{"id":8536,"date":"2024-08-14T15:44:28","date_gmt":"2024-08-14T15:44:28","guid":{"rendered":"https:\/\/longchangextracts.com\/?p=8536"},"modified":"2024-08-14T15:44:28","modified_gmt":"2024-08-14T15:44:28","slug":"erk-p27kip1-signaling-pathway","status":"publish","type":"post","link":"https:\/\/longchangextracts.com\/tr\/erk-p27kip1-sinyal-yolagi\/","title":{"rendered":"ERK\/P27Kip1 sinyal yolunun izorinofilin ile d\u00fczenlenmesi farelerde bleomisin kaynakl\u0131 pulmoner fibrozisi iyile\u015ftirir"},"content":{"rendered":"

ERK\/P27Kip1 sinyal yolunun izorinofilin ile d\u00fczenlenmesi farelerde bleomisin kaynakl\u0131 pulmoner fibrozisi iyile\u015ftirir
\nPulmoner fibrozis (PF), akci\u011fer fibroblastlar\u0131n\u0131n anormal proliferasyonu, ekstrasel\u00fcler matriksin (ECM) a\u015f\u0131r\u0131 birikimi, enflamatuar hasar ve doku yap\u0131s\u0131n\u0131n tahribat\u0131 ile karakterize, sonu\u00e7ta akci\u011fer skarlar\u0131n\u0131n olu\u015fumuna, akci\u011fer fonksiyon bozuklu\u011funa ve solunum yetmezli\u011fine yol a\u00e7an kronik bir interstisyel akci\u011fer hastal\u0131\u011f\u0131d\u0131r. Pulmoner fibrozis (PF) patogenezinde oksidatif stres, enflamatuar yan\u0131t, fibroblast proliferasyonu ve aktivasyonu ve anormal ECM birikimi gibi \u00e7e\u015fitli fakt\u00f6rler rol oynamaktad\u0131r. Daha da \u00f6nemlisi, akci\u011fer fibroblastlar\u0131n\u0131n miyofibroblastlara (MFb) proliferasyon ve farkl\u0131la\u015fma s\u00fcreci pulmoner fibrozis olu\u015fumunun anahtar\u0131 olabilir. \u00c7ok say\u0131da \u00e7al\u0131\u015fma, d\u00f6n\u00fc\u015ft\u00fcr\u00fcc\u00fc b\u00fcy\u00fcme fakt\u00f6r\u00fc - \u03b2 1 (TGF - \u03b2 1) gibi sitokinlerin uyar\u0131s\u0131 alt\u0131nda, akci\u011fer fibroblastlar\u0131n\u0131n \u00e7o\u011falabildi\u011fini ve alfa d\u00fcz kas aktin (\u03b1 - SMA) pozitif MFb'ye farkl\u0131la\u015fabildi\u011fini g\u00f6stermi\u015ftir. MFb, b\u00fcy\u00fck miktarda ECM ve pro-fibrotik fakt\u00f6r sentezi yoluyla, pulmoner fibrozun ilerlemesi i\u00e7in kilit bir patojenik mekanizma olarak kabul edilmektedir. Bu nedenle, akci\u011fer fibroblastlar\u0131n\u0131n \u00e7o\u011falma ve farkl\u0131la\u015fma mekanizmalar\u0131n\u0131 ara\u015ft\u0131rmak ve inhibit\u00f6r hedeflerini belirlemek, pulmoner fibrozisi hafifletmek i\u00e7in potansiyel bir strateji olabilir.<\/p>\n

