ABSTRACT
AIM: To observe the difference of cerebral injury following ischemia/reperfusion and mRNA expression of TGF-β1 between diabetic and non-diabetic rats.METHODS: At first, Wistar rats were divided into two groups,non-diabetes and diabetes, and then two groups followed by sham, middle cerebral artery occlusion(MCAO) 2h and reperfusion 24 h after MCAO 2 h respectively. TGF-β1 mRNA expression was measured by semi-quantitative reverse transcription polymerase chain reaction(RT-PCR); Cerebral damage was evaluated by histopathology.RESULTS: In the same condition of ischemia or ischemia/reperfusion, injuried area enlarged in DM groups; The expression level of TGF-β1 mRNA increased at the time of 2 h after MCAO in non-diabetic group and diabetic group, especialy significantly in non-diabetic group with MCAO 2 h, and decreased at the time of reperfusion 24 h after MCAO 2 h, but still higher than that in the sham group.CONCLUSION: Diabetes mellitus exacerbated brain lesion following ischemia/repefusion, increased TGF-β1 mRNA expresion after MCAO may be an anti-injury reaction,and anti-injury ability is decreased under diabetic condition
ABSTRACT
AIM: To study forms of cell death following cerebral ischemia/reperfusion in diabetic rats. METHODS: Based on the modles of diabetes and middle cerebral artery occlusion(MCAO), characteristics of cell death after ischemia/reperfusion were evaluated synthetically by the pathological, flow cytometry(FCM), TUNEL and the DNA agarose electrophoresis.RESULTS: The occurrence of cerebral injury after ischemia/reperfusion were accompanied by cell necrosis and cell apoptosis. And cell apoptosis was mainly located in ischeamic penumbra(IP) zone around the densely ischemic focus. Ischemic centre(IC)was characterized by cell necrosis. At the same time, the results showed that the process of ischemic cerebral injury worsen by diabetes mellitus was related to inducing cell apoptosis in IP and Mid zone.CONCLUSION: Neuronal damage following focal cerebral ischemia/reperfusion included cell necrosis and apoptosis, IC zone was mainly characterized by the former, however IP zone by the latter, and there had close internal relationship between them. Brain damage following cerebral ischemia/reperfusion was worsen instinctly under diabetic condition.
ABSTRACT
AIM: To observe the difference of cerebral injury following ischemia/reperfusion and mRNA expression of TGF-? 1 between diabetic and non-diabetic rats.METHODS: At first, Wistar rats were divided into two groups,non-diabetes and diabetes, and then two groups followed by sham, middle cerebral artery occlusion(MCAO) 2h and reperfusion 24 h after MCAO 2 h respectively. TGF-? 1 mRNA expression was measured by semi-quantitative reverse transcription polymerase chain reaction(RT-PCR); Cerebral damage was evaluated by histopathology.RESULTS: In the same condition of ischemia or ischemia/reperfusion, injuried area enlarged in DM groups; The expression level of TGF-? 1 mRNA increased at the time of 2 h after MCAO in non-diabetic group and diabetic group, especialy significantly in non-diabetic group with MCAO 2 h, and decreased at the time of reperfusion 24 h after MCAO 2 h, but still higher than that in the sham group.CONCLUSION: Diabetes mellitus exacerbated brain lesion following ischemia/repefusion, increased TGF-? 1 mRNA expresion after MCAO may be an anti-injury reaction,and anti-injury ability is decreased under diabetic condition.