{"id":4498,"date":"2024-08-04T14:35:10","date_gmt":"2024-08-04T14:35:10","guid":{"rendered":"https:\/\/longchangextracts.com\/?p=4498"},"modified":"2024-08-04T14:35:10","modified_gmt":"2024-08-04T14:35:10","slug":"%ce%b2-nicotinamide-mononucleotide","status":"publish","type":"post","link":"https:\/\/longchangextracts.com\/tr\/%ce%b2-nicotinamide-mononucleotide\/","title":{"rendered":"Oksijen ve glikozdan yoksun PC12 h\u00fccrelerinde \u03b2 - nikotinamid monon\u00fckleotidin otofaji \u00fczerine etkisi"},"content":{"rendered":"

\u0130skemik serebrovask\u00fcler hastal\u0131k iki t\u00fcr i\u00e7erir: ge\u00e7ici iskemik inme ve serebral enfarkt\u00fcs. Bunlar aras\u0131nda serebral enfarkt\u00fcs, geleneksel \u00c7in t\u0131bb\u0131 te\u015fhisinde iskemik inme (IS) olarak adland\u0131r\u0131l\u0131r ve beyin dokusu b\u00f6lgelerinde lokal kanlanma bozukluklar\u0131na yol a\u00e7an \u00e7e\u015fitli nedenlerden kaynaklanan, iskemik ve hipoksik lezyonlar ve beyin dokusunun nekrozu ile sonu\u00e7lanan ve daha sonra bir dizi n\u00f6rolojik fonksiyon bozuklu\u011fu \u00fcreten bir hastal\u0131kt\u0131r. Y\u00fcksek \u00f6l\u00fcm ve sakatl\u0131k oranlar\u0131n\u0131n yan\u0131 s\u0131ra karma\u015f\u0131k patolojik mekanizmalar\u0131, her y\u0131l d\u00fcnyaya \u00f6nemli bir ekonomik y\u00fck getirmektedir. Beyin h\u00fccrelerinde oksijen glukoz yoksunlu\u011fu (OGD), temel ve klinik \u00f6ncesi inme ara\u015ft\u0131rmalar\u0131nda yayg\u0131n olarak kullan\u0131lan en yayg\u0131n in vitro iskemik inme modelidir.
\nOtofaji, \u00f6karyotik h\u00fccrelerde yayg\u0131n olarak bulunur ve h\u00fccre sa\u011fkal\u0131m ve \u00f6l\u00fcm s\u00fcre\u00e7lerinin d\u00fczenlenmesinde \u00f6nemli bir rol oynar. \u00c7ok say\u0131da \u00e7al\u0131\u015fma, otofajinin iskemik beyin hasar\u0131n\u0131n olu\u015fumu ve geli\u015fimi ile yak\u0131ndan ili\u015fkili oldu\u011funu g\u00f6stermektedir. Baz\u0131 \u00e7al\u0131\u015fmalar n\u00f6ronal otofajinin iskemik beyin hasar\u0131n\u0131 hafifletebilece\u011fini g\u00f6sterirken, di\u011ferleri n\u00f6ronal otofajinin iskemik beyin hasar\u0131n\u0131 \u015fiddetlendirebilece\u011fini bildirmi\u015ftir, ancak spesifik mekanizma hala belirsizdir.
