Decreased Expression of Alpha Smooth Muscle Actin and Desmin Contributes to the Protection of Vitamin D3 against Diclofenac Induced Nephrotoxicity in Rats

Sahar Youssef, Marwa Salah

Abstract


Background: Diclofenac is widely prescribed for its analgesic and anti-inflammatory actions but it also has some harmful effects on the kidney. The current study was conducted to elucidate the possible mechanism of action of diclofenac sodium on kidney, and if it is affected by the addition of vitamin D.

Methods: Rats were divided into 4 equal groups. G1 was the control group that received no treatment; G2 was treated with intramuscular injection of vitamin D (1,000 IU/kg, 3days/week); G3 was treated with intramuscular injection of diclofenac sodium (3.6 mg/kg, 3 days/week) and G4 treated simultaneously with both diclofenac (3.6 mg/kg, 3 days/week) and vitamin D (1,000 IU/kg, 3days/week) intramuscularly for four weeks. Kidneys sections were stained with H&E, Masson’s trichrome and immunohistochemical staining against α –SMA and desmin followed by the morphometric and statistical analysis.

Results: Kidney sections from diclofenac sodium treated group showed degeneration and necrosis, small or atrophic glomeruli with dilated Bowman’s space and some of the renal tubular lining cells appeared vacuolated with small pyknotic nuclei. Renal fibrosis was confirmed by significant increase in collagen fibers, α –SMA and podocytes injury by significant increase of desmin.  However, in diclofenac- vitamin D treated group significantly the expression of α –SMA and desmin were decreased.

Conclusion: The current data suggested that vitamin D might play a protectant role against diclofenac induced kidney injury in rats through the preservation of the histological architecture of renal corpuscles, renal cortical tubules and down regulation of collagen, α – SMA and desmin.

Keywords: α-SMA; Desmin; Diclofenac Sodium; Vitamin D


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References


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