u00e1panyagjelek integr\u00e1l\u00e1s\u00e1\u00e9rt felel\u0151s, valamint els\u0151sorban a sejtek autof\u00e1gi\u00e1j\u00e1t, a ribosz\u00f3ma biogenezist, a feh\u00e9rje transzl\u00e1ci\u00f3t \u00e9s a lipidszint\u00e9zist szab\u00e1lyozza. az mTORT az autof\u00e1gia szelep\u00e9nek tekintik. Vizsg\u00e1latok kimutatt\u00e1k, hogy a foszforil\u00e1lt mTOR k\u00e9pes csillap\u00edtani az oxig\u00e9ncukor-megvon\u00e1s okozta s\u00e9r\u00fcl\u00e9seket, \u00e9s szerepet j\u00e1tszik a sejtek v\u00e9delm\u00e9ben. A 3-MA az autof\u00e1gia \u00e1ltal\u00e1nosan haszn\u00e1lt inhibitora. rAPA egy mTOR-inhibitor, amely az mTORC1 g\u00e1tl\u00e1s\u00e1val induk\u00e1lja az autof\u00e1gia megindul\u00e1s\u00e1t, \u00e9s autof\u00e1gia-aktiv\u00e1tornak is nevezik. Ebben a k\u00eds\u00e9rletben a 3-MA \u00e9s a rAPA csoportot az\u00e9rt \u00e1ll\u00edtottuk fel, hogy beavatkozzunk az OGD \u00e1ltal induk\u00e1lt autof\u00e1gia szab\u00e1lyoz\u00e1s\u00e1ba a PC12 sejtekben, \u00e9s a 3-MA, a rAPA \u00e9s a gy\u00f3gyszer kombin\u00e1ci\u00f3s csoportot is az\u00e9rt \u00e1ll\u00edtottuk fel, hogy megfigyelj\u00fck, hogy az NMN k\u00e9pes-e ellens\u00falyozni a 3-MA vagy a rAPA hat\u00e1s\u00e1t az OGD \u00e1ltal induk\u00e1lt autof\u00e1gi\u00e1ra a PC12 sejtekben.<\/p>\n

