Liu Y.,Childrens Hospital of Hebei ProvenceHebei Provence |
Shi L.,Childrens Hospital of Hebei ProvenceHebei Provence |
Liu C.,Childrens Hospital of Hebei ProvenceHebei Provence |
Zhu G.,Chest Hospital of Hebei ProvenceHebei Provence |
And 3 more authors.
International Journal of Clinical and Experimental Medicine | Year: 2015
To investigate the mechanism of combination therapy of propofol and sevoflurane on MAP2K3 level and myocardial apoptosis induced by ischemia-reperfusion (IR) in rat. A total of 30 SD rats were randomly separated into 3 groups: normal, IR (ligation of left coronary artery), and IR+ propofol and sevoflurane (IR+P+S). Different methods were used to detect the serum index associated IR injury. TUNEL assay was used to analyze the apoptotic cells of rat heart tissues. qRT-PCR was used to analyze the mRNA levels of cell apoptosis related proteins such as Bcl-2, Bax, and MAP2K3. Western blotting was used to detect the expression of Bcl-2, Bax, MAP2K3, and Caspase-3 of heart tissues. Compared with normal group, serum LDH, cTnI, and CK-MB levels in IR group were significantly increased with time increasing (P<0.05), while that in IR+P+S group were significantly decreased compared with that in IR group (P<0.05). The percentage of apoptotic cells of heart tissue in IR+P+S group was larger than that in IR group (P<0.05). Compared with IR group, mRNA expression of MAP2K3 and Bax were significantly decreased with Bcl-2 was significantly increased in IR+P+S group (P<0.05). Also, expression of MAP2K3, Caspase-3, and Bcl-2 in IR+P+S group were statistically lower while Bax was statistically higher than that in IR group (P<0.05). Our study suggested that combination therapy of propofol and sevoflurane may protect myocardial cells from damage during IR through decreasing MAP2K3 level and reducing cell apoptosis via Bcl-2/Bax pathway. © 2015 E-Century Publishing Corporation. All rights reserved.