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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Fujiwara, Hisayoshi Arai, Masazumi Chen, Xuehai Takemura, Genzou Fujiwara, Takako Minatoguchi, Shinya Wang, Ningyuan Lu, Chuanjiang Uno, Yoshihiro |
| Description | Author Affiliation: Wang N ( Second Department of Internal Medicine, Gifu University School of Medicine, 40 Tsukasa Machi, Gifu 500, Japan.) |
| Abstract | 1 We examined whether antidiabetic drug miglitol could reduce ischaemia/reperfusion-induced myocardial apoptosis by attenuating production. 2 Japanese white rabbits were subjected to 30-min coronary occlusion followed by 4-h reperfusion with miglitol (10 mg kg(-1), i.v., n=20) or saline (n=20). The infarct area was determined by myoglobin staining, and the infarct size (IS) was expressed as a percentage of the area at risk. DNA fragmentation was assessed by TUNEL method and DNA ladder formation. The expression of Bcl-XL and Bax was detected by immunohistochemical analysis and Western blot analysis. Myocardial interstitial 2,5-DHBA levels, an indicator of hydroxyl radicals, were measured during 30-min ischaemia and 30-min reperfusion in the absence (n=10) or presence of miglitol (10 mg kg(-1), i.v., n=10) using a microdialysis technique. 3 The IS was significantly reduced in the miglitol group (22.4+/-3.4%, n=10) compared to the control group (52.8+/-3.5%, n=10). Miglitol significantly decreased the 2,5-DHBA level during ischaemia and reperfusion and suppressed the incidence of TUNEL-positive myocytes in the ischaemic region (from 10.7+/-3.4 to 4.1+/-3.0%) and the intensity of DNA ladder formation. Miglitol significantly decreased the incidence of Bax-positive myocytes in the ischaemic region (7.4+/-1.7 vs 13.7+/-1.9% of the control) and significantly attenuated the upregulation of Bax protein in the ischaemic regions (from 179+/-17 to 90+/-12% of sham). There was no difference in the expression of Bcl-XL between the two groups. 4 These data suggest that miglitol reduces myocardial apoptosis by attenuating production of hydroxyl radicals and suppressing the upregulation of the expression of Bax protein. |
| ISSN | 00071188 |
| e-ISSN | 14765381 |
| Journal | British Journal of Pharmacology |
| Issue Number | 6 |
| Volume Number | 142 |
| Language | English |
| Publisher | Wiley Online Library(on behalf of The British Pharmacological Society) |
| Publisher Date | 2004-07-01 |
| Publisher Place | Great Britain (UK) |
| Access Restriction | Open |
| Subject Keyword | Apoptosis Drug Effects Glucosamine Analogs & Derivatives Pharmacology Hydroxyl Radical Metabolism Myocardium Proto-Oncogene Proteins C-bcl-2 Biosynthesis 1-Deoxynojirimycin Animals Blood Pressure Blotting, Western DNA Fragmentation Electrophoresis, Agar Gel Gentisates Heart Rate Hemodynamics Hypoglycemic Agents Imino Pyranoses Immunohistochemistry In Situ Nick-End Labeling Myocardial Infarction Pathology Myocardial Reperfusion Injury Physiopathology Myocytes, Cardiac Rabbits Time Factors Bcl-2-Associated X Protein Bcl-X Protein Comparative Study |
| Content Type | Text |
| Resource Type | Article |
| Subject | Pharmacology |
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