Protective activity of salidroside against ethanol-induced gastric ulcer via the MAPK/NF-κB pathway in vivo and in vitro

被引:164
|
作者
Chang, Xiayun [1 ]
Luo, Fen [1 ]
Jiang, Wenjiao [2 ]
Zhu, Lingpeng [1 ]
Gao, Jin [1 ]
He, He [1 ]
Wei, Tingting [1 ]
Gong, Shilin [2 ]
Yan, Tianhua [1 ]
机构
[1] China Pharmaceut Univ, Dept Physiol & Pharmacol, Nanjing 210009, Jiangsu, Peoples R China
[2] China Pharmaceut Univ, Sch Pharm, Nanjing 210009, Jiangsu, Peoples R China
关键词
Salidroside; Gastric ulcer; Ethanol; Inflammation; MAPKs/NF-kappa B; KINASE C-ZETA; GASTROPROTECTIVE ACTIVITY; SYNTHETIC SALIDROSIDE; OXIDATIVE DAMAGE; MUCOSAL DAMAGE; NITRIC-OXIDE; EXTRACT; INVOLVEMENT; CELL; ACTIVATION;
D O I
10.1016/j.intimp.2015.07.031
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Salidroside (Sal) is a traditional Chinese medicine with various pharmacological effects. The present study aimed to investigate the protective effect of Sal on-ethanol-induced acute gastric ulcer and H2O2-induced gastric epithelial cell damage. 0.2 ml ethanol and 400 mu M H2O2 were applied to establish a gastric ulcer model in vivo and in vitro respectively. The production of interleukin (IL)-6, interleuldn (IL)-1 beta and tumor necrosis factor (TNE)-alpha was analyzed, as well as myeloperoxidase (MPO), malondialdehyde (MDA) and superoxide dismutase (SOD). MIT assay was used to detect cell viability. In addition, MAPK/NF-kappa B signal pathway-related proteins p-ERK, p-JNK, p-p38, p-I kappa B alpha and p-NF-kappa Bp65 were analyzed to determine the underlying protective mechanism. Downstream genes such as cyclooxygenase-2 (COX-2), 5-lipoxygenase (5-LOX) and leukotrienes B-4 (LTB4) were also measured. Obtained data indicated that Sal inhibited the overproduction of pro-inflammatory cytokines and enhanced antioxidant activity. Collectively, it is assumed that Sal could alleviate ethanol-induced acute gastric ulcer and H2O2-induced gastric epithelial cell damage through the MAPK/NF-kappa B pathway. (C) 2015 Elsevier B.V. All rights reserved.
引用
收藏
页码:604 / 615
页数:12
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