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

Fluvastatin increases insulin-like growth factor-1 gene expression in rat model of metabolic syndrome

Insulin-like growth factor- 1 [IGF-1] was found to have a role in both glucose homeostasis and cardiovascular diseases. The present study was designed to compare the effects of fluvastatin and metformin on IGF- 1 mRNA expression within the liver and on other individual components of the metabolic syndrome induced in rats by high fructose feeding. Rats fed 60% fructose in diet for 6 weeks were treated daily with fluvastatin [3.75mg/kg/day] or metformin [200mg/kg/day] during the last 2 weeks and were compared with untreated fructose fed group. Fasting levels of plasma cholesterol, triglyceride, glucose, insulin, nitric oxide products, IGF- 1 and IGF- 1 mRNA within the liver as well as systolic blood pressure and body weight were determined. Compared to control rats, the fructose fed group developed hypertension, hyperlipidemia, hyperinsulinemia, hyperglycemia and endothelial dysfunction as well as decreased levels of plasma IGF- 1 and its mRNA within the liver. Fructose fed rats treated with fluvastatin or metformin for 2 weeks showed significant decrease in plasma cholesterol, triglyceride, insulin and glucose levels compared to untreated fructose fed group. Also, both drugs increased significantly plasma levels of nitric oxide products and IGF-1 together with significant increase in IGF-1 mRNA within the liver. However, only metformin treated rats showed significant decrease in systolic blood pressure compared to fructose fed group. This study showed that in a rat model of insulin resistance, fluvastatin improves the metabolic profile and increases plasma level of IGF-1 and its gene expression as effective as metformin