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膳食姜黄素可预防急性和慢性臭氧暴露引起的星形胶质细胞增生、小胶质细胞增生和细胞凋亡。

Dietary Curcumin Prevented Astrocytosis, Microgliosis, and Apoptosis Caused by Acute and Chronic Exposure to Ozone.

机构信息

Laboratorio de Neurofisiología, Departamento de Fisiología, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, 44340 Guadalajara, Jalisco, México.

Departamento de Medicina Veterinaria, Centro Universitario de Ciencias Biológicas y Agropecuarias, Universidad de Guadalajara, 45200 Zapopan, Jalisco, México.

出版信息

Molecules. 2019 Aug 5;24(15):2839. doi: 10.3390/molecules24152839.

DOI:10.3390/molecules24152839
PMID:31387223
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6696019/
Abstract

Ozone is the most oxidant tropospheric pollutant gas, causing damage through the formation of reactive oxygen and nitrogen species. Reactive species induce the nuclear factor-kappa B (NF-κB) activation leading to neuroinflammation characterized by astrocytosis, microgliosis, and apoptotic cell death. There is interest in evaluating the pharmacological activity of natural antioxidants to confer neuroprotection against the damage caused by ozone in highly polluted cities. Curcumin has been proven to exert a protective action in the central nervous system (CNS) of diverse experimental models, with no side effects. The aim of this work is to evaluate the effect of curcumin in a preventive and therapeutic manner against the astrocytosis, microgliosis, and apoptosis induced by ozone in rat hippocampus. Fifty Wistar rats were distributed into five experimental groups: The intact control, curcumin fed control, ozone-exposed group, and the preventive and therapeutic groups receiving the curcumin supplementation while exposed to ozone. Ozone caused astrocytosis and microgliosis, as well as apoptosis in the hippocampus. Meanwhile, curcumin was able to decrease the activation of microglia and astrocytes, and apoptotic cell death in both periods of exposure. Therefore, we propose that curcumin could be used as a molecule capable of counteracting the damage caused by ozone in the CNS.

摘要

臭氧是最具氧化性的对流层污染物气体,通过形成活性氧和氮物种而造成损害。活性物质诱导核因子-κB(NF-κB)的激活,导致以星形胶质细胞增生、小胶质细胞增生和细胞凋亡为特征的神经炎症。人们对评估天然抗氧化剂的药理学活性很感兴趣,以提供针对臭氧在高度污染城市中造成的损害的神经保护。姜黄素已被证明在各种实验模型的中枢神经系统(CNS)中发挥保护作用,且没有副作用。本工作旨在以预防和治疗的方式评估姜黄素对臭氧诱导的大鼠海马星形胶质细胞增生、小胶质细胞增生和细胞凋亡的作用。将 50 只 Wistar 大鼠分为五组:完整对照组、姜黄素喂养对照组、臭氧暴露组以及在暴露于臭氧时接受姜黄素补充的预防和治疗组。臭氧导致海马星形胶质细胞增生和小胶质细胞增生,以及细胞凋亡。同时,姜黄素能够减少两种暴露期内小胶质细胞和星形胶质细胞的激活以及细胞凋亡。因此,我们提出姜黄素可以作为一种能够抵抗臭氧在中枢神经系统造成损害的分子。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6d88/6696019/43e50be047b2/molecules-24-02839-g007.jpg
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