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C1q/CTRP1 exerts neuroprotective effects in TBI rats by regulating inflammation and autophagy
bioRxiv - Pathology Pub Date : 2020-12-29 , DOI: 10.1101/2020.12.29.424653
Ming Pei , Chaoqun Wang , Zhengdong Li , Jianhua Zhang , Ping Huang , Jiawen Wang , Jiang Huang , Donghua Zou , Yijiu Chen

Objective: C1q/CTRP1 is a newly discovered adiponectin protein, which is highly expressed in adipose and heart tissues. Recent studies have revealed that C1q/CTRP1 can regulate metabolism and inhibit inflammation. CTRP1 is also expressed in brain tissues and vascular cells of human and rat, and research on cerebral hemorrhage and cerebral ischemia-reperfusion injury demonstrates that the CTRP family can attenuate secondary brain injury and exert neuroprotective effects. Thus, this study was designed to explore the role of CTRP1 in traumatic brain injury (TBI) and the underlying mechanism. Main methods: Rats were assigned into rCTRP1 group, vehicle group, and sham group. Modified Feeney’s method was used to establish a closed traumatic brain injury model. Morris water maze was used for directional navigation, reverse searching and space exploration tests in rats. In addition, Golgi-Cox staining was utilized to visualize neurons, dendrites and dendritic spines. ELISA was conducted to detect the levels of inflammatory factors (IL-6 and TNF-α). Finally, Western blot was adopted to detect the relative expression of p -mTOR and autophagy-related proteins (Beclin-1 and LC3-II). Results: CTRP1 improved the behavioral and histopathological outcomes, inhibited the inflammatory response, activated mTOR and decreased autophagy-associated protein synthesis in TBI rats. Conclusion: CTRP1 exerts neuroprotective effects in TBI rats by regulating inflammation and autophagy and has potential therapeutic properties after TBI.

中文翻译:

C1q / CTRP1通过调节炎症和自噬作用在TBI大鼠中发挥神经保护作用

目的:C1q / CTRP1是一种新发现的脂联素蛋白,在脂肪和心脏组织中高表达。最近的研究表明,C1q / CTRP1可以调节新陈代谢并抑制炎症。CTRP1还在人和大鼠的脑组织和血管细胞中表达,对脑出血和脑缺血-再灌注损伤的研究表明,CTRP家族可以减轻继发性脑损伤并发挥神经保护作用。因此,本研究旨在探讨CTRP1在脑外伤(TBI)中的作用及其潜在机制。主要方法:将大鼠分为rCTRP1组,媒介物组和假组。改良的Feeney方法用于建立闭合性脑外伤模型。莫里斯水迷宫被用于定向导航,大鼠的反向搜索和太空探索测试。此外,高尔基-柯克斯染色被用来可视化神经元,树突和树突棘。进行ELISA以检测炎性因子(IL-6和TNF-α)的水平。最后,采用蛋白质印迹法检测p -mTOR和自噬相关蛋白(Beclin-1和LC3-II)的相对表达。结果:CTRP1改善了TBI大鼠的行为和组织病理学结果,抑制了炎症反应,激活了mTOR,并减少了自噬相关蛋白的合成。结论:CTRP1通过调节炎症和自噬作用,对TBI大鼠具有神经保护作用,在TBI后具有潜在的治疗作用。进行ELISA以检测炎性因子(IL-6和TNF-α)的水平。最后,采用蛋白质印迹法检测p -mTOR和自噬相关蛋白(Beclin-1和LC3-II)的相对表达。结果:CTRP1改善了TBI大鼠的行为和组织病理学结果,抑制了炎症反应,激活了mTOR,并减少了自噬相关蛋白的合成。结论:CTRP1通过调节炎症和自噬作用,对TBI大鼠具有神经保护作用,在TBI后具有潜在的治疗作用。进行ELISA以检测炎性因子(IL-6和TNF-α)的水平。最后,采用蛋白质印迹法检测p -mTOR和自噬相关蛋白(Beclin-1和LC3-II)的相对表达。结果:CTRP1改善了TBI大鼠的行为和组织病理学结果,抑制了炎症反应,激活了mTOR,并减少了自噬相关蛋白的合成。结论:CTRP1通过调节炎症和自噬作用,对TBI大鼠具有神经保护作用,在TBI后具有潜在的治疗作用。激活TTOR大鼠体内的mTOR并降低自噬相关蛋白的合成。结论:CTRP1通过调节炎症和自噬作用,对TBI大鼠具有神经保护作用,在TBI后具有潜在的治疗作用。激活TTOR大鼠体内的mTOR并减少自噬相关蛋白的合成。结论:CTRP1通过调节炎症和自噬作用,对TBI大鼠具有神经保护作用,在TBI后具有潜在的治疗作用。
更新日期:2020-12-30
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