\n\u03b2 - nikotinamid monon\u00fckleotid (NMN) \u00e7e\u015fitli g\u0131dalarda bulunur ve h\u00fccresel ya\u015flanman\u0131n d\u00fczenlenmesi ve normal v\u00fccut fonksiyonlar\u0131n\u0131n s\u00fcrd\u00fcr\u00fclmesi i\u00e7in \u00e7ok \u00f6nemlidir. Bir\u00e7ok \u00f6nemli h\u00fccre i\u00e7i sinyal yolunun iletimine kat\u0131l\u0131r. NMN'nin in vitro olarak uygulanmas\u0131n\u0131n, h\u00fccre ya\u015flanmas\u0131n\u0131 d\u00fczenlemek ve normal v\u00fccut fonksiyonlar\u0131n\u0131 s\u00fcrd\u00fcrmek i\u00e7in onu h\u0131zla NAD + 'ya d\u00f6n\u00fc\u015ft\u00fcrebilece\u011fine dair ara\u015ft\u0131rma raporlar\u0131 vard\u0131r. NMN, IS'nin neden oldu\u011fu NAD+ azalmas\u0131n\u0131 telafi edebilir ve serebral iskemide n\u00f6ronal hasar\u0131 iyile\u015ftirebilir. Bu, NMN'nin IS'de belirli bir rol oynad\u0131\u011f\u0131n\u0131 g\u00f6stermektedir. \u00c7al\u0131\u015fmalar, NMN'nin n\u00f6rovask\u00fcler rejenerasyonu te\u015fvik edebilece\u011fini, beyin mikrovask\u00fcler endotel fonksiyonunu, anti-inflamatuar ve anti apoptotik etkileri iyile\u015ftirebilece\u011fini g\u00f6stermi\u015ftir. NMN'nin otofajiyi d\u00fczenleyerek anti iskemik beyin hasar\u0131 etkileri g\u00f6sterebilece\u011fini \u00f6ne s\u00fcren birka\u00e7 \u00e7al\u0131\u015fma da vard\u0131r, ancak NMN'nin otofajiyi ve anti IS'yi d\u00fczenledi\u011fi spesifik mekanizma hen\u00fcz net de\u011fildir.
\nBu \u00e7al\u0131\u015fman\u0131n amac\u0131 oksijen glukoz yoksunlu\u011fu PC12 h\u00fccre modeli olu\u015fturmakt\u0131r. H\u00fccre sa\u011fkal\u0131m oran\u0131 in vitro MTT testi ile \u00f6l\u00e7\u00fclm\u00fc\u015f, otofagozomlar ve otolizozomlar transmisyon elektron mikroskobu ile tespit edilmi\u015f, otofagozom floresan yo\u011funlu\u011fu MDC ile g\u00f6zlenmi\u015f ve LC3-II\/LC3-I, Beclin1, p62 ve P-mTOR\/mTOR'un otofaji ile ili\u015fkili protein ekspresyonu Western blot ile tespit edilmi\u015ftir. Ama\u00e7, NMN'nin PC12 h\u00fccrelerinde OGD ile ind\u00fcklenen otofajik hasar \u00fczerindeki etkisini a\u00e7\u0131kl\u0131\u011fa kavu\u015fturmakt\u0131r.<\/p>\n

\"\"\"\"\"\"\"\"\"\"<\/p>\n

2017 Lancet \u00e7al\u0131\u015fmas\u0131, inmenin h\u0131zl\u0131 hastal\u0131k ilerlemesi, y\u00fcksek \u00f6l\u00fcm ve sakatl\u0131k oranlar\u0131 ile \u00c7in'de y\u0131llarca ya\u015fam kayb\u0131na neden olan ana hastal\u0131k oldu\u011funu g\u00f6stermi\u015ftir. Bunlar aras\u0131nda IS, t\u00fcm inmelerin 60% ila 70%'sini olu\u015fturmaktad\u0131r ve beynin belirli bir b\u00f6lgesine kan ak\u0131\u015f\u0131n\u0131n azalmas\u0131na yol a\u00e7an vask\u00fcler t\u0131kan\u0131kl\u0131ktan kaynaklanmaktad\u0131r. Serebral iskemi ve hipoksiden sonra, otofaji, apoptoz, oksidatif stres ve h\u00fccre i\u00e7i kalsiyum a\u015f\u0131r\u0131 y\u00fcklenmesi gibi bir dizi patolojik ve fizyolojik reaksiyonu tetikleyebilir. \u0130D'den kurtulanlar\u0131n uzun iyile\u015fme d\u00f6ng\u00fcs\u00fc k\u00fcresel ekonomik y\u00fck\u00fc art\u0131rm\u0131\u015ft\u0131r. G\u00fcn\u00fcm\u00fczde, \u0130D'nin \u00f6nlenmesi ve tedavisi i\u00e7in piyasada kullan\u0131lan ila\u00e7lar i\u00e7in bir\u00e7ok kontrendikasyon bulunmaktad\u0131r. Bu nedenle, \u0130S'nin \u00f6nlenmesi ve tedavisine y\u00f6nelik ila\u00e7lar\u0131n s\u00fcrekli olarak ara\u015ft\u0131r\u0131lmas\u0131 gerekmektedir. OGD, IS'yi in vitro olarak incelemek i\u00e7in klasik bir modeldir. PC12 h\u00fccre hatt\u0131, iskemi ve hipoksi hasar\u0131 ara\u015ft\u0131rmalar\u0131nda yayg\u0131n olarak kullan\u0131lan n\u00f6ronal hasar\u0131 incelemek i\u00e7in en yayg\u0131n kullan\u0131lan h\u00fccre hatlar\u0131ndan biridir. Bu nedenle, bu deneyde in vitro ara\u015ft\u0131rma i\u00e7in OGD PC12 h\u00fccre modeli kullan\u0131lm\u0131\u015ft\u0131r.
