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目的观察Apelin-13对小鼠脑外伤(Traumatic brain injury,TBI)自噬相关蛋白的影响,并初步探讨其对小鼠脑外伤后自噬相关蛋白调节的作用机制。方法取健康雄性CD-1小鼠,随机分为假手术(sham)组、生理盐水(saline)组、Apelin-13组。Apelin-13组和saline组在建立脑外伤模型前10min,分别注射Apelin-13(0.3μg/g)或等量生理盐水于侧脑室,然后利用Western-Blot检测脑外伤后24h、48h组大脑皮质自噬相关蛋白LC3、P62、Beclin-1和Bcl-2等的表达情况。结果与sham组相比,在脑外伤后24h、48h,saline组自噬相关蛋白LC3-Ⅱ/LC3-Ⅰ比值,Beclin-1的蛋白表达均被显著上调(P<0.01);同时Bcl-2、P62的蛋白表达水平被显著下调。然而,与saline组相比,Apelin-13组可显著下调自噬相关蛋白LC3-Ⅱ/LC3-Ⅰ比值和Beclin-1的蛋白表达水平(P<0.01);同时显著上调Bcl-2和P62的表达水平;亦明显降低Beclin-1/Bcl-2的比值。结论 Apelin-13可以明显抑制脑外伤后小鼠大脑皮质细胞的自噬活性,这一作用可能是通过调节Beclin-1、Bcl-2蛋白表达水平来实现的。
Objective To investigate the effect of Apelin-13 on the autophagy-related protein in mice with traumatic brain injury (TBI) and to explore its mechanism of autophagy-related protein regulation after traumatic brain injury in mice. Methods Healthy male CD-1 mice were randomly divided into sham group, saline group and Apelin-13 group. Apelin-13 group and saline group were injected with Apelin-13 (0.3μg / g) or normal saline into the lateral ventricle 10 min before the brain trauma model was established, and then the brain cortex was detected by Western-Blot The expression of autophagy-related proteins LC3, P62, Beclin-1, Bcl-2 and so on. Results Compared with sham group, the protein expression of LC3-Ⅱ / LC3-Ⅰ and Beclin-1 were significantly up-regulated in saline group (P <0.01) at 24h and 48h after traumatic brain injury, , P62 protein expression levels were significantly down-regulated. However, compared with the saline group, the Apelin-13 group significantly downregulated the expression of LC3-Ⅱ / LC3-Ⅰ and Beclin-1 (P <0.01), and significantly up-regulated the expressions of Bcl-2 and P62 The expression of Beclin-1 / Bcl-2 also significantly decreased. Conclusion Apelin-13 can significantly inhibit the autophagic activity of mouse cerebral cortex cells after traumatic brain injury, and this effect may be through the regulation of Beclin-1, Bcl-2 protein expression levels.