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Mine Inal - One of the best experts on this subject based on the ideXlab platform.
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Betaine (trimethylglycine) as a Nutritional Agent prevents oxidative stress after chronic ethanol consumption in pancreatic tissue of rats.
International journal for vitamin and nutrition research. Internationale Zeitschrift fur Vitamin- und Ernahrungsforschung. Journal international de vi, 2009Co-Authors: Güngör Kanbak, Ali Dokumacioglu, Aysegul Tektas, Kazim Kartkaya, Mine InalAbstract:In this study, we investigated the free radical-mediated cytotoxic effects of chronic ethanol consumption on the pancreatic tissue and a possible cytoprotective effect of betaine as a methyl donor and an important participant in the methionine cycle. Twenty-four male Wistar rats were divided into control, ethanol, and ethanol+betaine groups. Prior to sacrifice, all groups were fed 60 mL/diet per day for two months. Rats in the ethanol group were fed with ethanol 8 g/kg/day. The ethanol+betaine groups were fed ethanol plus betaine (0.5 % w/v). Malondialdehyde levels and adenosine deaminase, superoxide dismutase, and xanthine oxidase activities were determined in pancreatic tissues of rats. Compared to control group, MDA levels increased significantly in the ethanol group (p
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betaine trimethylglycine as a Nutritional Agent prevents oxidative stress after chronic ethanol consumption in pancreatic tissue of rats
International Journal for Vitamin and Nutrition Research, 2009Co-Authors: Güngör Kanbak, Ali Dokumacioglu, Aysegul Tektas, Kazim Kartkaya, Mine InalAbstract:In this study, we investigated the free radical-mediated cytotoxic effects of chronic ethanol consumption on the pancreatic tissue and a possible cytoprotective effect of betaine as a methyl donor and an important participant in the methionine cycle. Twenty-four male Wistar rats were divided into control, ethanol, and ethanol+betaine groups. Prior to sacrifice, all groups were fed 60 mL/diet per day for two months. Rats in the ethanol group were fed with ethanol 8 g/kg/day. The ethanol+betaine groups were fed ethanol plus betaine (0.5 % w/v). Malondialdehyde levels and adenosine deaminase, superoxide dismutase, and xanthine oxidase activities were determined in pancreatic tissues of rats. Compared to control group, MDA levels increased significantly in the ethanol group (p<0.05). MDA levels in the ethanol+betaine group were significantly decreased compared to the ethanol group (p<0.05). ADA activity in the ethanol+betaine group decreased significantly when compared to the ethanol group (p<0.05). XO activities in ethanol-fed rats were decreased significantly compared to the control group (p<0.05). XO activity in the betaine group was increased significantly (p<0.05) compared to the ethanol group. SOD activity in the ethanol group decreased significantly compared to control group (p<0.001). SOD activity in the ethanol+betaine group decreased significantly (p<0.05) compared to the control group. We think that betaine, as a Nutritional methylating Agent, may be effective against ethanol-mediated oxidative stress in pancreatic tissue.
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Effects of Chronic Ethanol Consumption on Brain Synaptosomes and Protective Role of Betaine
Neurochemical research, 2007Co-Authors: Güngör Kanbak, Ali Dokumacioglu, Kazim Kartkaya, Okan Can Arslan, Mine InalAbstract:To evaluate the cytotoxic effects of chronic ethanol consumption on brain cerebral synaptosomes and preventive role of betaine as a methyl donor andS-adenosylmethionine precursor, 24 male Wistar rats were divided into three groups: control, ethanol (8 g/kg/day) and ethanol plus betaine(0.5% w/v) group. Animals were fed 60 ml/diet per day for two months, then sacrificed. Malondialdehyde (MDA), protein carbonyl contents and adenosine deaminase (ADA) activities were determined in synaptosomal/mitochondrial enriched fraction isolated from rat cerebral cortexes. When compared to controls, ethanol containing diet significantly increased MDA levels (P 0.05). However, adding betaine to ethanol containing diet caused a significant decrease in MDA, protein carbonyl levels and adenosine deaminase activities (P < 0.05). These results indicate that betaine may appear as a protective Nutritional Agent against cytotoxic brain damage induced by chronic ethanol consumption.
Güngör Kanbak - One of the best experts on this subject based on the ideXlab platform.
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Betaine (trimethylglycine) as a Nutritional Agent prevents oxidative stress after chronic ethanol consumption in pancreatic tissue of rats.