Isorhynchophylline (IRN), geleneksel \u00c7in t\u0131bb\u0131 Hook Vine'dan izole edilen tetrasiklik bir indol alkaloiddir. \u00d6nceki \u00e7al\u0131\u015fmalar IRN'nin antioksidan, anti-enflamatuar, anti proliferatif ve n\u00f6roprotektif gibi \u00e7e\u015fitli etkilere sahip oldu\u011funu bulmu\u015ftur. Guo ve arkada\u015flar\u0131 IRN'nin pulmoner arter d\u00fcz kas h\u00fccrelerinin proliferasyonunu inhibe ederek ve pulmoner vask\u00fcler yeniden \u015fekillenmeyi azaltarak monokrotalin kaynakl\u0131 pulmoner arteriyel hipertansiyonu hafifletti\u011fini bulmu\u015flard\u0131r. Daha ileri ara\u015ft\u0131rmalar IRN'nin bron\u015fiyal d\u00fcz kas h\u00fccrelerinin \u00e7o\u011falmas\u0131n\u0131 inhibe ederek bron\u015fiyal ast\u0131m \u00fczerinde belirli bir hafifletici etkiye sahip oldu\u011funu bulmu\u015ftur. Son ara\u015ft\u0131rmalar, izorinofilinin farelerde silika kaynakl\u0131 akci\u011fer hasar\u0131 \u00fczerinde belirli bir koruyucu etkiye sahip oldu\u011funu bulmu\u015ftur. \u00d6nceki ara\u015ft\u0131rmalar\u0131m\u0131z, mimoza alkaloidlerinin, h\u00fccre d\u0131\u015f\u0131 d\u00fczenlenmi\u015f protein kinaz 1\/2 (ERK1\/2) fosforilasyonunu inhibe ederek ve p27Kip1 ekspresyonunu yukar\u0131 do\u011fru d\u00fczenleyerek TGF - \u03b2 1 taraf\u0131ndan ind\u00fcklenen pulmoner fibroblastlar\u0131n proliferasyonunu ve farkl\u0131la\u015fmas\u0131n\u0131 \u00f6nemli \u00f6l\u00e7\u00fcde inhibe edebilece\u011fini bulmu\u015ftur. IRN, ERK1\/2 fosforilasyonunu bask\u0131layarak anjiyotensin II (AngII) taraf\u0131ndan ind\u00fcklenen neonatal s\u0131\u00e7an ventrik\u00fcler miyositlerinin proliferasyonunu \u00f6nemli \u00f6l\u00e7\u00fcde inhibe eder. Yukar\u0131daki ara\u015ft\u0131rma ge\u00e7mi\u015fine dayanarak, bu \u00e7al\u0131\u015fma ERK1\/2 ve p27Kip1 sinyal yollar\u0131n\u0131 hedefleyerek IRN'nin anti PF etkisini ve mekanizmas\u0131n\u0131 ke\u015ffetmeyi ve anti PF etkileri olan geleneksel \u00c7in t\u0131bb\u0131n\u0131n ara\u015ft\u0131r\u0131lmas\u0131 ve geli\u015ftirilmesi i\u00e7in yeni fikirler sa\u011flamay\u0131 ama\u00e7lamaktad\u0131r.<\/p>\n

Pulmoner fibroz, fibroblastlar\u0131n a\u015f\u0131r\u0131 \u00e7o\u011falmas\u0131 ve h\u00fccre d\u0131\u015f\u0131 matriks birikimi ile karakterize, sonu\u00e7ta akci\u011fer yap\u0131s\u0131n\u0131n tahrip olmas\u0131na ve fibrotik lezyonlar\u0131n olu\u015fmas\u0131na yol a\u00e7an, k\u00f6t\u00fc prognozlu ilerleyici bir interstisyel hastal\u0131kt\u0131r. G\u00fcn\u00fcm\u00fczde pulmoner fibrozis tedavisinde kullan\u0131lan ba\u015fl\u0131ca ila\u00e7lar glukokortikoidler ve imm\u00fcnosupresanlard\u0131r, ancak bunlar\u0131n ciddi yan etkileri vard\u0131r. Son y\u0131llarda, pulmoner fibrozis ara\u015ft\u0131rmalar\u0131n\u0131n s\u00fcrekli derinle\u015fmesiyle