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从紫苏变种尖紫苏中分离得到的多糖对HO诱导的HT22海马细胞氧化应激的神经保护作用。

Neuroprotective effect of polysaccharide separated from Perilla frutescens Britton var. acuta Kudo against HO-induced oxidative stress in HT22 hippocampus cells.

作者信息

Byun Eui-Baek, Cho Eun-Ji, Kim Yi-Eun, Kim Woo Sik, Byun Eui-Hong

机构信息

a Advanced Radiation Technology Institute , Korea Atomic Energy Research Institute , Jeongeup , Korea.

b Department of Food Science and Technology , Kongju National University , Yesan , Republic of Korea.

出版信息

Biosci Biotechnol Biochem. 2018 Aug;82(8):1344-1358. doi: 10.1080/09168451.2018.1460572. Epub 2018 Apr 8.

Abstract

This study was carried out to evaluate the neuroprotective activity of polysaccharide extracts isolated from Perilla frutescens (PEPF) in HO-treated HT22 hippocampus cells. The PEPF treatment was found to increase the anti-oxidant activities of HT22 hippocampus cells. PEPF treatment resulted in a significant protection of HT22 hippocampus cells against HO-induced neurotoxicity, this protection ultimately occurred through an inhibition of ROS-mediated intracellular Ca levels leading to MAPKs and NF-κB, as well as the accumulation of PI3K/AKT and Nrf2-mediated HO-1/NQO1 pathways. Furthermore, PEPF not only decreased the expression of Bax, cytochrome c, and cleaved caspases-3, -8, and -9, but also increased the expression of PARP and Bcl-2 in the HO-treated HT22 hippocampus cells, which overall contributed to the neuroprotective action. PEPF retains its mitochondrial membrane potential and reduces the elevated levels of sub-G1 phase and apoptotic morphological features induced by HO. It also reduces the malondialdehyde levels and enhances the intracellular SOD activity.

摘要

本研究旨在评估从紫苏中分离得到的多糖提取物(PEPF)对过氧化氢(HO)处理的HT22海马细胞的神经保护活性。研究发现,PEPF处理可提高HT22海马细胞的抗氧化活性。PEPF处理能显著保护HT22海马细胞免受HO诱导的神经毒性,这种保护最终是通过抑制ROS介导的细胞内钙水平,从而影响丝裂原活化蛋白激酶(MAPKs)和核因子κB(NF-κB),以及磷脂酰肌醇-3激酶/蛋白激酶B(PI3K/AKT)和核因子E2相关因子2(Nrf2)介导的血红素加氧酶-1(HO-1)/醌氧化还原酶1(NQO1)信号通路的积累来实现的。此外,PEPF不仅降低了HO处理的HT22海马细胞中Bax、细胞色素c以及裂解的半胱天冬酶-3、-8和-9的表达,还增加了聚(ADP-核糖)聚合酶(PARP)和Bcl-2的表达,这些总体上促成了神经保护作用。PEPF维持其线粒体膜电位,并减少HO诱导的亚G1期水平升高和凋亡形态特征。它还降低了丙二醛水平并增强了细胞内超氧化物歧化酶(SOD)活性。

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