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The Effects of Rosiglitazone on Cardiomyocyte Apoptosis and Expression of Bax and Bcl-2 in Type 2 Diabetic Rats

Zhang Li-hui

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Abstract

Objective To investigate the effects of rosiglitazone on the cardiomyocyte apoptosis and expression of Bax and Bcl-2 in type 2 diabetic rats. Methods 8 weeks old SD rats were feeded with high calorie for one month, and then were intraperitoneally injected with a low dose of STZ (30mg/kg). The diabetic and control rats were killed at the 12th and 24th weeks after establishing model, respectively. Cardiomyocyte apoptosis was evaluated by TUNEL and flow cytometry. Flow cytometry was also used to detect the protein expression of Bax and Bcl-2. Results Compared with control group, apoptotic cells number, the Bax expression level and Bax/Bcl-2 ratio significantly increased in the diabetic rat hearts (P0.001). Bcl-2 expression level in the diabetic rat hearts was lower than that in control rat heart, but the difference between the two groups was not statistically significant. After rosiglitazone treatment, apoptotic rate of cardiomyocyte in the diabetic rats significantly decreased(P0.01), and Bax expression level decreased, and Bcl-2 expression level increased, but the difference in the level of Bax and Bcl-2 expression between the diabetic rats with or without treatment was not significant. Conclusion Cardiomyocyte apoptosis may play a role in the pathological lesion of diabetic myocardium. Cardiomyocyte apoptosis in diabetic rats could be partially inhibited by rosiglitazone, which was not related with Bax and Bcl-2.

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Objective To investigate the effects of rosiglitazone on the cardiomyocyte apoptosis and expression of Bax and Bcl-2 in type 2 diabetic rats. Methods 8 weeks old SD rats were feeded with high calorie for one month, and then were intraperitoneally injected with a low dose of STZ (30mg/kg). The diabetic and control rats were killed at the 12th and 24th weeks after establishing model, respectively. Cardiomyocyte apoptosis was evaluated by TUNEL and flow cytometry. Flow cytometry was also used to detect the protein expression of Bax and Bcl-2. Results Compared with control group, apoptotic cells number, the Bax expression level and Bax/Bcl-2 ratio significantly increased in the diabetic rat hearts (P0.001). Bcl-2 expression level in the diabetic rat hearts was lower than that in control rat heart, but the difference between the two groups was not statistically significant. After rosiglitazone treatment, apoptotic rate of cardiomyocyte in the diabetic rats significantly decreased(P0.01), and Bax expression level decreased, and Bcl-2 expression level increased, but the difference in the level of Bax and Bcl-2 expression between the diabetic rats with or without treatment was not significant. Conclusion Cardiomyocyte apoptosis may play a role in the pathological lesion of diabetic myocardium. Cardiomyocyte apoptosis in diabetic rats could be partially inhibited by rosiglitazone, which was not related with Bax and Bcl-2.

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Available abstract

Objective To investigate the effects of rosiglitazone on the cardiomyocyte apoptosis and expression of Bax and Bcl-2 in type 2 diabetic rats. Methods 8 weeks old SD rats were feeded with high calorie for one month, and then were intraperitoneally injected with a low dose of STZ (30mg/kg). The diabetic and control rats were killed at the 12th and 24th weeks after establishing model, respectively. Cardiomyocyte apoptosis was evaluated by TUNEL and flow cytometry. Flow cytometry was also used to detect the protein expression of Bax and Bcl-2. Results Compared with control group, apoptotic cells number, the Bax expression level and Bax/Bcl-2 ratio significantly increased in the diabetic rat hearts (P0.001). Bcl-2 expression level in the diabetic rat hearts was lower than that in control rat heart, but the difference between the two groups was not statistically significant. After rosiglitazone treatment, apoptotic rate of cardiomyocyte in the diabetic rats significantly decreased(P0.01), and Bax expression level decreased, and Bcl-2 expression level increased, but the difference in the level of Bax and Bcl-2 expression between the diabetic rats with or without treatment was not significant. Conclusion Cardiomyocyte apoptosis may play a role in the pathological lesion of diabetic myocardium. Cardiomyocyte apoptosis in diabetic rats could be partially inhibited by rosiglitazone, which was not related with Bax and Bcl-2.

Key concepts: Rosiglitazone, Apoptosis, TUNEL assay, Flow cytometry, Endocrinology, Internal medicine, BAX Protein, Medicine

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The Effects of Rosiglitazone on Cardiomyocyte Apoptosis and Expression of Bax and Bcl-2 in Type 2 Diabetic Rats — Research Paper | ScholarLens