Effect of Longxuetongluo capsule in protecting vascular endothelial cells against oxygen-glucose deprivation/reoxygenation-induced apoptosis.
10.19540/j.cnki.cjcmm.20180129.002
- Author:
Bo PAN
1
;
Zhen WU
1
;
Xiao-Pan GU
1
;
Zi-Yu LIU
1
;
Yun-Fang ZHAO
1
;
Wen-Zhe HUANG
2
;
Peng-Fei TU
1
;
Wei XIAO
2
;
Jiao ZHENG
1
;
Jun LI
1
Author Information
1. Modern Research Center for Traditional Chinese Medicine, School of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing 100029, China.
2. Jiangsu Kanion Pharmaceutical Co., Ltd., Lianyungang 222001, China.
- Publication Type:Journal Article
- Keywords:
Longxuetongluo capsule;
cell apoptosis;
oxygen-glucose deprivation/reoxygenation injury
- From:
China Journal of Chinese Materia Medica
2018;43(10):2118-2122
- CountryChina
- Language:Chinese
-
Abstract:
Focal cerebral ischemia reperfusion is an essential process during ischemic stroke. The apoptosis of vascular endothelial cells induced by ischemia/reperfusion (I/R) injury is an important cause for brain injury after focal cerebral ischemia. Longxuetongluo capsule (LTC) has been used for the treatment of ischemic stroke in clinic. However, its underlying action mechanism is still unclear. This study aimed to verify the protective effect and mechanisms of LTC on HUVEC cells against oxygen-glucose deprivation/reoxygenation (OGD/R) injury through MTT, LDH, flow cytometry, AO/EB staining and western blot assays. As a result, OGD/R significantly decreased the viability of HUVEC cells, which was significantly improved by LTC. LDH release assay showed that OGD/R significantly increased the lactate dehydrogenase (LDH) release, and LTC dramatically reduced the OGD/R-induced LDH release. Further mechanism study indicated that LTC dose-dependently inhibited the cleavage of PARP, caspase 3, and caspase 9 induced by OGD/R, suggesting that LTC could inhibit the activation of caspase 3/9 apoptosis pathway in the OGD/R-induced apoptosis of HUVEC cells. In conclusion, LTC could protect HUVEC cells against OGD/R injury by inhibiting the activation of mitochondria-related caspase 3/9 apoptosis pathway.
