YANG Yang, LIU Lan, WANG Wen-hua, et al. Protective Effect of Shenxiong Glucose Injection on HO-induced Oxidative Damage of HUVEC Cells[J]. Chinese journal of experimental traditional medical formulae, 2017, 23(1): 163-168.
YANG Yang, LIU Lan, WANG Wen-hua, et al. Protective Effect of Shenxiong Glucose Injection on HO-induced Oxidative Damage of HUVEC Cells[J]. Chinese journal of experimental traditional medical formulae, 2017, 23(1): 163-168. DOI: 10.13422/j.cnki.syfjx.2017010163.
Objective: To investigate the protective effect and mechanism of Shenxiong Glucose injection (SGI) on H2O2-induced oxidative damage of HUVEC cells. Method: The in vitro models of oxidative stress damage based on HUVEC cells were established by treatment with H2O2(130 mmol·L-1) for 0.5 h. SGI pretreated group:HUVEC cells were pretreated with SGI (6%
8%
10%) for 6 h
and then treated with H2O2 for 0.5 h. The cell viability was detected by MTS assay; ELISA method was used to determine lactate dehydrogenase(LDH) release
malondialdehyde(MDA) content as well as superoxide dismutase(SOD)
catalase(CAT)
glutathione peroxidase(GSH-Px) activities; gene and protein expression levels of Bcl-2
Bax and Caspase-3 in HUVEC cells were detected by Real-time PCR and Western blot. Result: After HUVEC cells were treated with H2O2(130 mmol·L-1) for 0.5 h
the survival rate of the cells decreased to about 50%with a proper range and good repeatability
so that oxidative damage models were established under this condition. As compared with the H2O2 group
the cells survival was significantly increased (P < 0.05
P < 0.01) after treatment with SGI for 6 h. SGI not only decreased the release of LDH
MDA (P < 0.05
P < 0.01)
but also significantly increased the activities of SOD
GSH-Px
and CAT (P < 0.05
P < 0.01). In addition
Real-time PCR and Western blot showed SGI can significantly up-regulate the expression level of Bcl-2 (P < 0.05
P < 0.01) and down-regulate the expression level of Caspase-3
Bax (P < 0.05
P < 0.01). Conclusions: SGI could protect the HUVEC cells against H2O2-induced oxidative damage in a certain range. The mechanism of action seemed to be relevant with inhibiting apoptosis.