2,3,5,4'-Tetrahydroxystilbene-2-O-β-D-glycoside attenuates the apoptotic responses of hypoxia/reoxygenation injury in bronchial epithelial cells through MAPK, HIF-1α and p53 pathway
10.16438/j.0513-4870.2017-0443
- VernacularTitle:二苯乙烯苷通过MAPK、HIF-1α和p53通路减轻缺氧/复氧损伤诱导的支气管上皮细胞凋亡
- Author:
Pu-qiao LIAN
1
;
Yan-nan FAN
1
;
Hui YANG
1
;
Li-xia FU
1
;
Yun-xiao LI
2
;
Qi HOU
1
Author Information
1. State Key Laboratory of Natural Products and Functions, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China
2. Beijing Friendship Hospital, Capital Medical University, Beijing 100050, China
- Publication Type:ORIGINAL ARTICLES
- Keywords:
2,3,5,4'-tetrahydroxystilbene-2-O-β-D-glycoside;
hypoxia/reoxygenation;
BEAS-2B cell;
apoptosis;
mitogen-activated protein kinase;
hypoxia inducible factor-1α;
p53
- From:
Acta Pharmaceutica Sinica
2017;52(7):1122-1132
- CountryChina
- Language:Chinese
-
Abstract:
This study was designed to investigate the effect of 2,3,5,4'-tetrahydroxystilbene-2-O-β-D-glycoside(TSG)on hypoxia/reoxygenation(H/R)-induced oxidative stress injury and its potential mechanism in human bronchial epithelial cell(BEAS-2B)cells. BEAS-2B cells were exposed to H/R treatment. Level of intracellular ROS was detected using DCFH-DA probe and fluorescence microplate reader. Production of MDA and activity of SOD were evaluated with MDA and SOD kits. Nucleus was shaped by DAPI staining. Translocation of Bax to mitochondria was observed in MCF-7/GFP-Bax cells. Change in mitochondrial membrane potential was detected by JC-1 staining. Release of cytochrome C from mitochondria was detected by immunofluorescence. Expressions of mitochondrial/cytoplasmic Bax and cytochrome C, caspase-9, caspase-3, phosphorylated MAPK, HIF-1α and phosphorylated p53(p-p53)were determined by Western blotting. TSG significantly improved cell viability and reduced H/R-induced ROS production in BEAS-2B cells, while significantly decreased MDA production. It inhibited Bax translocation and nucleus fracture, reversed the decrease in mitochondrial membrane potential and inhibited the release of cytochrome C and following activation of caspase-9/caspase-3. Simultaneously, TSG down-regulated the signals of SAPK JNK1/2 and p38 MAPK without an impact in ERK1/2. It attenuated expression of HIF-1α and phosphorylation of p53. This study suggests that TSG could protect BEAS-2B against H/R-induced apoptosis, perhaps through the MAPK, HIF-1α and p53 pathways.
