The Possible Protective Role of Ginger against Carbon Tetrachloride-Induced Nephrotoxicity in Rats. Histopathological and Morphometric Study

Document Type : Original Article

Authors

1 Departments of Forensic Medicine and Clinical Toxicology,Faculty of Medicine, Tanta University, Tanta, Egypt.

2 Departments of Anatomy,Faculty of Medicine, Tanta University, Tanta, Egypt.

3 Departments of Physiology,Faculty of Medicine, Tanta University, Tanta, Egypt.

4 Departments of Pharmacology, Faculty of Medicine, Tanta University, Tanta, Egypt.

Abstract

Carbon tetrachloride (CCl4) has long been known as a model toxicant. Several reports have discussed its toxic effects on different organs by inducing oxidative stress and free radical production. A number of antioxidant agents, including herbal extracts, have been reported to reduce CCl4 induced toxicity. Many studies have reported the beneficial effects of ginger including its antioxidant properties. This work was performed to assess the possible protective role of ginger against CCl4 induced renal injury in adult male albino rats. A total of 48 adult male rats were divided into 3 groups. Group I served as the control group. Group II received CCl4 by intraperitoneal injections, twice weekly, for 4 weeks. Group III received CCl4 (as previously described) and aqueous extract of ginger orally, once daily, for 4 weeks. At the end of the experiment, renal specimens were processed for light and electron microscopic examination. In addition, morphometric analysis was performed on electromicrographs to assess the filtration barrier integrity. Carbon tetrachloride treated rats showed renal corpuscles with shrunken, lobulated, and hypercellular glomeruli, podocyte affection, as well as mesangial cell proliferation. Morphometric analysis demonstrated disordered filtration barrier integrity. The use of ginger prevented most of these structural changes. Exposure to CCl4 resulted in nephrotoxicity associated with glomerular and tubular alterations in adult male rats. Ginger exhibited a protective effect against CCl4 induced renal damage.

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