Possible role of pomegranate fruit in reversing renal damage in rats exposed to Phenylhydrazine.

Background: Pomegranate granatum (molasses and peels) and its constituents showed protective effects against natural toxins such as phenylhydrazine (PHZ) as well as chemical toxicants such as arsenic, diazinon, and carbon tetrachloride. Aim: The current study aimed to assess the effect of pomegranate molasses (PM), white peel extract, and red peel extract on nephrotoxicity induced by PHZ. Methods: 80 male rats were divided into eight equal groups; a control group, PM pure group, white peel pomegranate pure group, red peel pomegranate pure group, PHZ group, PM + PHZ group, white peel pomegranate + PHZ group and red peel pomegranate + PHZ group. Kidney function, inflammation markers, antioxidant activities, and renal tissue histopathology were investigated. Results: The results revealed that PHZ group showed a significant increase in lactate Dehydrogenase (LDH), malondialdehyde (MDA), creatinine, uric acid, BUNBUN, C - reactive protein (CRP), tumor necrosis factor, thiobarbituric acid reactive substances (TBARSs), and total antioxidant capacity (TAC) with a significant decrease of catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD) as compared with a control group. Other pomegranate-treated and PHZ co-treated groups with pomegranate showed a significant decrease of LDH, MDA, creatinine, uric acid, BUN, tumor necrosis factor, TBARSs, and TAC with a significant increase of CAT, GPx, and SOD as compared with PHZ group. Conclusion: Collectively, our data suggest that red, white peels, and molasses have anti-toxic and anti-inflammatory effects on renal function and tissues.

Baicalein protects against hypertension associated with diabetes: effect on vascular reactivity and stiffness.

The present work investigated the possible protective effect of baicalein, a natural lipoxygenase enzyme inhibitor, on both insulin deficiency (ID) and insulin resistance (IR)-induced macro-vascular impairment. ID and IR were induced by STZ or fructose for 8 or 12 weeks respectively while baicalein was administered in the last six weeks. Blood pressure (BP) was recorded and isolated aorta reactivity to phenylephrine (PE) and acetylcholine (ACh) were studied. Blood levels of glucose, insulin, advanced glycation end products (AGEs) and tumour necrosis factor-α (TNF-α) were determined. Aortic nuclear transcription factor-κB (NF-κB) activation was assessed. Both models resulted in elevated BP, increased vasoconstriction and impaired relaxation KCl, elevated TNF-α and AGEs, NF-κB activation, marked infiltration of leukocytes in the adventitia, pyknosis of endothelial cells and marked collagen deposition. Baicalein ameliorated elevations in BP in models, prevented exaggerated vasoconstriction IR model and improved relaxation in ID model. Baicalein reduced AGEs and TNF-α level, decreased NF-κB activation and inhibited histopathological changes in both models. Baicalein offsets the hypertensive and the vascular impairment associated with both diabetic models via ameliorating functional and structural derangements of blood vessels.

Caffeic acid phenethyl ester, a 5-lipoxygenase enzyme inhibitor, alleviates diabetic atherosclerotic manifestations: effect on vascular reactivity and stiffness.

Atherosclerosis is a major macrovascular complication of diabetes that increases the risks for myocardial infarction, stroke, and other vascular diseases. The effect of a selective 5-lipoxygenase enzyme inhibitor; caffeic acid phenethyl ester (CAPE) on diabetes-induced atherosclerotic manifestations was investigated. Insulin deficiency or resistance was induced by STZ or fructose respectively. Atherosclerosis developed when rats were left for 8 or 12 weeks subsequent STZ or fructose administration respectively. CAPE (30 mg kg(-1) day(-1)) was given in the last 6 weeks. Afterwards, blood pressure (BP) was recorded. Then, isolated aorta reactivity to KCl and phenylephrine (PE) was studied. Blood glucose level, serum levels of insulin, tumor necrosis factor α (TNF-α) as well as advanced glycation end products (AGEs) were determined. Moreover aortic haem oxygenase-1 (HO-1) protein expression and collagen deposition were also assessed. Insulin deficiency and resistance were accompanied with elevated BP, exaggerated response to KCl and PE, elevated serum TNF-α and AGEs levels. Both models showed marked increase in collagen deposition. However, CAPE alleviated systolic and diastolic BP elevations and the exaggerated vascular contractility to both PE and KCl in both models without affecting AGEs level. CAPE inhibited TNF-α serum level elevation, induced aortic HO-1 expression and reduced collagen deposition. CAPE prevented development of hyperinsulinemia in insulin resistance model without any impact on the developed hyperglycemia in insulin deficiency model. In conclusion, CAPE offsets the atherosclerotic changes associated with diabetes via amelioration of the significant functional and structural derangements in the vessels in addition to its antihyperinsulinemic effect in insulin resistant model.