N-acetyl cysteine can blunt metabolic and cardiovascular effects via down-regulation of cardiotrophin-1 in rat model of fructose-induced metabolic syndrome.

In this study, we investigated the ability of N-acetyl cysteine (NAC) to alleviate the metabolic disorders in fructose-induced metabolic syndrome (MS) in male rats and to examine its protective effect on aortic and cardiac tissues via its influence on cardiotrophin-1 (CT-1) expression. NAC (20 mg/kg b.w./day) was administered to fructose induced MS animals for 12 weeks. Chronic fructose consumption (20% w/v) increased body weight gain, relative heart weight, systolic blood pressure (SBP), diastolic blood pressure (DBP), insulin resistance (IR), and associated with metabolic alterations. Histological and immunohistochemical examination revealed aortic stiffness and myocardial degeneration and fibrosis together with increased CT-1 expression. Treatment with NAC improved IR, SBP, DBP, and mitigated dyslipidaemia and oxidative stress. Additionally, NAC down-regulated CT-1 expression in the heart and aorta. These findings demonstrated the protective effect of NAC against aortic and myocardial degeneration and fibrosis through down-regulation of CT-1 in fructose induced MS animal model.

Omega-3 fatty acids decreases oxidative stress, tumor necrosis factor-alpha, and interleukin-1 beta in hyperthyroidism-induced hepatic dysfunction rat model.

Hyperthyroidism is associated with abnormalities of the liver. Omega-3 polyunsaturated fatty acids, especially their long-chain forms: eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) have beneficial health effects. The objectives of the present study were to assess hyperthyroidism-induced hepatic dysfunction in adult male rats and to evaluate the ameliorative effects of omega-3 on hyperthyroidism-induced hepatic dysfunction and the underlying mechanisms. Twenty four adult male rats were randomly divided into three equal groups; control group which received water for 6 weeks, hyperthyroid group which received L-thyroxine orally for 6 weeks and hyperthyroid omega-3 treated group which received L-thyroxine for 2 weeks and then co-treated with L-thyroxine and omega-3 oral compound containing 18% of EPA and 12% of DHA for 4 weeks. Hyperthyroid omega-3 treated group showed significantly increased final body weight and body weight gain, decreased liver weight to body weight ratio, decreased serum triiodo-l-thyronine level, increased serum thyroid stimulating hormone level, decreased serum levels of alanine transaminase, aspartate transaminase and tumor necrosis factor-alpha, increased hepatic levels of total antioxidant capacity and decreased hepatic levels of total peroxide and interleukin-1 beta when compared with the hyperthyroid group. Furthermore, histopathological studies revealed also marked improvement. We concluded that omega-3 had encouraging therapeutic effects against hyperthyroidism-induced hepatic dysfunction attributable to more than one mechanism: antioxidant, anti-inflammatory and anti-fibrotic effects.

Curcumin ameliorate DENA-induced HCC via modulating TGF-ß, AKT, and caspase-3 expression in experimental rat model.

Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide. In laboratory animal models, diethylnitrosamine (DENA) is a well-known agent that has a potent hepatocarcinogenic effect that is used to induce HCC. As curcumin has a potent anti-inflammatory effect with strong therapeutic potential against a variety of cancers, our present study aims to investigate its curative effects and the possible mechanisms of action against DENA-induced HCC in male rats. Investigation of biochemical and molecular parameters of HCC animal model liver showed an overexpression of TGF-ß and Akt proteins accompanied with a significant reduction of the proapoptotic marker caspase-3. DENA-induced hepatic cellular injury resulted also in a significant increase in liver function marker enzymes aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lipid peroxides in this group. Curcumin treatment partially reversed DENA-induced damage as it reduced the overexpression of the angiogenic and anti-apoptotic factors TGF-ß and Akt and improved caspase-3 expression. Also, it could partially normalize the serum values of liver marker enzymes and lipid peroxidation and improve liver architecture. Curcumin shows a unique chemotherapeutic effect in reversing DENA-induced HCC in rat model. This effect is possibly mediated through its proapoptotic, antioxidant, anti-angiogenic, as well as antimitotic effects. It interferes and modulates cell signaling pathways and hence turns death signals and apoptosis on within tumor cells.