Retracted: Effects of mTOR/NF‐κB signaling pathway and high thoracic epidural anesthesia on myocardial ischemia‐reperfusion injury via autophagy in rats

Abstract

We investigated the role of mammalian target of rapamycin/nuclear factor-kappa B (mTOR/NF-κB) signaling pathway in high thoracic epidural anesthesia (HTEA) against myocardial ischemia-reperfusion (I/R) injury in rats. The rat model of myocardial I/R injury was established. Ninety rats were divided into the normal, sham, I/R, eHTEA, the PDTC, and HTEA + PDTC groups. ELISA was applied to detect cardiac function indexes. HE staining was conducted to observe histopathological changes of myocardial tissues, and TTC staining was performed to detect the myocardial infarction size. TUNEL staining was adopted to detect the cell apoptosis rate. The mRNA and protein levels of mTOR, NF-κB, Fasl, Bcl-2 and Bax, and LC3-I, LC3-II, BNIP3, and Atg5 were detected by RT-qPCR and Western blotting, respectively. The findings indicated that compared with the normal and sham groups, the I/R, PDTC, and HTEA groups showed the larger myocardial infarction size and increased cell apoptosis rate, while the results in the HTEA + PDTC group were opposite. Compared with the normal and sham groups, the I/R group showed reduced mRNA and protein levels of Bcl-2, LC3, BNIP3, and Atg5, and elevated mRNA and protein levels of mTOR, p50, p65, Bax, and Fasl, while the HTEA + PDTC group revealed the opposite results, and the PDTC and HTEA group revealed the increased mRNA and protein levels of Bcl-2, LC3, BNIP3, Atg5, mTOR, p50, p65, Bax, and Fasl. These results prove that the inhibition of mTOR/NF-κB signaling pathway potentiates HTEA against myocardial IR injury by autophagy and apoptosis in rats.

Galectin‐3 exacerbates ox‐LDL‐mediated endothelial injury by inducing inflammation via integrin β1‐RhoA‐JNK signaling activation

“…(c and d) The expression of adhesion molecules (ICAM-1 and VCAM-1) was detected by WB (e). *p < 0.05, **p < 0.01 Wen, Lin, Wei, & Huang, 2018), myocardial infarction (Maracle et al, 2018) and heart failure (Hu et al, 2018). In our study, our results indicated Gal-3 effect was closely associated with the phosphorylation levels of p65, IKKα, and IKKβ levels, suggesting that Gal-3 may be involved in HUVECs inflammatory reaction on IKK-dependent NF-κB activation.…”

Physiological and pharmacological effects of melatonin on remote ischemic perconditioning after myocardial ischemia‐reperfusion injury in rats: Role of Cybb, Fas, NfκB, Irisin signaling pathway

“…Inhibition of early activation of NfκB may suppress the inflammatory response due to cytokines, thus by reducing the gene expression of intercellular adhesion molecules creates a protective effect on I/R damage . In the study of rat that performed by Huang et al, it was shown that autophagy‐related genes induced by inhibition of NfκB may play a vital role in reducing myocardial I/R injury. Melatonin can reduce the upregulation of various pro‐inflammatory cytokines, such as interleukins and TNFα, by preventing the translocation of NfκB into the nucleus .…”

Practical guidelines for rigor and reproducibility in preclinical and clinical studies on cardioprotection

“…A mixture of ketamine (50–75 mg/kg) and xylazine (1–5 mg/kg) induces anesthesia [464], while a single injection of pentobarbital [15–80 mg/kg] is also used [216, 446, 464]. However, in a recent study ketamine/xylazine induced bradycardia and increased serum-free fatty acids, while both ketamine/xylazine and isoflurane induced hyperglycemia.…”