热应激对小鼠心肌的影响及其机制研究

Effect of Heat Stress on Blood Biochemical Indicator and Myocardial Ultrastructure in Mice

为探讨热应激时间对小鼠心肌损伤的影响及其具体作用机制,本试验通过不同的高温(41℃)时间(0、1、2、3 h)处理小鼠,通过酶联免疫、放射免疫、组织学方法以及Western Blot,检测小鼠血清生化指标、心肌组织病理变化以及内质网应激蛋白的表达。结果表明:随着热应激时间的延长,血液中的CK、CK-MB、LDH和COR都呈上升趋势,热应激组显著高于常温对照组,且应激组间差异显著(P<0.05);光镜和电镜发现热应激小鼠心肌纤维、肌细胞等都不同程度地受损,心肌细胞凋亡、线粒体空泡化、内质网肿胀等程度加剧。Western Blot结果表明,内质网应激蛋白BiP和CHOP随着热应激时间延长表达量逐渐升高。综上,内质网应激可能参与了热应激导致的小鼠心肌损伤。

This experiment was conducted to study the effect of heat stress on serum e nzymograms, corfiso] and fissure pathological changes by enzyme linked immunosorbentassaying, radioimmunoassay and histopathology methods. The ICR mice were exposed to 41℃ for 1, 2, 3 hours as the heat stress model and 21℃ as control. The results showed that with the heat stress duration expanding, the activity of CK, CK-MB and LDH had increased significantly （P〈0. 05）, the activity of serum cortisol in treatments was higher than that of control group （P〈0. 05）, but there was no significant difference between treatmens. Under light microscope and transmission electron microscope （TEM）, cardiac muscle fibers and myocardial cells had been impaired in different extents, myocardial nucleus shrinked, even apoptosised, rERdilated, chondriosome swelled, the cristae were disorganized and vacuoled, the flesh fibers were shrinked. These above results suggested that heat stress can lead to myoeardium impairment by disturbing energy metagolism and increaseing the activity of cortisol.