Myocardial Infaction analysis

We also examined whether Gper1 expression is required for acute E2-induced improvement of heart viability by determining the myocardial infarct size in sham or hearts subjected to I/R. 3A. Hearts were sectioned and analyzed at the end of the perfusion or reperfusion periods. As expected, acute E2 treatment reduced myocardial infarct size significantly in WT animals. Supporting the functional data, acute E2 treatment had the same protective action (as in the WT animals) when hearts from Esr1and Esr2 knockouts were used but lost its protective effect in the absence of Gper1 as hearts from Gper1-/- animals displayed a robust infarcted area regardless of E2 treatment.我们通过检测假手术（sham）或缺血再灌注（I/R，Ischemia/Reperfusion）处理心脏的心肌梗死面积，探究G蛋白偶联雌激素受体1（Gper1）的表达是否为急性雌二醇（E2，Estradiol）改善心脏存活能力所必需。3A. 在灌注或再灌注阶段结束时，对心脏进行切片并分析。正如预期，急性E2处理可显著降低野生型（WT，Wild Type）动物的心肌梗死面积。与功能实验结果相佐证，当使用雌激素受体α（Esr1）与雌激素受体β（Esr2）基因敲除动物的心脏时，急性E2处理仍可发挥与野生型动物中一致的保护作用；但在缺失Gper1的情况下，E2处理不再具有保护效应，无论是否给予E2处理，Gper1基因敲除纯合子（Gper1-/-）动物的心脏均呈现大面积梗死区域。