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硫化氢可保护C57BL/6小鼠模型免受实验性脑型疟疾的侵害。

Hydrogen sulfide protects against the development of experimental cerebral malaria in a C57BL/6 mouse model.

作者信息

Jiang Ping, Xu Zhishen, Xiao Baiquan, Han Zhong, Huang Jiehong, Xu Jianbang, Lun Zhaorong, Zhou Wenliang

机构信息

School of Life Sciences, Sun Yat‑Sen University, Guangzhou, Guangdong 510275, P.R. China.

出版信息

Mol Med Rep. 2017 Aug;16(2):2045-2050. doi: 10.3892/mmr.2017.6854. Epub 2017 Jun 23.

DOI:10.3892/mmr.2017.6854
PMID:28656241
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5561995/
Abstract

Hydrogen sulfide (H2S) has anti‑inflammatory and neuroprotective properties, particularly during pathological processes. Experimental cerebral malaria (ECM), which is caused by vascular leakage into the brain, is characterized by inflammation, neurological deficits and cerebral hemorrhage. The present study investigated the correlation between ECM genesis and the levels of H2S. The results indicated that the levels of H2S derived from the brain decreased over time following ECM infection, and that the low H2S bioavailability was partially caused by decreased expression of the H2S generating enzyme, cystathionine‑β‑synthase. Administration of NaHS (an exogenous donor of H2S) provided protection against ECM. NaHS inhibited the destruction of the blood brain barrier and the secretion of proinflammatory biomarkers, including interluekin‑18, matrix metalloproteinase‑9 and serum cluster of differentiation 40 into the brain during ECM. In conclusion, these results suggested that low levels of H2S in brain contributed to the progression of ECM, and that H2S donor administration may represent a potential protective therapy against ECM.

摘要

硫化氢(H₂S)具有抗炎和神经保护特性,尤其是在病理过程中。实验性脑型疟疾(ECM)由血管渗漏入脑引起,其特征为炎症、神经功能缺损和脑出血。本研究调查了ECM发生与H₂S水平之间的相关性。结果表明,ECM感染后,脑源性H₂S水平随时间下降,且低H₂S生物利用度部分是由H₂S生成酶胱硫醚-β-合酶表达降低所致。给予NaHS(一种外源性H₂S供体)可预防ECM。NaHS可抑制ECM期间血脑屏障的破坏以及促炎生物标志物(包括白细胞介素-18、基质金属蛋白酶-9和血清分化簇40)向脑内的分泌。总之,这些结果表明脑内低水平H₂S促成了ECM的进展,给予H₂S供体可能是一种针对ECM的潜在保护性治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4083/5561995/338627bc9397/MMR-16-02-2045-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4083/5561995/eb625f349ce3/MMR-16-02-2045-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4083/5561995/79b80218f485/MMR-16-02-2045-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4083/5561995/02320930149e/MMR-16-02-2045-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4083/5561995/2a814efdb8c8/MMR-16-02-2045-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4083/5561995/338627bc9397/MMR-16-02-2045-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4083/5561995/eb625f349ce3/MMR-16-02-2045-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4083/5561995/79b80218f485/MMR-16-02-2045-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4083/5561995/02320930149e/MMR-16-02-2045-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4083/5561995/2a814efdb8c8/MMR-16-02-2045-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4083/5561995/338627bc9397/MMR-16-02-2045-g04.jpg

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