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Role of adenylyl cyclase activator in controlling experimental diabetic nephropathy in rats

Lakhwinder Singh1, Surbhi Rana2, Sidharth Mehan3

  • 1Head Department of Applied Science CGC College of Engineering Landran, Punjab, India.

International Journal of Physiology, Pathophysiology and Pharmacology
|December 6, 2018
PubMed

Insights

Forskolin, an adenylyl cyclase activator, shows potential in preventing diabetic nephropathy in rats. High doses significantly improved kidney function and structure, offering a promising therapeutic avenue.

Area of Science:

  • Pharmacology
  • Nephrology
  • Biochemistry

Background:

  • Diabetic nephropathy is a major complication of diabetes mellitus.
  • Identifying effective treatments to prevent kidney damage is crucial.

Purpose of the Study:

  • To investigate the protective role of the adenylyl cyclase activator, Forskolin, against diabetic nephropathy in a rat model.
  • To assess Forskolin's effects on renal function, oxidative stress, and histological changes.

Main Methods:

  • Experimental diabetic nephropathy was induced in male Wistar rats using a high-fat diet and streptozotocin.
  • Rats were treated with varying doses of Forskolin, Glibenclamide, or Atorvastatin.
  • Renal function, lipid profile, oxidative stress markers, and histopathology were evaluated.

Main Results:

  • Forskolin at intermediate (20 mg/kg) and high (30 mg/kg) doses significantly attenuated diabetes-induced increases in renal function parameters and oxidative stress.
  • High-dose Forskolin treatment reduced vacuolar degeneration of tubules and glomerulosclerosis.
  • Synergistic effects were observed when Forskolin was co-administered with standard drugs.

Conclusions:

  • Forskolin effectively prevents renal structural and functional abnormalities in diabetic rats.
  • It reduces hyperglycemia, renal dysfunction biomarkers, hypertrophy, dyslipidemia, and oxidative stress.
  • Forskolin demonstrates potential for preventing diabetic nephropathy without affecting body weight.
Keywords:
Dyslipidaemiaglutathionehypertrophysuperoxide dismutase and histopathologythiobarbituric acid reactive substances

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