Chemopreventive effect of galangin against benzo(a)pyrene-induced stomach tumorigenesis through modulating aryl hydrocarbon receptor in Swiss albino mice

被引:13
作者
Wang, L. [1 ]
Xue, J. [2 ]
Wei, F. [3 ]
Zheng, G. [1 ]
Cheng, M. [4 ]
Liu, S. [5 ]
机构
[1] Xinjiang Med Univ, Dept Gastrointestinal Surg, Affiliated Hosp 5, Urumqi, Xinjiang, Peoples R China
[2] Sun Yat Sen Univ, Affiliated Hosp 5, Dept Blood Transfus, Zhuhai, Guangdong, Peoples R China
[3] Cent Hosp Haining, Dept Gastroenterol, Haining City, Zhejiang, Peoples R China
[4] Tongji Univ, Shanghai Tianyou Hosp, Dept Gen Surg, Shanghai, Peoples R China
[5] Shengli Oilfield Cent Hosp, Dept Gastrointestinal Surg, Dongying 257034, Shandong, Peoples R China
关键词
Galangin; stomach cancer; benzo(a)pyrene; antioxidants; aryl hydrocarbon receptor; POLYCYCLIC AROMATIC-HYDROCARBONS; HEPATOCELLULAR-CARCINOMA; OXIDATIVE STRESS; ADDUCT FORMATION; GASTRIC-CANCER; TISSUES; TRANSFORMATION; PURIFICATION; GLUTATHIONE; ACTIVATION;
D O I
10.1177/0960327121997979
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
The present study was aimed to evaluate the chemopreventive potential of galangin against benzo(a)pyrene (BaP)-induced stomach carcinogenesis in Swiss albino mice. Stomach cancer was induced in experimental mice using BaP oral administration. The mice were treated with galangin (10 mg/kg b.wt.) before and during BaP administration. Oral administration of galangin at a dose of 10 mg/kg b.wt. significantly (p < 0.05) prevented the tumor incidence, tumor volume in the experimental animals. Further, galangin pretreatment prevents BaP-induced lipid peroxidation and restores BaP-mediated loss of cellular antioxidants status. It has also been found that galangin prevents BaP-induced activation of phase I detoxification enzymes. Furthermore, galangin pretreatment prevented the BaP-induced overexpression of cytochrome P450s isoform genes (CYP1A1, CYP1B1), aryl hydrocarbon receptor system (AhR, ARNT), transcriptional activators (CBP/p300, NF-kB), tumor growth factors, proto-oncogenes, invasion markers (TGFB, SRC-1, MYC, iNOS, MMP2, MMP9) and Phase II metabolic isoenzyme genes (GST) in the stomach tissue homogenate when compared to the control groups. The western blot results confirm that galangin (10 mg/kg. b.wt.) treatment significantly prevented the BaP-mediated expression of ArR, ARNT, and CYP1A1 proteins in the mouse stomach tissue. Therefore, the present results confirm that galangin prevents BaP-induced stomach carcinogenesis probably through modulating ArR and ARNT expression in the experimental mice.
引用
收藏
页码:1434 / 1444
页数:11
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