A Beclin-1, LC3 \u00e9s p62 feh\u00e9rj\u00e9k szintje az autof\u00e1gia szerep\u00e9nek fontos detektora lehet.A Beclin1 az autof\u00e1gia egyik j\u00f3l ismert szab\u00e1lyoz\u00f3ja, \u00e9s pozit\u00edvan korrel\u00e1l az autof\u00e1gi\u00e1val.A Beclin1 k\u00f6lcs\u00f6nhat\u00e1sba l\u00e9p olyan feh\u00e9rj\u00e9kkel, mint a VPS15, VPS34 \u00e9s ATG14 az autof\u00e1gia \u00e9s a membr\u00e1ntranszport funkci\u00f3inak ell\u00e1t\u00e1sa \u00e9rdek\u00e9ben.Az LC3 az \u00e9leszt\u0151ben az ATG8 ubikvitinszer\u0171 m\u00f3dos\u00edt\u00f3 homol\u00f3gja, az LC3 az \u00e9leszt\u0151ben az ATG8 ubikvitinszer\u0171 m\u00f3dos\u00edt\u00f3 homol\u00f3gja, \u00e9s felt\u00e9telezhet\u0151en szerepet j\u00e1tszik az autof\u00e1gi\u00e1ban. Az LC3 elvesz\u00edti C-termin\u00e1lis marad\u00e9k\u00e1t az ATG4-gyel val\u00f3 kezel\u00e9s ut\u00e1n, \u00e9s LC3-I-v\u00e9 alakul \u00e1t. Az LC3-I ubikvitin\u00e1ci\u00f3-szer\u0171 enzimatikus reakci\u00f3k kaszk\u00e1dj\u00e1n megy kereszt\u00fcl, kovalensen k\u00f6t\u0151dik az autofagosz\u00f3ma membr\u00e1nban l\u00e9v\u0151 lipidmolekul\u00e1hoz, a foszfatidil-etanolaminhoz, \u00e9s \u00e1talakul LC3-II-v\u00e9, \u00e9s az LC3-II \u00e9s az LC3-I ar\u00e1ny\u00e1nak n\u00f6veked\u00e9se az autof\u00e1gia emelkedett szintj\u00e9t jelzi. A p62 az autof\u00e1gi\u00e1s aktivit\u00e1st t\u00fckr\u00f6z\u0151 markerfeh\u00e9rje, \u00e9s feh\u00e9rjeszintje korrel\u00e1l az autof\u00e1gia szintj\u00e9vel. p62 az autof\u00e1gi\u00e1s aktivit\u00e1s markerfeh\u00e9rje, \u00e9s feh\u00e9rjeszintje negat\u00edvan korrel\u00e1l az autof\u00e1gi\u00e1val, azaz, amikor autof\u00e1gia t\u00f6rt\u00e9nik, a p62 feh\u00e9rje lebomlik a citoplazm\u00e1ban; amikor az autof\u00e1gia aktivit\u00e1sa gyeng\u00fcl \u00e9s az autof\u00e1gia funkci\u00f3ja hib\u00e1s, a p62 feh\u00e9rje felhalmoz\u00f3dik a citoplazm\u00e1ban. Ebben a k\u00eds\u00e9rletben Western blot seg\u00edts\u00e9g\u00e9vel meger\u0151s\u00edtett\u00e9k, hogy az NMN k\u00e9pes lefel\u00e9 szab\u00e1lyozni a Beclin1 \u00e9s az LC3-II\/LC3-I feh\u00e9rj\u00e9k relat\u00edv expresszi\u00f3j\u00e1t, \u00e9s felfel\u00e9 szab\u00e1lyozni a P-mTOR\/mTOR \u00e9s a p62 feh\u00e9rj\u00e9k expresszi\u00f3j\u00e1t. Ezenk\u00edv\u00fcl transzmisszi\u00f3s elektronmikroszk\u00f3pi\u00e1t \u00e9s MDC-m\u00f3dszert is alkalmaztunk annak meger\u0151s\u00edt\u00e9s\u00e9re, hogy az NMN k\u00e9pes cs\u00f6kkenteni az autof\u00e1gikus vezikul\u00e1k, az autof\u00e1gikus lizosz\u00f3m\u00e1k, valamint a fluoreszcens foltok sz\u00e1m\u00e1t \u00e9s intenzit\u00e1s\u00e1t az OGD PC12 sejtekben. A fentiek azt jelzik, hogy az NMN k\u00e9pes g\u00e1tolni az OGD \u00e1ltal kiv\u00e1ltott autof\u00e1gi\u00e1t a PC12 sejtekben.
\n\u00d6sszefoglalva, azt sugalljuk, hogy az NMN bizonyos d\u00f3zisa ellen\u00e1ll az OGD \u00e1ltal kiv\u00e1ltott autof\u00e1gi\u00e1s k\u00e1rosod\u00e1snak a PC12 sejtekben, \u00edgy citoprotekt\u00edv hat\u00e1st fejt ki, \u00e9s ez a v\u00e9d\u0151hat\u00e1s az mTOR-ral kapcsolatos \u00fatvonallal \u00e1llhat \u00f6sszef\u00fcgg\u00e9sben. A jelen tanulm\u00e1ny bizonyos c\u00e9lreferenci\u00e1t ny\u00fajthat az NMN sz\u00e1m\u00e1ra az OGD \u00e1ltal kiv\u00e1ltott sejtes autof\u00e1gia-k\u00e1rosod\u00e1s megel\u0151z\u00e9s\u00e9re, \u00e9s felhalmozhat bizonyos laborat\u00f3riumi adatokat a term\u00e9szetes vegy\u00fclet NMN fejleszt\u00e9s\u00e9hez.<\/p>","protected":false},"excerpt":{"rendered":"

K\u00e9miai n\u00e9v: B\u00e9ta-nikotinamid-mononukleotid<\/p>\n

CAS-sz\u00e1m: 1094-61-7<\/p>\n

Molekul\u00e1ris k\u00e9plet: C11H15N2O8P<\/p>\n

Molekulat\u00f6meg:334,22<\/p>\n

Megjelen\u00e9s: Feh\u00e9r por<\/p>\n

Assay:97%~100.0%<\/p>","protected":false},"featured_media":0,"comment_status":"open","ping_status":"closed","template":"","meta":[],"product_brand":[],"product_cat":[113],"product_tag":[],"class_list":{"0":"post-6829","1":"product","2":"type-product","3":"status-publish","5":"product_cat-organic-intermediate","7":"first","8":"instock","9":"shipping-taxable","10":"product-type-simple"},"yoast_head":"\nChina beta-nicotinamide mononucleotide Manufacturer CAS 1094-61-7 - Longchang Chemical<\/title>\n<meta name=\"description\" content=\"beta-nicotinamide mononucleotide CAS 1094-61-7 Organic Intermediate is an organic intermediate for chemical synthesis and formulation manufacturing.\" \/>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/longchangchemical.com\/hu\/product\/beta-nicotinamide-mononucleotide-cas-1094-61-7\/\" \/>\n<meta property=\"og:locale\" content=\"hu_HU\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"China beta-nicotinamide mononucleotide Manufacturer CAS 1094-61-7 - 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