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鹿茸多肽通过Nrf-2/HO-1/NF-κB通路对脑缺血/再灌注(I/R)损伤的保护作用。

Protective effect of pilose antler peptide on cerebral ischemia/reperfusion (I/R) injury through Nrf-2/OH-1/NF-κB pathway.

作者信息

Bai Luning, Shi Wei, Liu Jiping, Zhao Xiaoping, Zhang Yi, Zhou Zhengguo, Hou Wen, Chang Tao

机构信息

Medical College of Xi'an Jiao Tong University Xi'an 71000, PR China; Affiliated hospital of Shaanxi University of Chinese Medicine, Xianyang, 712046, PR China.

Medical College of Xi'an Jiao Tong University Xi'an 71000, PR China.

出版信息

Int J Biol Macromol. 2017 Sep;102:741-748. doi: 10.1016/j.ijbiomac.2017.04.091. Epub 2017 Apr 25.

Abstract

The purpose of the current study was to detect the effect of pilose antler peptide (PAP) on cerebral ischemia and explore its potential mechanism. Middle cerebral artery occlusion (MCAO) was performed to investigate the effects of PAP on cerebral ischemia. The rats were randomly divided into five groups: sham group, model(I/R) group, I/R+Clopidogrel group, I/R+PAP (50mg/kg) group, I/R+PAP (100mg/kg) group. The results showed that PAP significantly reduced brain infarct size, inhibited cerebral edema, decreased th eneurological deficits. Treatment with PA reduced the contents of malondialdehyde(MDA) and restore the activity of superoxide dismutase(SOD) in serum and brains. Lig also could effectively decrease the levels of interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in serum and brain tissues of the MCAO rats. Western blot results demonstrated that PAP up-regulated the expressions of Nrf-2 and HO-1, also blocked the phosphorylations of IκB kinases(IKK)α, IKKβ, inhibitor of NF-κB(IκB)α, nuclear factor kappa B(NF-κB) p65 in I/R-induced brains. Our findings suggested that PAP effectively attenuated the I/R-induced cerebral ischemia through Nrf-2/HO-1/NF-κB pathway.

摘要

本研究旨在检测鹿茸多肽(PAP)对脑缺血的影响并探讨其潜在机制。采用大脑中动脉闭塞(MCAO)法研究PAP对脑缺血的影响。将大鼠随机分为五组:假手术组、模型(I/R)组、I/R+氯吡格雷组、I/R+PAP(50mg/kg)组、I/R+PAP(100mg/kg)组。结果显示,PAP显著减小脑梗死体积,抑制脑水肿,减轻神经功能缺损。PAP治疗降低了血清和脑组织中丙二醛(MDA)含量,恢复了超氧化物歧化酶(SOD)活性。PAP还可有效降低MCAO大鼠血清和脑组织中白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)水平。蛋白质印迹结果表明,PAP上调Nrf-2和HO-1的表达,还阻断I/R诱导脑内IκB激酶(IKK)α、IKKβ、核因子κB抑制蛋白(IκB)α、核因子κB(NF-κB)p65的磷酸化。我们的研究结果提示,PAP通过Nrf-2/HO-1/NF-κB通路有效减轻I/R诱导的脑缺血。

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