SAM, a cystathionine beta-synthase activator, promotes hydrogen sulfide to promote neural repair resulting from massive cerebral infarction induced by middle cerebral artery occlusion

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成果类型：

期刊论文

作者：

Wang, Fang;Zhou, Hao;Zhang, Xiaoxia

通讯作者：

Zhang, XX

作者机构：

[Zhang, Xiaoxia; Wang, Fang; Zhang, XX] Changsha Social Work Coll, Dept Med, 22 Xiangzhang Rd, Changsha 410004, Hunan, Peoples R China.

[Zhou, Hao] Hunan Univ Chinese Med, Affiliated Hosp 2, Dept Urol, Changsha 410001, Hunan, Peoples R China.

通讯机构：

[Zhang, XX ] C

Changsha Social Work Coll, Dept Med, 22 Xiangzhang Rd, Changsha 410004, Hunan, Peoples R China.

语种：

英文

关键词：

*ERK/MAPK signaling pathway;*Hydrogen sulfide;*Massive cerebral infarct;*NMDAR;*Sympathetic hyperactivity

期刊：

Metabolic Brain Disease

ISSN：

0885-7490

年：

2022

卷：

期：

页码：

1641-1654

DOI：

10.1007/s11011-022-00976-9

机构署名：

本校为其他机构

院系归属：

第二中医临床医学院

摘要：

Neurologic deterioration after massive cerebral infarct should be identified at an early stage for medical and surgical treatments. We investigated the effect of hydrogen sulfide on the excitotoxity of PC12 cells exposed to oxygen–glucose deprivation (OGD) and its effect on the apoptosis of brain tissues in rats with middle cerebral artery occlusion (MCAO). Rats with MCAO were treated with SAM, a cystathionine beta-synthase (CBS) activator, or AOAA, a CBS inhibitor. Hydrogen sulfide content in the brain tissues of infarcted patients or rats wi...

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SAM, a cystathionine beta-synthase activator, promotes hydrogen sulfide to promote neural repair resulting from massive cerebral infarction induced by middle cerebral artery occlusion

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