Background Cardiac failure is a leading cause of the mortality of diabetic patients. In part this is due to a specific cardiomyopathy, referred to as diabetic cardiomyopathy. Oxidative stress is widely considered to b...Background Cardiac failure is a leading cause of the mortality of diabetic patients. In part this is due to a specific cardiomyopathy, referred to as diabetic cardiomyopathy. Oxidative stress is widely considered to be one of the major factors underlying the pathogenesis of the disease. This study aimed to test whether the antioxidant α-lipoic acid （α-LA） could attenuate mitochondrion-dependent myocardial apoptosis through suppression of mitochondrial oxidative stress to reduce diabetic cardiomyopathy. Methods A rat model of diabetes was induced by a single tail intravenous injection of streptozotocin （STZ） 45 mg/kg. Experimental animals were randomly assigned to 3 groups： normal control （NC）, diabetes （DM） and DM treated with α-LA （α-LA）. The latter group was administered with a-LA （100 mg/kg ip per day）, the remainder received the same volume vehicle. At weeks 4, 8, and 12 after the onset of diabetes, cardiac apoptosis was examined by TUNEL assay. Cardiomyopathy was evaluated by assessment of cardiac structure and function. Oxidative damage was evaluated by the content of malondialdehyde （MDA）, reduced glutathione （GSH） and the activity of manganese superoxide diamutase （Mn-SOD） in the myocardial mitochondria. Expression of caspase-9 and caspase-3 proteins was determined by immunohistochemistry and mitochondrial cytochrome c release was detected by Western blotting Results At 4, 8, and 12 weeks after the onset of diabetes, significant reductions in TUNEL-positive cells, caspase-9,-3 expression, and mitochondrial cytochrome c release were observed in the α-LA group compared to the DM group. In the DM group, the content of MDA in the myocardial mitochondria was significantly increased, and there was a decrease in both the mitochondrial GSH content and the activities of Mn-SOD. They were significantly improved by α-LA treatment. HE staining displayed structural abnormalities in diabetic hearts, while α-LA reversed this structural derangement. The index of cardiac functi展开更多
Objective:To investigate the bioactive-constituents of Shemamruthaa(SM),a herbal combination and its therapeutic effects on the mitochondrial functions with reference to lipid peroxidation(LPO),antioxidant status,citr...Objective:To investigate the bioactive-constituents of Shemamruthaa(SM),a herbal combination and its therapeutic effects on the mitochondrial functions with reference to lipid peroxidation(LPO),antioxidant status,citric acid cycle enzymes and electron transport chain enzymes in mammary tissues of 7,12-dimethylbenz(a)-anthracene(DMBA)induced mammary carcinoma in rat model.Methods:Adult Female Sprague-Dawley rats were used for the study and were divided into four groups.CroupⅠserved as control and CroupⅡrats were induced mammary carcinoma by administration of DMBA(25 mg/kg b.w.)orally.The normal and cancer-induced rats(GroupⅢ)were treated with SM(400 mg/kg b.w./day)orally by gastric incubation for 14days.CroupⅣrats served as SM-treated control animals.Results:Cancer-induced rats showed a considerably increased level of LPO with concomitant decreased levels of antioxidants,citric acid cycle enzymes,electron transport chain enzymes and cytochrome contents in the mammary tissue.Treatment with SM brought back the aforementioned biochemical parameters to near normal.Conclusions:From the results,it can be inferred that Shemamruthaa possesses significant anticancer effect through its role in attenuation of LPO,prevention of membrane damage and restoring membrane integrity.展开更多
文摘Background Cardiac failure is a leading cause of the mortality of diabetic patients. In part this is due to a specific cardiomyopathy, referred to as diabetic cardiomyopathy. Oxidative stress is widely considered to be one of the major factors underlying the pathogenesis of the disease. This study aimed to test whether the antioxidant α-lipoic acid （α-LA） could attenuate mitochondrion-dependent myocardial apoptosis through suppression of mitochondrial oxidative stress to reduce diabetic cardiomyopathy. Methods A rat model of diabetes was induced by a single tail intravenous injection of streptozotocin （STZ） 45 mg/kg. Experimental animals were randomly assigned to 3 groups： normal control （NC）, diabetes （DM） and DM treated with α-LA （α-LA）. The latter group was administered with a-LA （100 mg/kg ip per day）, the remainder received the same volume vehicle. At weeks 4, 8, and 12 after the onset of diabetes, cardiac apoptosis was examined by TUNEL assay. Cardiomyopathy was evaluated by assessment of cardiac structure and function. Oxidative damage was evaluated by the content of malondialdehyde （MDA）, reduced glutathione （GSH） and the activity of manganese superoxide diamutase （Mn-SOD） in the myocardial mitochondria. Expression of caspase-9 and caspase-3 proteins was determined by immunohistochemistry and mitochondrial cytochrome c release was detected by Western blotting Results At 4, 8, and 12 weeks after the onset of diabetes, significant reductions in TUNEL-positive cells, caspase-9,-3 expression, and mitochondrial cytochrome c release were observed in the α-LA group compared to the DM group. In the DM group, the content of MDA in the myocardial mitochondria was significantly increased, and there was a decrease in both the mitochondrial GSH content and the activities of Mn-SOD. They were significantly improved by α-LA treatment. HE staining displayed structural abnormalities in diabetic hearts, while α-LA reversed this structural derangement. The index of cardiac functi
基金supported by the Department of Medical Biochemistry.University of Madras.Chennai-600113.Tamil Nadu,India
文摘Objective:To investigate the bioactive-constituents of Shemamruthaa(SM),a herbal combination and its therapeutic effects on the mitochondrial functions with reference to lipid peroxidation(LPO),antioxidant status,citric acid cycle enzymes and electron transport chain enzymes in mammary tissues of 7,12-dimethylbenz(a)-anthracene(DMBA)induced mammary carcinoma in rat model.Methods:Adult Female Sprague-Dawley rats were used for the study and were divided into four groups.CroupⅠserved as control and CroupⅡrats were induced mammary carcinoma by administration of DMBA(25 mg/kg b.w.)orally.The normal and cancer-induced rats(GroupⅢ)were treated with SM(400 mg/kg b.w./day)orally by gastric incubation for 14days.CroupⅣrats served as SM-treated control animals.Results:Cancer-induced rats showed a considerably increased level of LPO with concomitant decreased levels of antioxidants,citric acid cycle enzymes,electron transport chain enzymes and cytochrome contents in the mammary tissue.Treatment with SM brought back the aforementioned biochemical parameters to near normal.Conclusions:From the results,it can be inferred that Shemamruthaa possesses significant anticancer effect through its role in attenuation of LPO,prevention of membrane damage and restoring membrane integrity.
