Histological study on the role of ginger against cisplatin-induced testicular toxicity in albino rats

Chemotherapy with cisplatin has adverse effects on spermatogenesis. Therefore, this work aimed at investigating the protective role of ginger against cisplatin-induced testicular toxicity in male albino rats. Twenty-four adult albino rats were used in this study. They were divided into three groups. The first group served as the control group; the second group was injected with cisplatin [12 mg/kg once]; and the third group was injected with cisplatin [12 mg/kg once] and then given ginger [310 mg/kg orally] for 26 days. Testicular specimens were processed for light microscopic examination using H and E. Other specimens were processed for electron microscopic examination. Cisplatin had damaging effects on the seminiferous tubules. Some areas of the tubules showed complete depletion of germ cells. Other areas showed some spermatogonia or primary spermatocytes. Sertoli cells showed a variable degree of degenerative changes in the form of destruction of cellular processes and cell junction. Interruption of the nuclear envelope of spermatids and loss of intercellular bridges were noticed. Treating with ginger resulted in normal Sertoli cells and cell junctions. The germ cells lining the tubules were more or less normal except for some intercellular vacuolations. The use of ginger has some protective effects on the testicular structure; hence, a larger number of experiments with higher doses of ginger or longer administration period could be beneficial for patients taking chemotherapeutic drugs

effect of Nigella sativa on the diabetic liver in male albino rats with a special focus on the role of hepatic oval cells

Liver-related complications are a significant cause of death in diabetes and are often unrecognized. This study was designed to evaluate the hepatoprotective properties of Nigella sativa [NS] in streptozotocin-induced diabetes in rats. Moreover, the effect of NS on hepatic oval cells in the liver of diabetic rats was determined. Rats were divided into three groups: group I was the control group; group II included diabetic rats [single intraperitoneal injection of streptozotocin [50 mg/kg body weight]]; and group III included diabetic rats treated with NS [300 mg/kg/day, administered orally] for 4 weeks. Liver sections were subjected to H and E, masson staining, and immunohistochemical staining of proliferating cell nuclear antigen, alpha-smooth muscle actin, and insulin protein. Plasma levels of aspartate aminotransferase, alanine aminotransferase, and albumin levels were measured. Liver hepatocyte growth factor gene expression was also measured by reverse transcription PCR. Compared with the untreated diabetic group, NS preserved the hepatic architecture in diabetic rats as assessed histologically and biochemically. NS has a significant effect on liver regeneration as indicated by a significant increase in liver hepatocyte growth factor gene expression and a significant increase in proliferating cell nuclear antigen immunohistochemical staining. Hepatic fibrosis in diabetic rats was reduced by NS treatment as shown by the significant decrease in collagen deposition and alpha-smooth muscle actin immunohistochemical staining. Moreover, NS maintains functional insulin-producing hepatic oval cells as indicated by immunohistochemistry. This study showed the hepatoprotective effect of NS in experimentally induced diabetes in rats. NS also maintained functional insulin-producing hepatic oval cells in the liver of diabetic-treated rats

effect of red grape seed extract on the experimental model of ulcerative colitis in male albino rats: a histological, immunohistochemical and biochemical study

Ulcerative colitis [UC] is a chronic inflammatory disorder of the large bowel. Red grape seed extract [GSE] has antioxidative, anti-inflammatory and antimicrobial activities. This study was designed to evaluate the protective properties of GSE on an animal model of acetic acid-induced UC. Rats were divided into three groups: group I - the control group; group II - the UC group in which UC was induced by a single intracolonic injection of 2 ml of 3% acetic acid; and group III - the GSE-treated group in which rats were administered GSE at 400 mg/kg/day, orally for 4 days, after induction of UC. Colon sections were subjected to H and E, and immunohistochemical staining of vascular endothelial growth factor [VEGF] and alpha-smooth muscle actin [alpha-SMA]. Tumour necrosis factor-alpha [TNF-alpha], interleukin [IL]-6 and IL-10 were determined in blood by enzyme-linked immunosorbent assay. The UC group showed patchy mucosal ulceration, mononuclear cell infiltration extending to the muscularis externa, increased blood vessels in the mucosa and wide separation of muscle fibers in the muscularis externa. UC significantly increased the plasma levels of proinflammatory cytokines TNF-alpha and IL-6 and significantly decreased immunoregulatory cytokine IL-10 level in plasma. On histologic assessment it was observed that GSE protected the colon from acetic acid-induced UC by preserving colonic crypts and their lining epithelium while decreasing mononuclear cell infiltration. This histological improvement was associated with a significant decrease in the plasma levels of TNF-alpha and IL-6 and a significant increase in plasma IL-10 level. Moreover, GSE significantly decreased the VEGF and alpha-SMA immunostaining in colonic tissues as compared with the UC group. This study proved the protective effect of GSE in experimentally induced UC in rats