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Eriodictyol attenuates MCAO-induced brain injury and neurological deficits via reversing the autophagy dysfunction
Frontiers in Systems Neuroscience ( IF 3.1 ) Pub Date : 2021-04-19 , DOI: 10.3389/fnsys.2021.655125
Chuanxiang Wang , Zhequan Ma , Zuqiang Wang , Shuping Ming , Yanbing Ding , Sufang Zhou , Hongyu Qian

The present study was designed to investigate the protective effect of eriodictyol on MCAO-induced brain injury and its regulation of neural function and to explore the mechanism of its regulation of autophagy in rats. Brain injury was induced by middle cerebral artery occlusion (MCAO) in adult rats and pretreated with eriodictyol (low dose: 20 mg/kg; medium dose: 40 mg/kg; high dose: 80 mg/kg) or saline. Rats in the treatment group had a smaller volume of infarction and improved neurological outcome and reduced the latency to the platform, increased the time spent in the correct quadrant compared to MCAO rats pretreated with saline. ELISA kits results confirmed that eriodictyol reduced the inflammatory response induced by MCAO. The results of apoptosis and proliferation by Nissl staining and immunofluorescence detection indicated that eriodictyol could inhibit apoptosis and promote the proliferation in MCAO rats. The expressions of LC3, ATG5, p62, and Beclin1 were used to evaluate the autophagy, as well as the reversal of the autophagy activator (rapamycin) on the neuroprotective effect of eriodictyol, which suggested the protective effect of eriodictyol on brain injury may be related to the inhibition of autophagy. In summary, we, therefore, suggested that eriodictyol could reduce the inflammation response of brain injury and inhibit neuroapoptosis, directly affecting autophagy to alleviate brain injury. It will provide theoretical support for eriodictyol in the treatment of ischemic stroke. Keywords: Eriodictyol; Autophagy; Middle cerebral artery occlusion (MCAO); Inflammation; Apoptosis

中文翻译:

雌三醇通过逆转自噬功能障碍减轻MCAO诱导的脑损伤和神经功能缺损

本研究旨在探讨去氧雌烟醇对MCAO诱导的脑损伤的保护作用及其对神经功能的调节作用,并探讨其对大鼠自噬的调节作用。成年大鼠的大脑中动脉闭塞(MCAO)诱发了脑损伤,并用去氧雌二醇(低剂量:20 mg / kg;中剂量:40 mg / kg;高剂量:80 mg / kg)或生理盐水预处理。与用盐水预处理的MCAO大鼠相比,治疗组的大鼠梗死面积较小,神经系统结局改善,平台等待时间减少,在正确象限中花费的时间增加。ELISA试剂盒结果证实,雌三醇减少了MCAO诱导的炎症反应。Nissl染色和免疫荧光检测的结果表明,雌三醇可以抑制MCAO大鼠的细胞凋亡并促进其增殖。使用LC3,ATG5,p62和Beclin1的表达来评估自噬以及自噬激活剂(雷帕霉素)逆转对eriodictyol的神经保护作用,这表明eriodictyol对脑损伤的保护作用可能是相关的。抑制自噬。综上所述,因此,我们提出,二十碳三烯醇可以减轻脑损伤的炎症反应并抑制神经细胞凋亡,直接影响自噬以减轻脑损伤。它将为eriodictyol治疗缺血性中风提供理论支持。关键字:雌三醇;自噬 脑中动脉闭塞(MCAO);炎; 细胞凋亡
更新日期:2021-04-19
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