The Protective Effect of Quercetin-3-O-β -D-Glucuronopyranoside on Ethanol-induced Damage in Cultured Feline Esophageal Epithelial Cells

被引:7
作者
Cho, Jung Hyun [1 ]
Park, Sun Young [1 ]
Lee, Ho Sung [1 ]
Whang, Wan Kyunn [2 ]
Sohn, Uy Dong [1 ]
机构
[1] Chung Ang Univ, Coll Pharm, Dept Pharmacol, Seoul 156756, South Korea
[2] Chung Ang Univ, Coll Pharm, Dept Pharmacognosy, Seoul 156756, South Korea
关键词
Flavonoid; Hydrogen peroxide; ERK; Esophageal epithelial cell; Ethanol; OXYGEN SPECIES PRODUCTION; ACTIVATED PROTEIN-KINASE; ALCOHOL-RELATED DISEASES; REACTIVE OXYGEN; HEME OXYGENASE-1; MAP KINASE; OXIDATIVE STRESS; INDUCED CYTOTOXICITY; ANTIOXIDANT ACTIVITY; CYTOKINE PRODUCTION;
D O I
10.4196/kjpp.2011.15.6.319
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Quercetin-3-O-beta -D-glucuronopyranoside (QGC) is a flavonoid glucoside extracted from Rumex Aquaticus Herba. We aimed to explore its protective effect against ethanol-induced cell damage and the mechanism involved in the effect in feline esophageal epithelial cells (EEC). Cell viability was tested and 2',7'-dichlorofluorescin diacetate assay was used to detect intracellular H2O2 production. Western blotting analysis was performed to investigate MAPK activation and interleukin 6 (IL-6) expression. Exposure of cells to 10% ethanol time-dependently decreased cell viability. Notably, exposure to ethanol for 30 min decreased cell viability to 43.4%. When cells were incubated with 50 mu M QGC for 12 h prior to and during ethanol treatment, cell viability was increased to 65%. QGC also inhibited the H2O2 production and activation of ERK 1/2 induced by ethanol. Pretreatment of cells with the NADPH oxidase inhibitor, diphenylene iodonium, also inhibited the ethanol-induced ERK 1/2 activation. Treatment of cells with ethanol for 30 or 60 min in the absence or presence of QGC exhibited no changes in the IL-6 expression or release compared to control. Taken together, the data indicate that the cytoprotective effect of QGC against ethanol-induced cell damage may involve inhibition of ROS generation and downstream activation of the ERK 1/2 in feline EEC.
引用
收藏
页码:319 / 326
页数:8
相关论文
共 71 条
[1]   Role of mitochondria in alcoholic liver injury [J].
Adachi, M ;
Ishii, H .
FREE RADICAL BIOLOGY AND MEDICINE, 2002, 32 (06) :487-491
[2]   MAP kinase signaling in diverse effects of ethanol [J].
Aroor, AR ;
Shukla, SD .
LIFE SCIENCES, 2004, 74 (19) :2339-2364
[3]  
Aviram M, 2000, FREE RADICAL RES, V33, pS85
[4]   EFFECTS OF ACUTE AND CHRONIC ETHANOL EXPOSURE ON INTESTINAL MICROVILLUS MEMBRANE LIPID-COMPOSITION AND FLUIDITY [J].
BJORKMAN, DJ ;
JESSOP, LD .
ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH, 1994, 18 (03) :560-565
[5]  
Borska Sylwia, 2004, Folia Morphol (Warsz), V63, P103
[6]   Proinflammatory cytokines alter/reduce esophageal circular muscle contraction in experimental cat esophagitis [J].
Cao, WB ;
Cheng, L ;
Behar, J ;
Fiocchi, C ;
Biancani, P ;
Harnett, KM .
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, 2004, 287 (06) :G1131-G1139
[7]   Mammalian MAP kinase signalling cascades [J].
Chang, LF ;
Karin, M .
NATURE, 2001, 410 (6824) :37-40
[8]   Protective effects of estradiol on ethanol-induced bone loss involve inhibition of reactive oxygen species generation in osteoblasts and downstream activation of the extracellular signal-regulated kinase/signal transducer and activator of transcription 3/receptor activator of nuclear factor-κB ligand signaling cascade [J].
Chen, Jin-Ran ;
Shankar, Kartik ;
Nagarajan, Shanmugam ;
Badger, Thomas M. ;
Ronis, Martin J. J. .
JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS, 2008, 324 (01) :50-59
[9]   Effects of ethanol on mitogen-activated protein kinase and stress-activated protein kinase cascades in normal and regenerating liver [J].
Chen, JP ;
Ishac, EJN ;
Dent, P ;
Kunos, G ;
Gao, B .
BIOCHEMICAL JOURNAL, 1998, 334 :669-676
[10]   Platelet-activating factor and prostaglandin E2 impair esophageal ACh release in experimental esophagitis [J].
Cheng, L ;
Cao, WB ;
Fiocchi, C ;
Behar, J ;
Biancani, P ;
Harnett, KM .
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, 2005, 289 (03) :G418-G428