Study on the ameliorating effect of miR-221-3p on the nerve cells injury induced by sevoflurane

Abstract

Purpose: Sevoflurane is a widely used anesthetics, however, it has been reported that sevoflurane has neurotoxic effects. Studies have shown that miR-221-3p can ameliorate neuron damage. This study was to investigate whether miR-221-3p could reduce the neurotoxic effect of sevoflurane on nerve cells. Materials and methods: The rat hippocampal neuron cells were treated with sevoflurane or cultured normally. And we constructed neuron cells that overexpressed or low expression of miR-221-3p in the presence or absence of sevoflurane. The cells were transfected with CDKN1B or siCDKN1B, and co-transfected with miR-221-3p mimic and CDKN1B or miR-221-3p inhibitor and siCDKN1B. Cell viability and apoptosis were detected by CCK-8 and flow cytometer. Target gene of miR-221-3p were predicted by TargetScan and luciferase reporter assay. The expressions of related genes were detected by western blotting and quantitative real-time polymerase chain reaction. Results: Sevoflurane decreased miR-221-3p level and increased CDKN1B level, inhibited cell viability and promoted apoptosis. Overexpress of miR-221-3p decreased CDKN1B level, up-regulated cell viability and inhibited apoptosis, and reversed the effects of sevoflurane on cell viability and apoptosis, while the effects low expression of miR-221-3p was contrary. CDKN1B was the target gene of miR-221-3p, which inhibited cell viability and promoted apoptosis, and reversed the effects of miR-221-3p mimic, whereas siCDKN1B did the opposite effects. Conclusions: Sevoflurane can cause nerve cell injury, and miR-221-3p may promote cell activity and inhibit apoptosis by inhibiting CDKN1B expression, thereby ameliorating cell injury induced by sevoflurane.

Plasma microRNA-221-3p as a biomarker for POCD after non-cardiac surgery

“…However, this observation found that high postoperative plasma microRNA-221-3p level was independent risk factors for POCD, the mechanism may be related to its proinflammatory effect. With regards to the regulatory mechanism of microRNA-221-3p in related diseases, Wang et al found that microRNA-221-3p ameliorated sevoflurane-induced cell injury by promoting cellular activity and inhibiting apoptosis through suppression of CDKN1B expression [ 28 ]. Numerous studies implicated a relationship between microR-221-3p and inflammation, microRNA-221-3p could mediate the antitumor effects of IFN-α [ 29 ], microRNA-221-3p and microRNA-92a-3p are reportedly associated with smoking-induced inflammation in COPD (chronic obstructive pulmonary disease) [ 30 ], microRNA-221-3p could drive the shift of macrophages towards pro-inflammatory functions by inhibiting the activation of JAK3/STAT3 [ 31 ].…”

GAS5, a long noncoding RNA, contributes to annulus fibroblast osteogenic differentiation and apoptosis in intervertebral disk degeneration via the miR-221-3p/SOX11 axis

“…Moreover, the authors revealed that miR-221-3p suppresses the osteogenic differentiation of degenerated AFs [ 11 ]. It has also been reported that miR-221-3p can suppress cell apoptosis in several diseases [ 12 , 13 ], and excessive AF apoptosis is highly associated with IVDD progression [ 14 ]. Therefore, miR-221-3p may be a potent regulator that protects against IVDD.…”