birlikte, pulmoner fibrozis tedavisinde geleneksel \u00c7in t\u0131bb\u0131 kullan\u0131m\u0131n\u0131n ara\u015ft\u0131r\u0131lmas\u0131 ve uygulanmas\u0131 giderek artm\u0131\u015ft\u0131r. Geleneksel \u00c7in t\u0131bb\u0131 ve aktif bile\u015fenleri, enflamatuar fakt\u00f6rlerin ekspresyonunu azaltarak, akci\u011fer fibroblastlar\u0131n\u0131n proliferasyonunu inhibe ederek, akci\u011fer fibroblastlar\u0131n\u0131n apoptozunu ind\u00fckleyerek ve fibroz s\u00fcrecini bloke ederek iyi bir anti pulmoner fibroz aktivitesi g\u00f6stermi\u015ftir. Fibrozis semptomlar\u0131n\u0131 etkili bir \u015fekilde iyile\u015ftirebilir ve hastal\u0131\u011f\u0131n ilerlemesini geciktirebilirler. \u00d6nceki \u00e7al\u0131\u015fmalar, metilprednizolon ve oksimatrin gibi geleneksel \u00c7in t\u0131bb\u0131ndaki alkaloid monomerlerinin pulmoner fibrozu hafifletmede belirli etkilere sahip oldu\u011funu bulmu\u015ftur. Ara\u015ft\u0131rma grubumuz da erken a\u015famada mimoza alkaloidleri ve rutaekarpinin bleomisin kaynakl\u0131 pulmoner fibroz \u00fczerinde belirli bir hafifletici etkiye sahip oldu\u011funu bulmu\u015ftur. Di\u011fer \u00e7al\u0131\u015fmalar Danshensu ve Danshensu B gibi geleneksel \u00c7in ila\u00e7lar\u0131n\u0131n akci\u011fer fibroblastlar\u0131n\u0131n \u00e7o\u011falmas\u0131n\u0131 ve farkl\u0131la\u015fmas\u0131n\u0131 engelleyerek bleomisin kaynakl\u0131 pulmoner fibrozu iyile\u015ftirdi\u011fini g\u00f6stermi\u015ftir. \u00d6nceki \u00e7al\u0131\u015fmalar IRN'nin PASMC'lerin proliferasyonunu inhibe ederek ve pulmoner vask\u00fcler yeniden \u015fekillenmeyi azaltarak MCT kaynakl\u0131 PAH'\u0131 hafifletti\u011fini ve bron\u015fiyal d\u00fcz kas h\u00fccrelerinin proliferasyonunu inhibe ederek bron\u015fiyal ast\u0131m \u00fczerinde belirli bir hafifletici etkiye sahip oldu\u011funu bulmu\u015ftur. Bununla birlikte, bu \u00e7al\u0131\u015fma IRN ile 21 g\u00fcnl\u00fck tedaviden sonra, PF farelerinin akci\u011fer dokusunda kolajen birikiminin ve kolajen I ekspresyonunun \u00f6nemli \u00f6l\u00e7\u00fcde azald\u0131\u011f\u0131n\u0131, \u03b1 SMA ekspresyonunun \u00f6nemli \u00f6l\u00e7\u00fcde azald\u0131\u011f\u0131n\u0131 ve akci\u011fer hasar\u0131n\u0131n derecesinin \u00f6nemli \u00f6l\u00e7\u00fcde azald\u0131\u011f\u0131n\u0131 bulmu\u015ftur. Daha ileri in vitro deneyler, IRN'nin akci\u011fer fibroblastlar\u0131n\u0131n TGF - \u03b2 1 ile ind\u00fcklenen proliferasyonunu \u00f6nemli \u00f6l\u00e7\u00fcde inhibe edebilece\u011fini, TGF - \u03b2 1 ile ind\u00fcklenen h\u00fccre g\u00f6\u00e7\u00fcn\u00fc \u00f6nemli \u00f6l\u00e7\u00fcde azaltabilece\u011fini ve akci\u011fer fibroblastlar\u0131nda TGF - \u03b2 1 ile ind\u00fcklenen alfa SMA ve kolajen I ekspresyonunu de\u011fi\u015fen derecelerde inhibe edebilece\u011fini ortaya koymu\u015ftur. Bu sonu\u00e7lar, izorinofilinin pulmoner fibroblastlar\u0131n proliferasyonunu ve farkl\u0131la\u015fmas\u0131n\u0131 inhibe ederek BLM ile ind\u00fcklenen pulmoner fibrozisi iyile\u015ftirebilece\u011fini d\u00fc\u015f\u00fcnd\u00fcrmektedir.<\/p>\n

Ara\u015ft\u0131rmalar, pulmoner fibroblastlar\u0131n \u00e7o\u011falmas\u0131n\u0131n, g\u00f6\u00e7 etmesinin ve MFb'ye farkl\u0131la\u015fmas\u0131n\u0131n pulmoner fibrozis geli\u015fiminde \u00f6nemli bir rol oynad\u0131\u011f\u0131n\u0131 g\u00f6stermi\u015ftir. Bunlar aras\u0131nda TGF - \u03b2 1, fibroblastlar\u0131n MFb'ye do\u011fru \u00e7o\u011falmas\u0131nda ve farkl\u0131la\u015fmas\u0131nda kilit bir rol oynamaktad\u0131r. Ara\u015ft\u0131rmalar, TGF - \u03b2 1'in Smad sinyal yolunu aktive ederek akci\u011fer fibroblastlar\u0131n\u0131n \u00e7o\u011falmas\u0131n\u0131 ve farkl\u0131la\u015fmas\u0131n\u0131 te\u015fvik edebilece\u011fini ve ayr\u0131ca MAPK sinyal yolunu aktive ederek akci\u011fer fibroblastlar\u0131n\u0131n \u00e7o\u011falmas\u0131n\u0131 ve farkl\u0131la\u015fmas\u0131n\u0131 ind\u00fckleyebilece\u011fini bulmu\u015ftur. Siklin ba\u011f\u0131ml\u0131 kinaz inhibit\u00f6r proteini p27Kip1, CDK inhibit\u00f6rlerinin Cip\/Kip ailesinin bir \u00fcyesidir ve protein kinaz CDK2\/siklin E'nin negatif bir d\u00fczenleyicisidir. G0\/G1 faz\u0131nda h\u00fccre d\u00f6ng\u00fcs\u00fcn\u00fc bloke edebilir. H\u00fccre d\u00f6ng\u00fcs\u00fcn\u00fcn G0\/G1 faz\u0131nda p27Kip1 seviyesi nispeten y\u00fcksektir. Mitotik uyar\u0131m alt\u0131nda, p27Kip1 h\u0131zla bozunarak CDK2\/cyclin E'nin h\u00fccre \u00e7o\u011falmas\u0131n\u0131 desteklemesine izin verir. Ara\u015ft\u0131rma grubumuz, TGF - \u03b2 1'in ERK1\/2 fosforilasyon seviyesini y\u00fckselterek ve p27Kip1 ekspresyonunu inhibe ederek pulmoner fibroblastlar\u0131n proliferasyonunu ve farkl\u0131la\u015fmas\u0131n\u0131 ind\u00fckledi\u011fini, ERK1\/2 inhibit\u00f6r\u00fc PD98059'un ise ERK1\/2 fosforilasyonunu inhibe ederek ve p27Kip1 ekspresyonunu y\u00fckselterek TGF - \u03b2 1 taraf\u0131ndan ind\u00fcklenen pulmoner fibroblastlar\u0131n proliferasyonunu ve aktivasyonunu inhibe etti\u011fini bulmu\u015ftur. Bu arada, mimoza alkaloidlerinin p27Kip1 ekspresyonunu d\u00fczenleyerek TGF - \u03b2 1 ile ind\u00fcklenen pulmoner fibroblastlar\u0131n proliferasyonunu ve