Introduction and objectives: The purpose of the study was to observe different expression of connexin 43 between culprit arteries and nonculprit arteries in ischemia-reperfusion model and investigate on the mechanism of nonculprit arteries lesions progression. Methods: Rabbit hyperlipidemia ischemia-reperfusion model was established, vascular smooth muscles of culprit arteries and nonculprit arteries were divided into 4 groups: ① culprit arteries control group, ② nonculprit arteries control group, ③ culprit arteries ischemia-reperfusion group, ④ nonculprit arteries ischemia-reperfusion group. Immunohistochemistry analysis of connexin 43 was performed in each group. Smooth muscle cells of nonculprit arteries were divided into 4 groups: ① normal control group. ② hyperlipidemia control group. ③ angiotensin II intervention group. ④ mitogen-activated protein kinase pathway inhibitor pretreatment plus angiotensin II intervention group. Expression of connexin 43 was analysed in each group. Results: Fluorescence immunohistochemistry analysis of connexin 43 showed there was significant difference between culprit arteries ischemia-reperfusion group and nonculprit arteries ischemia-reperfusion group (1723.52±138.64 vs 2136.15±237.82, P<0.001). Expression of connexin 43 in angiotensin II intervention group was higher than that in hyperlipidemia control group (1.79±0.31 vs 1.25±0.21, P<0.05), expression of connexin 43 in mitogen-activated protein kinase pathway inhibitor pretreatment plus angiotensin II intervention group was lower than that in angiotensin II intervention group [(0.85±0.19 vs 1.79±0.31, P<0.05), (0.99±0.13 vs 1.79±0.31, P<0.05), (0.81±0.15 vs 1.79±0.31, P<0.05) respectively]. Conclusions: Expression of connexin 43 in nonculprit arteries was higher than that in culprit arteries, it may be involved in angiotensin II--mitogen-activated protein kinase pathway. IJCEP
Introduction and objectives: The purpose of the study was to observe different expression of connexin 43 between culprit arteries and nonculprit arteries in ischemia-reperfusion model and investigate on the mechanism of nonculprit arteries lesions progression. Methods:Rabbit hyperlipidemia ischemia-reperfusion model was established, vascular smooth muscles of culprit arteries and nonculprit arteries were divided into 4 groups: ① culprit arteries control group, ② nonculprit arteries control group, ③ culprit arteries ischemia-reperfusion group, ④ nonculprit arteries ischemia-reperfusion group. Immunohistochemistry analysis of connexin 43 was performed in each group. Smooth muscle cells of nonculprit arteries were divided into 4 groups: ① normal control group. ② hyperlipidemia control group. ③ angiotensin II intervention group. ④ mitogen-activated protein kinase pathway inhibitor pretreatment plus angiotensin II intervention group. Expression of connexin 43 was analysed in each group. Results: Fluorescence immunohistochemistry analysis of connexin 43 showed there was significant difference between culprit arteries ischemia-reperfusion group and nonculprit arteries ischemia-reperfusion group (1723.52±138.64 vs 2136.15±237.82, P<0.001). Expression of connexin 43 in angiotensin II intervention group was higher than that in hyperlipidemia control group (1.79±0.31 vs 1.25±0.21, P<0.05), expression of connexin 43 in mitogen-activated protein kinase pathway inhibitor pretreatment plus angiotensin II intervention group was lower than that in angiotensin II intervention group [(0.85±0.19 vs 1.79±0.31, P<0.05), (0.99±0.13 vs 1.79±0.31, P<0.05), (0.81±0.15 vs 1.79±0.31, P<0.05) respectively]. Conclusions: Expression of connexin 43 in nonculprit arteries was higher than that in culprit arteries, it may be involved in angiotensin II--mitogen-activated protein kinase pathway. IJCEP