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Study on the mechanism of inhibiting iron death of AGS cells in Jiawei Qifang Weitong Granules |
ZHANG Qinglang1 MO Xueni2 WANG Ting2 TANG Meiwen1 |
1.Graduate School, Guangxi University of Chinese Medicine, Guangxi Zhuang Autonomous Region, Nanniang 530200, China; 2.Affairs Office, Academic Guangxi University of Chinese Medicine, Guangxi Zhuang Autonomous Region, Nanniang 530200, China |
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Abstract Objective To investigate the mechanism of Jiawei Qifang Weitong Granules on inhibiting iron death of in gastric cancer cells. Methods Wistar rats were selected to prepare drug-containing serum. Gastric cancer AGS cells were divided into AGS group, blank serum group, and drug-containing serum group. The drug-containing serum was prepared by the conversion method of 19.4 g/(kg·d) intragastric administration of supplemented Qifang Weitong Granules fors seven days. Blank serum was prepared by routine feeding of rats in blank serum group. After two days of intervention, the cell activity and morphology of each group were detected, the contents of malondialdehyde (MDA) and glutathione (GSH) were detected by colorimetry, and the mRNA contents and protein expression levels of SLC7A11, P53 and GPX4 were detected by RT-qPCR and Western blot. Results The cell proliferation rate of drug-containing serum group was lower than that of blank serum group (P<0.05). The mRNA contents of SLC7A11 and GPX4 in drug-containing serum group were lower than those in blank serum group, and the mRNA contents of P53 were higher than those in blank serum group (P<0.01). The expression levels of SLC7A11 and GPX4 in drug-containing serum group were lower than those in blank serum group, and the expression level of P53 was higher than that in blank serum group (P<0.01). The MDA content in drug-containing serum group was lower than that in blank serum group, and the GSH content was higher than that in blank serum group (P<0.01). Conclusion Jiawei Qifang Weitong Granules can inhibit the proliferation of gastric cancer cells, and its effect may be related to the inhibition of ferroptosis signal.
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