\nNMN, insan v\u00fccudunda do\u011fal olarak bulunan ve bir\u00e7ok g\u0131dada da bulunan 334,22 molek\u00fcl a\u011f\u0131rl\u0131\u011f\u0131na sahip bir maddedir. Nikotinamid fosforibosiltransferaz reaksiyonunun bir \u00fcr\u00fcn\u00fcd\u00fcr ve ayn\u0131 zamanda NAD+'nin temel \u00f6nc\u00fclerinden biridir. \u00c7al\u0131\u015fmalar, organizmalardaki NMN seviyelerini d\u00fczenlemenin kardiyovask\u00fcler ve serebrovask\u00fcler hastal\u0131klar, n\u00f6rodejeneratif hastal\u0131klar ve ya\u015fa ba\u011fl\u0131 dejeneratif hastal\u0131klar \u00fczerinde iyi terap\u00f6tik ve onar\u0131c\u0131 etkilere sahip oldu\u011funu bulmu\u015ftur. NMN uygulamas\u0131n\u0131n s\u0131\u00e7an MCAO modellerinde enfarkt\u00fcs boyutunu ve n\u00f6rolojik hasar\u0131 azaltabilece\u011fine dair ara\u015ft\u0131rma raporlar\u0131 da bulunmaktad\u0131r. Bu deneyde, OGD'nin PC12 h\u00fccrelerinin hayatta kalma oran\u0131n\u0131 azaltabilece\u011fini g\u00f6stermek i\u00e7in MTT deneyi kullan\u0131lm\u0131\u015ft\u0131r. NMN, OGD PC12 h\u00fccrelerinin hayatta kalma oran\u0131n\u0131 400, 800 ve 1600 \u03bc mol\/L konsantrasyonlarda art\u0131rabilir ve en y\u00fcksek hayatta kalma oran\u0131 800 \u03bc mol\/L konsantrasyonda g\u00f6zlenmi\u015ftir; Bununla birlikte, NMN200 ve 3200 \u03bc mol\/L konsantrasyonlar\u0131 aras\u0131nda h\u00fccre hayatta kalma oran\u0131nda \u00f6nemli bir fark yoktu, bu da 200 \u03bc mol\/L konsantrasyonun OGD kaynakl\u0131 PC12 h\u00fccre hayatta kalma oran\u0131n\u0131 iyile\u015ftirmek i\u00e7in hen\u00fcz etkili konsantrasyona ula\u015fmad\u0131\u011f\u0131n\u0131 g\u00f6sterirken, 3200 \u03bc mol\/L konsantrasyonu a\u015f\u0131r\u0131 konsantrasyon nedeniyle h\u00fccrelerde belirli hasara neden olmu\u015f olabilir.
