Effect of quercetin on inhibiting gefitinib‑activated non‑small cell lung cancer‑induced cell pyroptosis in cardiomyocytes via modulating mitochondrial autophagy mediated by the SHP2/ROS/AMPK/XBP‑1/DJ‑1 signaling pathway
Abstract
It has been reported that treatment of patients with non-small cell lung cancer (NSCLC) with gefitinib increases the risk of QT interval prolongation. Therefore, the present study aimed to investigate whether quercetin could delay gefitinib-induced cardiomyocyte apoptosis and its underlying mechanism. A total of 32 nude mice were divided into the sham, NSCLC, NSCLC + gefitinib and NSCLC + gefitinib + quercetin groups. Cardiac fibrosis in mouse heart tissues was assessed by Masson's trichrome staining. Additionally, immunohistochemical staining was performed to detect the expression levels of Src homology-2 domain-containing protein tyrosine phosphatase (SHP2), X-box binding protein 1 (XBP-1), phosphorylated (p)-stimulator of interferon genes (STING) and Nod-like receptor protein 3. Bioinformatics analysis was carried auto to predict the association between quercetin and the SHP2/reactive oxygen species (ROS) axis. Furthermore, the effects of adenosine triphosphate (ATP) + gefitinib, SHP2 silencing and H2O2 on ROS levels, as well as on the p-AMP-activated protein kinase (AMPK)/XBP-1/Parkinsonism associated deglycase (DJ-1) axis, mitochondrial autophagy and apoptosis were assessed via detecting the expression levels of the corresponding proteins in cardiomyocytes by western blot analysis. JC-1 immunofluorescence was performed to evaluate mitochondrial membrane damage. The results showed that NSCLC could not significantly affect cardiac function. In addition, compared with…
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