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Astragaloside IV reverses MNNG ‐induced precancerous lesions of gastric carcinoma in rats: R egulation on glycolysis through mi RNA ‐34a/ LDHA pathway
Author(s) -
Zhang Chengzhe,
Cai Tiantian,
Zeng Xiaohui,
Cai Dake,
Chen Yuxing,
Huang Xuejun,
Gan Haining,
Zhuo Juncheng,
Zhao Ziming,
Pan Huafeng,
Li Siyi
Publication year - 2018
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.6070
Subject(s) - lactate dehydrogenase a , histopathology , microbiology and biotechnology , glycolysis , chemistry , blot , real time polymerase chain reaction , immunohistochemistry , biology , pathology , biochemistry , medicine , immunology , gene , enzyme
This study was designed to investigate the precancerous lesions of gastric carcinoma (PLGC)‐reversing mechanisms of astragaloside IV (ASIV) in N‐methyl‐N′‐nitro‐N‐nitrosoguanidine (MNNG)‐induced PLGC rats. All rats were sacrificed after 10‐week treatment. Gastric tissue was analyzed by using histopathology and electron microscope. To be fully evidenced, LDHA, p53, TIGAR, MCT1, MCT4, HIF‐1α, CD147, and miRNA‐34a were detected by Western blotting and Real‐time Quantitative polymerase chain reaction (RT‐qPCR). As histopathology and electron microscope showed, it can be clearly observed that the area of dysplasia was reduced in ASIV groups, indicating that MNNG‐induced PLGC was markedly reversed by ASIV. Moreover, compared with model group, a significant decrease in gene expressions of LDHA, MCT1, MCT4, HIF‐1α, CD147, and TIGAR was observed whereas miRNA‐34a level was increased in ASIV groups. A significant up‐regulation induced by MNNG in protein levels of LDHA, MCT1, MCT4, HIF‐1α, and CD147 was attenuated in rats treated with ASIV. In contrast, the decreased expression of TIGAR was restored by ASIV. Interestingly, up‐regulation of p53 expression induced by MNNG was further increased in ASIV groups. In brief, these results implied that abnormal glycolysis was relieved by ASIV via regulation of the expressions of LDHA, p53, TIGAR, MCT1, MCT4, HIF‐1α, CD147, and miRNA‐34a.