International journal for vitamin and nutrition research. Internationale Zeitschrift fur Vitamin- und Ernahrungsforschung. Journal international de vi, 2009Co-Authors: Güngör Kanbak, Ali Dokumacioglu, Aysegul Tektas, Kazim Kartkaya, Mine InalAbstract:In this study, we investigated the free radical-mediated cytotoxic effects of chronic ethanol consumption on the pancreatic tissue and a possible cytoprotective effect of betaine as a methyl donor and an important participant in the methionine cycle. Twenty-four male Wistar rats were divided into control, ethanol, and ethanol+betaine groups. Prior to sacrifice, all groups were fed 60 mL/diet per day for two months. Rats in the ethanol group were fed with ethanol 8 g/kg/day. The ethanol+betaine groups were fed ethanol plus betaine (0.5 % w/v). Malondialdehyde levels and adenosine deaminase, superoxide dismutase, and xanthine oxidase activities were determined in pancreatic tissues of rats. Compared to control group, MDA levels increased significantly in the ethanol group (p
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betaine trimethylglycine as a Nutritional Agent prevents oxidative stress after chronic ethanol consumption in pancreatic tissue of rats
International Journal for Vitamin and Nutrition Research, 2009Co-Authors: Güngör Kanbak, Ali Dokumacioglu, Aysegul Tektas, Kazim Kartkaya, Mine InalAbstract:In this study, we investigated the free radical-mediated cytotoxic effects of chronic ethanol consumption on the pancreatic tissue and a possible cytoprotective effect of betaine as a methyl donor and an important participant in the methionine cycle. Twenty-four male Wistar rats were divided into control, ethanol, and ethanol+betaine groups. Prior to sacrifice, all groups were fed 60 mL/diet per day for two months. Rats in the ethanol group were fed with ethanol 8 g/kg/day. The ethanol+betaine groups were fed ethanol plus betaine (0.5 % w/v). Malondialdehyde levels and adenosine deaminase, superoxide dismutase, and xanthine oxidase activities were determined in pancreatic tissues of rats. Compared to control group, MDA levels increased significantly in the ethanol group (p<0.05). MDA levels in the ethanol+betaine group were significantly decreased compared to the ethanol group (p<0.05). ADA activity in the ethanol+betaine group decreased significantly when compared to the ethanol group (p<0.05). XO activities in ethanol-fed rats were decreased significantly compared to the control group (p<0.05). XO activity in the betaine group was increased significantly (p<0.05) compared to the ethanol group. SOD activity in the ethanol group decreased significantly compared to control group (p<0.001). SOD activity in the ethanol+betaine group decreased significantly (p<0.05) compared to the control group. We think that betaine, as a Nutritional methylating Agent, may be effective against ethanol-mediated oxidative stress in pancreatic tissue.
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Effects of Chronic Ethanol Consumption on Brain Synaptosomes and Protective Role of Betaine
Neurochemical research, 2007Co-Authors: Güngör Kanbak, Ali Dokumacioglu, Kazim Kartkaya, Okan Can Arslan, Mine InalAbstract:To evaluate the cytotoxic effects of chronic ethanol consumption on brain cerebral synaptosomes and preventive role of betaine as a methyl donor andS-adenosylmethionine precursor, 24 male Wistar rats were divided into three groups: control, ethanol (8 g/kg/day) and ethanol plus betaine(0.5% w/v) group. Animals were fed 60 ml/diet per day for two months, then sacrificed. Malondialdehyde (MDA), protein carbonyl contents and adenosine deaminase (ADA) activities were determined in synaptosomal/mitochondrial enriched fraction isolated from rat cerebral cortexes. When compared to controls, ethanol containing diet significantly increased MDA levels (P 0.05). However, adding betaine to ethanol containing diet caused a significant decrease in MDA, protein carbonyl levels and adenosine deaminase activities (P < 0.05). These results indicate that betaine may appear as a protective Nutritional Agent against cytotoxic brain damage induced by chronic ethanol consumption.
Kazim Kartkaya - One of the best experts on this subject based on the ideXlab platform.
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Betaine (trimethylglycine) as a Nutritional Agent prevents oxidative stress after chronic ethanol consumption in pancreatic tissue of rats.
