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目的探讨自噬相关因子LC3、Bnip-3及凋亡相关因子Bcl-2、Bax在实验性糖尿病大鼠脑组织损伤中的作用。方法 30只SD大鼠随机分为糖尿病组和对照组。糖尿病组一次性腹腔注射1%链脲佐菌素(60 mg/kg体质量),对照组一次性腹腔注射柠檬酸缓冲液,饲养12周后活杀大鼠,留取脑组织标本。经HE染色观察其病理学改变,采用免疫组化S-P法检测大鼠脑组织中LC3、Bnip-3、Bcl-2及Bax的表达。结果与对照组大鼠相比,糖尿病大鼠脑组织病理学显示细胞排列紊乱,分布不均,胞体缩小,胞质淡红色,正常形态神经细胞数减少;LC3、Bnip-3及Bax阳性数较对照组明显升高,差异有统计学意义(P<0.05);Bcl-2阳性数较对照组明显降低,差异有统计学意义(P<0.001);LC3与Bnip-3呈弱正相关(P<0.05),与Bcl-2及Bax不相关;Bnip-3与Bax呈正弱相关(P<0.05),与Bcl-2无相关;Bcl-2与Bax无相关。结论糖尿病大鼠脑组织中LC3、Bnip-3及Bax存在过度表达,Bcl-2呈弱表达,表明自噬因子与凋亡因子参与了糖尿病大鼠脑组织损伤的过程,可能是脑组织损伤的机制之一。
Objective To investigate the role of autophagy-related factors (LC3), Bnip-3 and apoptosis-related factors Bcl-2 and Bax in brain injury in experimental diabetic rats. Methods Thirty SD rats were randomly divided into diabetic group and control group. Rats in the diabetic group were given 1% streptozotocin (60 mg / kg body weight) by intraperitoneal injection. Citric acid buffer was intraperitoneally injected into the control group. After 12 weeks of feeding, the rats were killed and the brain tissue samples were collected. The pathological changes were observed by HE staining. The expression of LC3, Bnip-3, Bcl-2 and Bax in rat brain was detected by immunohistochemical S-P method. Results Compared with the control group, the histopathology of diabetic rats showed that the cells arranged in disorder, unevenly distributed, the cell bodies shrinking, the cytoplasm was pink and the number of normal neurons decreased. The positive numbers of LC3, Bnip-3 and Bax (P <0.05). The positive number of Bcl-2 was significantly lower than that of the control group (P <0.001), while the positive rate of LC3 was lower than that of Bnip-3 <0.05), but not with Bcl-2 and Bax. Bnip-3 was positively correlated with Bax (P <0.05), but not with Bcl-2. Bcl-2 had no correlation with Bax. Conclusion The over-expression of LC3, Bnip-3 and Bax in brain tissue of diabetic rats and the low expression of Bcl-2 suggest that autophagy and apoptosis factors are involved in the process of brain injury in diabetic rats, which may be the result of brain injury One of the mechanisms.