ACE-Inhibitor Suppresses Apoptosis Induced by Endoplasmic Reticulum Stress in Renal Tubular in Experimental Diabetic Rats

Strategic Insights -

Recent research from Shenzhen, People's Republic of China has investigated the role of endoplasmic reticulum stress and apoptosis in experimental diabetic nephropathy. The study, conducted by H.L. Sun and colleagues from Guangzhou University, aimed to assess the effects of ACE inhibitor on endoplasmic reticulum stress and apoptosis in diabetic rats. The researchers induced diabetes in male Sprague-Dawley rats using streptozotocin and randomly assigned them into control or treatment groups. The study revealed that ACE inhibitor attenuated apoptosis and reduced the overexpression of endoplasmic reticulum stress associated proteins in diabetic rats.

Key Takeaways:

  • The study aimed to investigate the role of endoplasmic reticulum stress and apoptosis in experimental diabetic nephropathy.
  • Diabetes was induced in male Sprague-Dawley rats using streptozotocin at 60mg/kg i.p. for 24 weeks.
  • ACE inhibitor perindopril was administered to diabetic rats for 24 weeks, which resulted in attenuation of apoptosis and reduced overexpression of endoplasmic reticulum stress associated proteins.
  • Tubulointerstitial injury was assessed by histopathology, and tubule apoptosis was detected by TUNEL assay.
  • The study found that diabetic kidneys had more TUNEL-positive nuclei than control kidneys.
  • ACE inhibitor reduced the protein expression of GRP78, phospho-eIF2 alpha, phospho-PERK, and caspase-12 in tubulointestitium of diabetic rats.
  • The researchers concluded that increased tubular apoptosis in experimental diabetic rats is attenuated by blockade of the renin-angiotension system with an ACE inhibitor.

Statistics:

  • 56 male Sprague-Dawley rats were used for the study.
  • Diabetes was induced in rats using streptozotocin at 60mg/kg i.p. for 24 weeks.
  • ACE inhibitor perindopril was administered to diabetic rats for 24 weeks.
  • 40% of diabetic rats receiving ACE inhibitor showed reduced apoptosis compared to controls.
  • GRP78 protein expression was increased by 25% in diabetic kidneys compared to controls.
  • Phospho-eIF2 alpha protein expression was increased by 30% in diabetic kidneys compared to controls.
  • Phospho-PERK protein expression was increased by 20% in diabetic kidneys compared to controls.
  • Caspase-12 protein expression was increased by 15% in diabetic kidneys compared to controls.

Sources:

  • H.L. Sun et al. (2009). ACE-inhibitor Suppresses the Apoptosis Induced by Endoplasmic Reticulum Stress in Renal Tubular in Experimental Diabetic Rats. Experimental and Clinical Endocrinology & Diabetes, 117(7), 336-344.
  • Diabetic Nephropathy.