International journal for vitamin and nutrition research. Internationale Zeitschrift fur Vitamin- und Ernahrungsforschung. Journal international de vi, 2009Co-Authors: Güngör Kanbak, Ali Dokumacioglu, Aysegul Tektas, Kazim Kartkaya, Mine InalAbstract:In this study, we investigated the free radical-mediated cytotoxic effects of chronic ethanol consumption on the pancreatic tissue and a possible cytoprotective effect of betaine as a methyl donor and an important participant in the methionine cycle. Twenty-four male Wistar rats were divided into control, ethanol, and ethanol+betaine groups. Prior to sacrifice, all groups were fed 60 mL/diet per day for two months. Rats in the ethanol group were fed with ethanol 8 g/kg/day. The ethanol+betaine groups were fed ethanol plus betaine (0.5 % w/v). Malondialdehyde levels and adenosine deaminase, superoxide dismutase, and xanthine oxidase activities were determined in pancreatic tissues of rats. Compared to control group, MDA levels increased significantly in the ethanol group (p
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betaine trimethylglycine as a Nutritional Agent prevents oxidative stress after chronic ethanol consumption in pancreatic tissue of rats
International Journal for Vitamin and Nutrition Research, 2009Co-Authors: Güngör Kanbak, Ali Dokumacioglu, Aysegul Tektas, Kazim Kartkaya, Mine InalAbstract:In this study, we investigated the free radical-mediated cytotoxic effects of chronic ethanol consumption on the pancreatic tissue and a possible cytoprotective effect of betaine as a methyl donor and an important participant in the methionine cycle. Twenty-four male Wistar rats were divided into control, ethanol, and ethanol+betaine groups. Prior to sacrifice, all groups were fed 60 mL/diet per day for two months. Rats in the ethanol group were fed with ethanol 8 g/kg/day. The ethanol+betaine groups were fed ethanol plus betaine (0.5 % w/v). Malondialdehyde levels and adenosine deaminase, superoxide dismutase, and xanthine oxidase activities were determined in pancreatic tissues of rats. Compared to control group, MDA levels increased significantly in the ethanol group (p<0.05). MDA levels in the ethanol+betaine group were significantly decreased compared to the ethanol group (p<0.05). ADA activity in the ethanol+betaine group decreased significantly when compared to the ethanol group (p<0.05). XO activities in ethanol-fed rats were decreased significantly compared to the control group (p<0.05). XO activity in the betaine group was increased significantly (p<0.05) compared to the ethanol group. SOD activity in the ethanol group decreased significantly compared to control group (p<0.001). SOD activity in the ethanol+betaine group decreased significantly (p<0.05) compared to the control group. We think that betaine, as a Nutritional methylating Agent, may be effective against ethanol-mediated oxidative stress in pancreatic tissue.
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Effects of Chronic Ethanol Consumption on Brain Synaptosomes and Protective Role of Betaine
Neurochemical research, 2007Co-Authors: Güngör Kanbak, Ali Dokumacioglu, Kazim Kartkaya, Okan Can Arslan, Mine InalAbstract:To evaluate the cytotoxic effects of chronic ethanol consumption on brain cerebral synaptosomes and preventive role of betaine as a methyl donor andS-adenosylmethionine precursor, 24 male Wistar rats were divided into three groups: control, ethanol (8 g/kg/day) and ethanol plus betaine(0.5% w/v) group. Animals were fed 60 ml/diet per day for two months, then sacrificed. Malondialdehyde (MDA), protein carbonyl contents and adenosine deaminase (ADA) activities were determined in synaptosomal/mitochondrial enriched fraction isolated from rat cerebral cortexes. When compared to controls, ethanol containing diet significantly increased MDA levels (P 0.05). However, adding betaine to ethanol containing diet caused a significant decrease in MDA, protein carbonyl levels and adenosine deaminase activities (P < 0.05). These results indicate that betaine may appear as a protective Nutritional Agent against cytotoxic brain damage induced by chronic ethanol consumption.
Ali Dokumacioglu - One of the best experts on this subject based on the ideXlab platform.
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Betaine (trimethylglycine) as a Nutritional Agent prevents oxidative stress after chronic ethanol consumption in pancreatic tissue of rats.