\nTip II programl\u0131 h\u00fccre \u00f6l\u00fcm\u00fc olarak da bilinen otofaji, h\u00fccrelerin otofaji ile ilgili genlerin d\u00fczenlemesi alt\u0131nda, hayatta kalmalar\u0131n\u0131, farkl\u0131la\u015fmalar\u0131n\u0131, b\u00fcy\u00fcmelerini ve stabilitelerini korumak i\u00e7in hasarl\u0131, denat\u00fcre veya ya\u015flanan makromolek\u00fclleri ve organelleri bozmak i\u00e7in lizozomlar\u0131 kulland\u0131klar\u0131 s\u00fcreci ifade eder. Ara\u015ft\u0131rmalar otofajinin IS'den sonra ind\u00fcklendi\u011fini ve IS'nin patolojik s\u00fcreciyle birlikte otofajinin de ortaya \u00e7\u0131kt\u0131\u011f\u0131n\u0131 ve geli\u015fti\u011fini, IS'nin akut, subakut, iyile\u015fme ve sekel a\u015famalar\u0131nda farkl\u0131 d\u00fczenleyici roller oynad\u0131\u011f\u0131n\u0131 g\u00f6stermektedir.
\nMTOR, 289 kDa nispi molek\u00fcler a\u011f\u0131rl\u0131\u011fa sahip atipik bir serin\/treonin protein kinazd\u0131r. Farkl\u0131 proteinlerin ba\u011flanmas\u0131yla mTORCl ve mTORC2 olmak \u00fczere iki farkl\u0131 kompleks olu\u015fturabilir. MTORCl rapamisine duyarl\u0131d\u0131r ve esas olarak h\u00fccresel otofaji, ribozom biyogenezi, protein translasyonu ve lipid sentezini d\u00fczenleyen b\u00fcy\u00fcme fakt\u00f6rleri ve besin sinyallerinin entegrasyonundan sorumludur. MTORT, otofaji i\u00e7in bir valf olarak kabul edilir. Ara\u015ft\u0131rmalar, fosforile mTOR'un oksidatif glikoz yoksunlu\u011fu hasar\u0131n\u0131 hafifletebilece\u011fini ve h\u00fccrelerde koruyucu bir rol oynayabilece\u011fini g\u00f6stermi\u015ftir. 3-MA yayg\u0131n olarak kullan\u0131lan bir otofaji inhibit\u00f6r\u00fcd\u00fcr. RAPA, otofaji aktivat\u00f6r\u00fc olarak da bilinen mTORC1'i inhibe ederek otofajiyi ind\u00fckleyebilen bir mTOR inhibit\u00f6r\u00fcd\u00fcr. Bu deney, PC12 h\u00fccrelerinde OGD ile ind\u00fcklenen otofajiye m\u00fcdahale etmek ve d\u00fczenlemek i\u00e7in 3-MA ve RAPA gruplar\u0131n\u0131 kurdu; Ayn\u0131 zamanda, NMN'nin PC12 h\u00fccrelerinde OGD ile ind\u00fcklenen otofaji \u00fczerinde 3-MA veya RAPA'n\u0131n etkilerine kar\u015f\u0131 koyup koyamayaca\u011f\u0131n\u0131 g\u00f6zlemlemek i\u00e7in 3-MA, RAPA ve ila\u00e7 kombinasyon gruplar\u0131 da kuruldu.
