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Objective: We designed this study to observe the effect of galangin on damaged mitochondria in the liver of diabetic rats., Methods: Male albino Wistar rats were made diabetic by injecting streptozotocin (STZ) intraperitoneally (40 mg kg -1 body weight (BW)). Galangin (8 mg kg -1 BW) or glibenclamide (600 µg kg -1 BW) was given orally daily once for 45 days to both healthy and diabetic rats., Results: Diabetic rats showed significant (P < 0.05) increase in liver mitochondrial oxidant [Thiobarbituric acid reactive substance (TBARS)] level and a significant decrease in enzymatic [superoxide dismutase (SOD), glutathione peroxidase (GPx)] and non-enzymatic (reduced glutathione (GSH)) antioxidant levels when compared with healthy rats. The mitochondrial enzymes isocitrate dehydrogenase (ICDH), alpha-ketoglutarate dehydrogenase (α-KGDH), succinate dehydrogenase (SDH) and malate dehydrogenase (MDH) and mitochondrial respiratory chain enzymes NADH-dehydrogenase and Cytochrome c-oxidase were decreased significantly (P < 0.05) in diabetic rats when compared with healthy rats. A natural flavonoid galangin administered to hyperglycemia-induced rats resulted in the following findings as compared to hyperglycemia-induced control rats: the oxidant levels decreased significantly (P < 0.05); the enzymatic and non-enzymatic antioxidant levels increased significantly (P < 0.05) and the function of mitochondrial enzymes and the mitochondrial respiratory chain enzymes increased significantly (P < 0.05)., Conclusion: From the results, we conclude that galangin could maintain liver mitochondrial function in diabetic rats.

Mortality in ovarian cancer is predominantly due to acquired chemoresistance and tumor recurrence. UBIQUITIN CONJUGATING ENZYME E2 or RAD6 expression increases in cell lines and patient tumors in response to platinum-based chemotherapy and promotes both activation of DNA damage response pathways and expression of stemness genes and a stem cell-like phenotype driving ovarian cancer chemoresistance.

Objective: To examine the effect of galangin on hyperglycemia-mediated oxidative stress in streptozotocin (STZ)-induced diabetic rats., Methods: Diabetes was induced by intraperitoneal administration of low-dose STZ (40 mg/kg body weight (BW)) into male albino Wistar rats. Galangin (8 mg/kg BW) or glibenclamide (600 µg/kg BW) was given orally, once daily for 45 days to normal and STZ-induced diabetic rats., Results: Diabetic rats showed significantly increased levels of plasma glucose, thiobarbituric acid reactive substances, lipid hydroperoxides, and conjugated dienes. The levels of insulin and non-enzymatic antioxidants (vitamin C, vitamin E, reduced glutathione) and the activity of enzymatic antioxidants (superoxide dismutase, catalase, glutathione peroxidase, and glutathione-S-transferase (GST)) were decreased significantly in diabetic control rats. These altered plasma glucose, insulin, lipid peroxidation products, enzymatic and non-enzymatic antioxidants ions were reverted to near-normal level after the administration of galangin and glibenclamide., Conclusion: The present study shows that galangin decreased oxidative stress and increased antioxidant status in diabetic rats, which may be due to its antidiabetic and antioxidant potential.

Objective: The aim of the present study was to evaluate the protective effect of kaempferol against oxidative stress in streptozotocin (STZ)-induced diabetic rats., Methods: Diabetes was induced in male, adult albino rats of the Wistar strain, by intraperitoneal administration of STZ (40 mg/kg body weight (BW)). Kaempferol (100 mg/kg BW) or glibenclamide (600 µg/kg BW) was administered orally once daily for 45 days to normal and STZ-induced diabetic rats., Results: The STZ-induced diabetic rats showed significantly increased levels of plasma glucose, thiobarbituric acid reactive substances, lipid hydroperoxides, and conjugated dienes in plasma, liver, kidney, and heart whereas they showed significantly decreased level of plasma insulin. The levels of non-enzymic antioxidants (vitamin C, vitamin E, reduced glutathione) in plasma, liver, kidney, and heart and the activities of enzymatic antioxidants (superoxide dismutase, catalase, glutathione peroxidase, and glutathione-S-transferase) in liver, kidney, and heart were significantly decreased in diabetic rats. Administration of kaempferol to diabetic rats was showed brought back in plasma glucose, insulin, lipid peroxidation products, enzymatic, and non-enzymatic antioxidants to near normal., Conclusion: The present study indicates that kaempferol has a good antioxidant property, as evidenced by its increase of antioxidant status and decrease of lipid peroxidation markers, thus providing protection from the risks of diabetic complications.

Context: Kaempferol is a flavonoid found in many edible plants (e.g. tea, cabbage, beans, tomato, strawberries, and grapes) and in plants or botanical products commonly used in traditional medicine. Numerous preclinical studies have shown that kaempferol have a wide range of pharmacological activities, including antioxidant, anti-inflammatory, anticancer, cardioprotective, neuroprotective, and antidiabetic activities., Objective: The present study investigates the effect of kaempferol on membrane-bound ATPases in erythrocytes and in liver, kidney, and heart of streptozotocin (STZ)-induced diabetic rats., Materials and Methods: Diabetes was induced into adult male albino rats of the Wistar strain, by intraperitoneal administration of STZ (40 mg/kg body weight (BW)). Kaempferol (100 mg/kg BW) or glibenclamide (600 µg/kg BW) was administered orally once daily for 45 d to normal and STZ-induced diabetic rats. The effects of kaempferol on membrane-bound ATPases (total ATPase, Na(+)/K(+)-ATPase, Ca(2+)-ATPase, and Mg(2+)-ATPase) activity in erythrocytes and in liver, kidney, and heart were determined., Results: In our study, diabetic rats had significantly (p < 0.05) decreased activities of total ATPases, Na(+)/K(+)-ATPase, Ca(2+)-ATPase, and Mg(2+)-ATPase in erythrocytes and tissues. Oral administration of kaempferol (100 mg/kg BW) or glibenclamide (600 µg/kg BW) for a period of 45 d resulted in significant (p < 0.05) reversal of these enzymes' activities to near normal in erythrocytes and tissues when compared with diabetic control rats., Discussion and Conclusion: Thus, obtained results indicate that administration of kaempferol has the potential to restore deranged activity of membrane-bound ATPases in STZ-induced diabetic rats. Further detailed investigation is necessary to discover kaempferol's action mechanism.

Betle leaf chewing is an old traditional practice in India and other countries of East Asia. We have investigated the antioxidant and antihyperlipidaemic potential of an alcoholic leaf-extract of Piper betle against D-galactosamine (D-GalN; 400 mg/kg body weight, i.p. single dose) intoxication in male albino Wistar rats. Rats were treated with leaf-extract (200 mg/kg body weight) by intragastric intubations daily for 20 days. The animals were divided randomly into five groups of six animals each as control, control plus extract, D-GalN control, D-GalN-rats on treatment with extract or silymarin, a standard drug. We observed an increase in the plasma levels of thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides, and a decrease in vitamin C, vitamin E and reduced glutathione concentrations. Very low density lipoprotein cholesterol and low density lipoprotein cholesterol increased significantly while high density lipoprotein cholesterol decreased. Further, increase in the levels of total cholesterol, phospholipids, triglycerides, free fatty acids in the plasma and tissues of liver and kidney were observed in D-GalN-treated rats. Administration of P. betle leaf-extract prevented the increase or decrease of these parameters and brought towards normality. These results suggest that P. betle could afford a significant antioxidant and antihyperlipidaemic effect against D-GalN-intoxication.