aktivasyonunu inhibe etti\u011fini de bulduk. \u00d6nceki \u00e7al\u0131\u015fmalar IRN'nin ERK1\/2 fosforilasyonunu inhibe ederek ve p27Kip1 ekspresyonunu d\u00fczenleyerek MCT ile ind\u00fcklenen PAH'\u0131 hafifletti\u011fini ve b\u00f6ylece trombosit aktive edici fakt\u00f6r ile ind\u00fcklenen PASMC'leri bask\u0131lad\u0131\u011f\u0131n\u0131 bulmu\u015ftur. Daha ileri ara\u015ft\u0131rmalar IRN'nin MAPK sinyal yolunu bask\u0131layarak miyokardiyal hipertrofi geli\u015fimini engelledi\u011fini de ortaya koymu\u015ftur. Bu \u00e7al\u0131\u015fma, 3 hafta boyunca IRN uygulamas\u0131n\u0131n pulmoner fibrozisli farelerin akci\u011fer dokusunda TGF - \u03b2 1 ekspresyonunu \u00f6nemli \u00f6l\u00e7\u00fcde azaltt\u0131\u011f\u0131n\u0131, ERK1\/2 fosforilasyonunu inhibe etti\u011fini, p27Kip1 ekspresyonunu yukar\u0131 reg\u00fcle etti\u011fini ve CDK2\/cyclin E1 ekspresyonunu a\u015fa\u011f\u0131 reg\u00fcle etti\u011fini bulmu\u015ftur. Daha ileri in vitro deneyler IRN'nin TGF - \u03b2 1 ile ind\u00fcklenen ERK1\/2 fosforilasyonunu \u00f6nemli \u00f6l\u00e7\u00fcde inhibe edebildi\u011fini, p27Kip1 ekspresyonunu \u00f6nemli \u00f6l\u00e7\u00fcde yukar\u0131 reg\u00fcle edebildi\u011fini ve CDK2\/cyclin E1 ekspresyonunu \u00f6nemli \u00f6l\u00e7\u00fcde a\u015fa\u011f\u0131 reg\u00fcle edebildi\u011fini ortaya koymu\u015ftur. Bu sonu\u00e7lar IRN'nin ERK\/p27Kip1'i d\u00fczenleyerek pulmoner fibroblastlar\u0131n proliferasyonunu ve farkl\u0131la\u015fmas\u0131n\u0131 inhibe edebilece\u011fini g\u00f6stermektedir.<\/p>\n

\u00d6zetle, \u00e7al\u0131\u015fmam\u0131z IRN'nin ERK sinyal yolunu bask\u0131layarak ve p27Kip1 ekspresyonunu yukar\u0131 d\u00fczenleyerek fibroblastlar\u0131n miyofibroblastlara d\u00f6n\u00fc\u015f\u00fcm\u00fcn\u00fc engelleyebilece\u011fini ve b\u00f6ylece BLM kaynakl\u0131 PF'yi hafifletebilece\u011fini g\u00f6stermektedir. Bu \u00e7al\u0131\u015fma IRN'nin klinik uygulamas\u0131 i\u00e7in yeni teorik temeller ve PF tedavisi i\u00e7in yeni fikirler sunmaktad\u0131r.<\/p>","protected":false},"excerpt":{"rendered":"

Regulation of ERK\/P27Kip1 signaling pathway by isorhynchophylline improves bleomycin induced pulmonary fibrosis in mice Pulmonary fibrosis (PF) is a chronic interstitial lung disease characterized by abnormal proliferation of lung fibroblasts, excessive accumulation of extracellular matrix (ECM), inflammatory damage, and tissue structure destruction, ultimately leading to the formation of lung scars, lung dysfunction, and respiratory failure. 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