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神经球蛋白通过 PI3K/Akt/Bax 依赖性机制保护大鼠免受脓毒症相关性脑病的影响。

Neuroglobin Protects Rats from Sepsis-Associated Encephalopathy via a PI3K/Akt/Bax-Dependent Mechanism.

机构信息

Department of Critical Care Medicine, Xiangya Hospital, Central South University, Changsha, 410008, China.

出版信息

J Mol Neurosci. 2017 Sep;63(1):1-8. doi: 10.1007/s12031-017-0933-x. Epub 2017 Jun 10.

Abstract

Sepsis-associated encephalopathy (SAE) is a common complication of sepsis, and has no generally accepted treatment due to its complicated pathophysiology. Previously, we demonstrated the protective role of neuroglobin (Ngb) in SAE rats, but the exact mechanism has not been determined. To investigate the potential neuroprotective roles and mechanisms of Ngb, Sprague-Dawley rats were used. Overexpression of Ngb via intracerebroventricular injection with Ngb plasmids attenuated brain damage assessed by hematoxylin and eosin (HE) staining and neurological dysfunction assessed by Morris water maze test. Western blot analysis also showed that the phosphorylation of Akt increased and the protein level of Bax decreased. Furthermore, the protective effect can be abolished by PI3K/Akt pathway inhibitor LY294002. Our results demonstrate that Ngb can protect rats from SAE via a PI3K/Akt/Bax-dependent mechanism.

摘要

脓毒症相关性脑病(SAE)是脓毒症的常见并发症,由于其复杂的病理生理学,目前尚无被普遍接受的治疗方法。先前,我们在 SAE 大鼠中证明了神经球蛋白(Ngb)的保护作用,但确切的机制尚未确定。为了研究 Ngb 的潜在神经保护作用和机制,我们使用了 Sprague-Dawley 大鼠。通过脑室内注射 Ngb 质粒过表达 Ngb,通过苏木精和伊红(HE)染色评估脑损伤和 Morris 水迷宫试验评估神经功能障碍,结果显示损伤减轻,神经功能障碍改善。Western blot 分析还表明,Akt 的磷酸化增加,Bax 的蛋白水平降低。此外,PI3K/Akt 通路抑制剂 LY294002 可以消除这种保护作用。我们的研究结果表明,Ngb 可以通过 PI3K/Akt/Bax 依赖性机制来保护大鼠免受 SAE 的侵害。

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