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Expression of SIRT1 and P53 in Rat Lens Epithelial cells in Experimentally Induced DM.

AbstractPURPOSE:
To determine the etiopathogenesis of diabetic cataract by studying changes in relative expressions of silent information regulator protein-1 (SIRT1) and P53 in rat lens epithelial cells (LECs) in experimentally induced diabetes mellitus (DM).
METHODS:
Six-week-old male SD rats (n = 120) were randomly divided into experimental (n = 80 rats) and control (n = 40 rats) groups. DM was induced in the experimental group (diabetic model) by intraperitoneal (i.p.) injection of 60 mg/kg streptozotocin (STZ). Control group rats were injected similarly with phosphate-buffered saline (PBS). Four and eight weeks after successful induction of DM, relative expressions of SIRT1 and P53 in LECs were analyzed using quantitative real-time (qRT) fluorescence polymerase chain reaction (qRT-PCR) and Western blot analysis.
RESULTS:
Expression of both SIRT1 and P53 was observed in LECs of control and experimental group rats at 4 and 8 weeks but was significantly greater in experimental compared with control group rats (p < 0.05).
CONCLUSIONS:
Expression of both SIRT1 and P53 increases in the early stages of diabetic cataract formation, indicating that they play potentially important roles in the pathogenesis of diabetic cataract.
AuthorsKeke Xu, Shubin Wu, Zhijian Li, Hong Lou, Jiayu Yao, Hong Sun, Yin Sun, Yuxia Dai
JournalCurrent eye research (Curr Eye Res) Vol. 43 Issue 4 Pg. 493-498 (04 2018) ISSN: 1460-2202 [Electronic] England
PMID29199862 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Tumor Suppressor Protein p53
  • RNA
  • Sirt1 protein, rat
  • Sirtuin 1
Topics
  • Animals
  • Apoptosis
  • Cataract (etiology, genetics, metabolism)
  • Diabetes Mellitus, Experimental
  • Epithelial Cells (metabolism, pathology)
  • Gene Expression Regulation
  • Lens, Crystalline (metabolism, pathology)
  • Male
  • RNA (genetics)
  • Rats
  • Rats, Sprague-Dawley
  • Real-Time Polymerase Chain Reaction
  • Sirtuin 1 (biosynthesis, genetics)
  • Tumor Suppressor Protein p53 (biosynthesis, genetics)

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