氧化应激
肺癌
安普克
癌症研究
医学
肺
肿瘤科
内科学
生物
细胞生物学
激酶
蛋白激酶A
作者
Zhuxiu Jiang,Yao Zhong,Jiahao Chen,Xiang Guo,Jingjing Wang,Zhibo Xu
出处
期刊:PubMed
日期:2024-11-01
卷期号:54 (6): 774-781
摘要
To understand the influence of MIR-451 on LKB1-AMPK signal pathway and oxidative stress index in lung cancer mice. 40 rats were divided into four groups: ZC group (no lung cancer model), model group (lung cancer model), intervention group (rats with MiR-451 agomir injected), and NC group (rats with MiR-451 agomir control injected), 10 mice/group. The levels of MDA (malondialdehyde) and SOD (superoxide dismutase) in the four groups were detected, as well as the overall weights of the lungs and spleens. Lung tissue pathological changes were assessed by HE and LKB1-AMPK protein level and mRNA by Western blot and PCR. Compared to ZC group, the MDA levels in model and NC group were higher (p<0.05). In comparison with model and NC groups, the MDA level in intervention group was lower (p<0.05), while SOD was inversely associated with MDA levels. The lung and spleen indexes were similar in the NC and model groups (p>0.05). The lung index was lower and spleen index was higher in intervention group than in the other two groups (p<0.05). LKB1 and AMPK protein levels in model and NC groups were significantly elevated over the ZC group (P<0.05), and the LKB1 and AMPK protein levels of intervention group were the highest (P<0.05); LKB1 and AMPK mRNA levels of model and NC group were minor than ZC and intervention group (P<0.05). MiR-451 agonist shows a favorable response in a lung cancer model, reducing MDA levels and increasing SOD levels and improving lung weight as well as increasing LKB1-AMPK protein and mRNA expression.
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