Modulation of cell death by aldose reductase andpoly(adp-ribose) polymerase (PARP) in diabetic hearts
Başlık çevirisi mevcut değil.
- Tez No: 710237
- Danışmanlar: PROF. DR. RAVİCHANDRAN RAMASAMY
- Tez Türü: Yüksek Lisans
- Konular: Kardiyoloji, Cardiology
- Anahtar Kelimeler: Belirtilmemiş.
- Yıl: 2008
- Dil: İngilizce
- Üniversite: Columbia University
- Enstitü: Yurtdışı Enstitü
- Ana Bilim Dalı: Belirtilmemiş.
- Bilim Dalı: Belirtilmemiş.
- Sayfa Sayısı: 32
Özet
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Özet (Çeviri)
Hyperglycemia causes generation of oxidative stress through several pathways, including excess aldose reductase flux, in diabetic heart tissue. Downstream events of excess aldose reductase flux in diabetic hearts, activates a nuclear repair enzyme, Poly(ADP-ribose) Polymerase and results in apoptosis, due to DNA damage exerted via oxidative stress. In this thesis, we assessed the role of a Poly(ADP-ribose) Polymerase inhibitor, 1,5- isoquinolinediol (ISQ), on the excess aldose reductase flux mediated mitochondria dependent apoptotic signaling in diabetic rat hearts. We showed that streptozotocin induced diabetic hearts had significantly lowered aldose reductase expression and activity via inhibition of Poly (ADP-ribose) Polymerase. In contrast, generation of oxidative stress was not altered by Poly (ADP-ribose) Polymerase inhibition in diabetic state. Furthermore, we were able to demonstrate the potential benefits of 1,5-isoquinolinediol treatment in terms of preventing mitochondria dependent apoptotic signaling via less caspase-3 activity, less Poly(ADP-ribose) Polymerase cleavage fragment expression, higher Bcl-xL expression and less cytochrome-c release into cytosol under continuous oxidative stress of diabetic state. In conclusion, our data indicates that Poly (ADP-ribose) Polymerase inhibition may afford protection against aldose reductase flux mediated mitochondria dependent apoptosis in diabetic hearts.
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