International journal for vitamin and nutrition research. Internationale Zeitschrift fur Vitamin- und Ernahrungsforschung. Journal international de vi, 2009Co-Authors: Güngör Kanbak, Ali Dokumacioglu, Aysegul Tektas, Kazim Kartkaya, Mine InalAbstract:In this study, we investigated the free radical-mediated cytotoxic effects of chronic ethanol consumption on the pancreatic tissue and a possible cytoprotective effect of betaine as a methyl donor and an important participant in the methionine cycle. Twenty-four male Wistar rats were divided into control, ethanol, and ethanol+betaine groups. Prior to sacrifice, all groups were fed 60 mL/diet per day for two months. Rats in the ethanol group were fed with ethanol 8 g/kg/day. The ethanol+betaine groups were fed ethanol plus betaine (0.5 % w/v). Malondialdehyde levels and adenosine deaminase, superoxide dismutase, and xanthine oxidase activities were determined in pancreatic tissues of rats. Compared to control group, MDA levels increased significantly in the ethanol group (p
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betaine trimethylglycine as a Nutritional Agent prevents oxidative stress after chronic ethanol consumption in pancreatic tissue of rats
International Journal for Vitamin and Nutrition Research, 2009Co-Authors: Güngör Kanbak, Ali Dokumacioglu, Aysegul Tektas, Kazim Kartkaya, Mine InalAbstract:In this study, we investigated the free radical-mediated cytotoxic effects of chronic ethanol consumption on the pancreatic tissue and a possible cytoprotective effect of betaine as a methyl donor and an important participant in the methionine cycle. Twenty-four male Wistar rats were divided into control, ethanol, and ethanol+betaine groups. Prior to sacrifice, all groups were fed 60 mL/diet per day for two months. Rats in the ethanol group were fed with ethanol 8 g/kg/day. The ethanol+betaine groups were fed ethanol plus betaine (0.5 % w/v). Malondialdehyde levels and adenosine deaminase, superoxide dismutase, and xanthine oxidase activities were determined in pancreatic tissues of rats. Compared to control group, MDA levels increased significantly in the ethanol group (p<0.05). MDA levels in the ethanol+betaine group were significantly decreased compared to the ethanol group (p<0.05). ADA activity in the ethanol+betaine group decreased significantly when compared to the ethanol group (p<0.05). XO activities in ethanol-fed rats were decreased significantly compared to the control group (p<0.05). XO activity in the betaine group was increased significantly (p<0.05) compared to the ethanol group. SOD activity in the ethanol group decreased significantly compared to control group (p<0.001). SOD activity in the ethanol+betaine group decreased significantly (p<0.05) compared to the control group. We think that betaine, as a Nutritional methylating Agent, may be effective against ethanol-mediated oxidative stress in pancreatic tissue.
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Effects of Chronic Ethanol Consumption on Brain Synaptosomes and Protective Role of Betaine
Neurochemical research, 2007Co-Authors: Güngör Kanbak, Ali Dokumacioglu, Kazim Kartkaya, Okan Can Arslan, Mine InalAbstract:To evaluate the cytotoxic effects of chronic ethanol consumption on brain cerebral synaptosomes and preventive role of betaine as a methyl donor andS-adenosylmethionine precursor, 24 male Wistar rats were divided into three groups: control, ethanol (8 g/kg/day) and ethanol plus betaine(0.5% w/v) group. Animals were fed 60 ml/diet per day for two months, then sacrificed. Malondialdehyde (MDA), protein carbonyl contents and adenosine deaminase (ADA) activities were determined in synaptosomal/mitochondrial enriched fraction isolated from rat cerebral cortexes. When compared to controls, ethanol containing diet significantly increased MDA levels (P 0.05). However, adding betaine to ethanol containing diet caused a significant decrease in MDA, protein carbonyl levels and adenosine deaminase activities (P < 0.05). These results indicate that betaine may appear as a protective Nutritional Agent against cytotoxic brain damage induced by chronic ethanol consumption.
Yuqing Zhao - One of the best experts on this subject based on the ideXlab platform.
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Hypoglycemic Effects of Licochalcone A on the Streptozotocin-Induced Diabetic Mice and Its Mechanism Study.
Journal of agricultural and food chemistry, 2021Co-Authors: Zhonghua Luo, Qingqing Gao, Dongyu Miao, Yuqing ZhaoAbstract:Type 2 diabetes mellitus (T2DM) is a type of metabolic illness based on relatively insufficient insulin secretion and insulin resistance (IR) as pathophysiological bases. Currently, it is the main type of diabetes. Hypoglycemic and hypolipidemic effects of licochalcone A (LicA) on high-fat diet and streptozocin-caused T2DM were studied. LicA can remarkably decline the IR index and blood glucose and serum lipid levels. Also, the treatment of LicA can improve the "three more and one less" phenomenon in T2DM mice, such as excessive drinking, eating, urine, and weight loss. In addition, LicA can improve oral glucose tolerance, pancreatic injury, and liver enlargement in T2DM mice. Network pharmacology analysis demonstrated that the observed pharmacological effects were mediated by regulating the insulin signal transduction pathway. Therefore, the PI3K/Akt-signaling pathway was selected for verification; it was demonstrated that LicA could improve the insulin-signaling pathway, protect islet cells, improve IR, reduce blood glucose levels, and alleviate lipid metabolism disorder. Its mechanism of influence may be closely related to LicA up-regulating the liver and pancreas IRS-2/PI3K/AKT-signaling pathway. Among them, the high-dose group of LicA had the best effect, which provided an idea for the use of LicA as a Nutritional Agent in the cure of T2DM.
