S-Allylcysteine as an Inhibitor of Benzo(a)pyrene-Induced Precancerous Carcinogenesis in Human Lung Cells via Inhibiting Activation of Nuclear Factor-Kappa B

被引:1
作者
Wang, Kaiming [1 ,2 ,3 ]
Qi, Qiuchen [4 ]
Zhang, Fang [3 ]
Zhang, Yongchun [3 ,5 ]
Yang, Min [6 ]
Zhao, Zhongxi [3 ]
机构
[1] Univ Jinan, Sch Biol Sci & Technol, 336 West Rd Nan Xinzhuang, Jinan 250022, Shandong, Peoples R China
[2] Tarim Univ, Engn Lab Chem Resources Utilizat South Xinjiang X, Alar, Peoples R China
[3] Shandong Univ, Sch Pharmaceut Sci, 44 West Rd Wenhua, Jinan 250012, Shandong, Peoples R China
[4] Shandong Univ, Dept Clin Lab, Hosp 2, Jinan, Shandong, Peoples R China
[5] Qilu Univ Technol, Sch Chem & Pharmaceut Engn, Jinan, Shandong, Peoples R China
[6] Shandong Xinhua Pharmaceut Co Ltd, Zibo, Peoples R China
关键词
benzo(a)pyrene; S-allylcysteine; carcinogenesis; A549; reactive oxygen species; nuclear factor-kappa B; INDUCED OXIDATIVE INJURY; DIALLYL TRISULFIDE; GARLIC EXTRACT; PLANT-EXTRACTS; IN-VITRO; CANCER; STRESS; GROWTH; EXPRESSION; A549;
D O I
10.1177/1934578X19896915
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
Oil-soluble organosulfur compounds in garlic are known for the anticancer effect. However, there are limited experimental studies to describe the effect of S-allylcysteine (SAC), a main water-soluble derivative of garlic, in carcinogenesis. This study investigates the prevention function of SAC on carcinogen benzo(a)pyrene (B(a)P)-induced precancerous activity in human lung cells (A549). A549 cells were either pretreated (PreTM) or concurrently treated (CoTM) with 1 mu M B(a)P and either 10 or 50 mu M SAC. The 50 mu M CoTM group inhibited B(a)P-induced cell proliferation by approximately 100%. The 50 mu M SAC CoTM and PreTM inhibited the B(a)P-induced G2/M phase shift by 119% and 100%, respectively. Furthermore, the SAC PreTM exhibited the potential to reduce the generation of reactive oxygen species (ROS) in cells relative to the B(a)P group by approximately 100%. The CoTM and PreTM elevated superoxide dismutase (SOD) by at least 70% compared with B(a)P group. In this study, we demonstrated that the mechanisms involved in the inhibitory role of SAC in B(a)P-induced carcinogenesis, including suppression of cell proliferation and DNA damage, cell cycle regulation, attenuation of ROS formation, increase of SOD activity, and inhibition of nuclear factor-kappa B (NF-kappa B) activity, which indicated that SAC is potentially a novel therapeutic candidate for the prevention and treatment of B(a)P-induced human lung cancer.
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页数:8
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