Astragaloside IV suppresses post-ischemic natural killer cell infiltration and activation in the brain: involvement of histone deacetylase inhibition.
10.1007/s11684-020-0783-8
- Author:
Baokai DOU
1
;
Shichun LI
1
;
Luyao WEI
1
;
Lixin WANG
1
;
Shiguo ZHU
1
;
Zhengtao WANG
2
;
Zunji KE
3
;
Kaixian CHEN
4
;
Zhifei WANG
5
Author Information
1. School of Basic Medical Sciences, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China.
2. Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China.
3. Academy of Integrative Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China.
4. Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China. kxchen@simm.ac.cn.
5. School of Basic Medical Sciences, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China. zfwang@shutcm.edu.cn.
- Publication Type:Journal Article
- Keywords:
astragaloside IV;
brain ischemia;
histone deacetylase;
natural killer cells;
nuclear factor-κB
- MeSH:
Animals;
Brain;
Histone Deacetylases;
Killer Cells, Natural;
Rats;
Saponins/pharmacology*;
Triterpenes/pharmacology*
- From:
Frontiers of Medicine
2021;15(1):79-90
- CountryChina
- Language:English
-
Abstract:
Natural killer (NK) cells, a type of cytotoxic lymphocytes, can infiltrate into ischemic brain and exacerbate neuronal cell death. Astragaloside IV (ASIV) is the major bioactive ingredient of Astragalus membranaceus, a Chinese herbal medicine, and possesses potent immunomodulatory and neuroprotective properties. This study investigated the effects of ASIV on post-ischemic brain infiltration and activation of NK cells. ASIV reduced brain infarction and alleviated functional deficits in MCAO rats, and these beneficial effects persisted for at least 7 days. Abundant NK cells infiltrated into the ischemic hemisphere on day 1 after brain ischemia, and this infiltration was suppressed by ASIV. Strikingly, ASIV reversed NK cell deficiency in the spleen and blood after brain ischemia. ASIV inhibited astrocyte-derived CCL2 upregulation and reduced CCR2