\nBeclin-1, LC3 ve p62 proteinlerinin seviyeleri, otofaji i\u00e7in \u00f6nemli tespit g\u00f6stergeleri olarak hizmet edebilir. Beclin1, otofaji ile pozitif korelasyon g\u00f6steren olgun bir otofaji d\u00fczenleyicisidir. Beclin1, otofaji ve membran ta\u015f\u0131ma i\u015flevlerini yerine getirmek i\u00e7in VPS15, VPS34, ATG14 gibi proteinlerle etkile\u015fime girer. LC3, mayada otofajide rol oynad\u0131\u011f\u0131na inan\u0131lan ubikitin benzeri de\u011fi\u015ftirici ATG8'in bir homologudur. ATG4 ile muameleden sonra LC3, C-terminal kal\u0131nt\u0131s\u0131n\u0131 kaybeder ve LC3-I'e d\u00f6n\u00fc\u015f\u00fcr. LC3-I, otofagozom membran\u0131ndaki lipid molek\u00fcl\u00fc fosfatidiletanolamine kovalent olarak ba\u011flanarak LC3-II'ye d\u00f6n\u00fc\u015fen enzimatik reaksiyonlar gibi bir dizi ubikitinasyona u\u011frar. LC3-II\/LC3-I oran\u0131ndaki art\u0131\u015f, otofaji seviyelerinde bir art\u0131\u015f oldu\u011funu g\u00f6sterir. P62, otofaji aktivitesini yans\u0131tan bir marker proteindir ve protein seviyesi otofaji ile negatif korelasyon g\u00f6sterir. Yani, otofaji ger\u00e7ekle\u015fti\u011finde, p62 proteini sitoplazmada s\u00fcrekli olarak bozulur; otofaji aktivitesi zay\u0131flad\u0131\u011f\u0131nda ve otofaji i\u015flevi bozuldu\u011funda, p62 proteini sitoplazmada s\u00fcrekli olarak birikecektir. Bu deney, Western blot teknolojisi arac\u0131l\u0131\u011f\u0131yla NMN'nin Beclin1 ve LC3-II\/LC3-I proteinlerinin g\u00f6receli ekspresyon seviyelerini a\u015fa\u011f\u0131 \u00e7ekebilece\u011fini ve P-mTOR\/mTOR ve p62 proteinlerinin ekspresyon seviyelerini yukar\u0131 \u00e7ekebilece\u011fini do\u011frulam\u0131\u015ft\u0131r. Ayr\u0131ca, NMN'nin OGD PC12 h\u00fccrelerinde otofagozom ve otolizozom say\u0131s\u0131n\u0131 ve yo\u011funlu\u011funu azaltabildi\u011fini do\u011frulamak i\u00e7in transmisyon elektron mikroskopisi ve MDC y\u00f6ntemi kullan\u0131lm\u0131\u015ft\u0131r. Yukar\u0131dakiler, NMN'nin PC12 h\u00fccrelerinde OGD ile ind\u00fcklenen otofajiyi inhibe edebilece\u011fini g\u00f6stermektedir.
\n\u00d6zetle, belirli bir NMN dozunun PC12 h\u00fccrelerinde OGD kaynakl\u0131 otofajik hasara kar\u015f\u0131 koyabilece\u011fini ve b\u00f6ylece h\u00fccresel koruyucu bir etki uygulayabilece\u011fini ve bu koruyucu etkinin mTOR ile ilgili yolaklarla ili\u015fkili olabilece\u011fini d\u00fc\u015f\u00fcnd\u00fcrmektedir. Bu \u00e7al\u0131\u015fma, OGD kaynakl\u0131 otofajik hasar\u0131n NMN taraf\u0131ndan \u00f6nlenmesi ve tedavisi i\u00e7in belirli bir hedef referans\u0131 sa\u011flayabilir ve do\u011fal bile\u015fik NMN'nin geli\u015ftirilmesi i\u00e7in laboratuvar verilerini biriktirebilir.<\/p>","protected":false},"excerpt":{"rendered":"

Ischemic cerebrovascular disease includes two types: transient ischemic stroke and cerebral infarction. Among them, cerebral infarction is named as ischemic stroke (IS) in traditional Chinese medicine diagnosis, which is a disease caused by various reasons leading to local blood supply disorders in brain tissue regions, resulting in ischemic and hypoxic lesions and necrosis of brain […]<\/p>","protected":false},"author":1,"featured_media":0,"comment_status":"closed","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[20],"tags":[],"yoast_head":"\nThe effect of \u03b2 - nicotinamide mononucleotide on autophagy in oxygen glucose deprived PC12 cells - China Chemical Manufacturer<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/longchangextracts.com\/tr\/\u03b2-nicotinamide-mononucleotide\/\" \/>\n<meta property=\"og:locale\" content=\"tr_TR\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"The effect of \u03b2 - nicotinamide mononucleotide on autophagy in oxygen glucose deprived PC12 cells - China Chemical Manufacturer\" \/>\n<meta property=\"og:description\" content=\"Ischemic cerebrovascular disease includes two types: transient ischemic stroke and cerebral infarction. 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