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维持机体氧供与氧耗相对平衡是防治缺氧/复氧损伤的重要措施。吗啡可降低代谢,降低氧耗。细胞凋亡是缺血再灌注损伤发病机制中的重要环节,半胱氨酸蛋白酶3(caspase-3)是凋亡的关键酶和执行者。本文拟通过观察缺氧/复氧损伤肾脏组织中caspase-3蛋白的变化,探讨吗啡缺氧预处理发挥肾脏保护作用的可能机制。经自制面罩吸入8%O23 h后吸入空气复氧3 h,建立全身缺氧/复氧肾损伤兔动物模型,缺氧/复氧结束后分别取肾脏组织,采用Envision两步法行caspase-3免疫组化染色。实验结果表明:正常对照组肾脏组织中极少的caspase-3阳性细胞表达。单纯缺氧/复氧组和吗啡缺氧预处理组阳性蛋白表达指数分别为(29.3±5.7)%和(12.16+1.23)%(P<0.05)。结果提示:吗啡缺氧预处理可以下调兔肾脏缺氧/复氧损伤时caspase-3的表达,进而对缺氧/复氧损伤肾脏组织发挥保护作用。
Maintaining the relative balance between oxygen supply and oxygen consumption is an important measure to prevent hypoxia / reoxygenation injury. Morphine reduces metabolism and reduces oxygen consumption. Apoptosis is an important part of the pathogenesis of ischemia-reperfusion injury. Caspase-3 is the key enzyme and executor of apoptosis. This paper intends to observe the changes of caspase-3 protein in renal tissues by hypoxia / reoxygenation injury and to explore the possible mechanism of morphine hypoxic preconditioning playing a protective role in the kidney. After inhalation of 8% O23 h by self-made mask, air was taken in for 3 h. The animal models of hypoxia / reoxygenation injury were established and the kidneys were taken out after hypoxia / reoxygenation respectively. Envision was used to perform caspase-3 Immunohistochemistry. The experimental results show that there are very few caspase-3 positive cells in the normal control group. The positive expression rates of protein in hypoxia / reoxygenation group and morphine hypoxic preconditioning group were (29.3 ± 5.7)% and (12.16 ± 1.23)%, respectively (P <0.05). The results suggest that morphine hypoxic preconditioning can down-regulate the expression of caspase-3 in hypoxia / reoxygenation injury in rabbit kidney, which may play a protective role in hypoxia / reoxygenation injury of kidney.