Effect of electroacupuncture on haemodynamic changes during intubation for general anaesthesia is mediated by nitric oxide synthase‑3 via the regulation of microRNA‑155, microRNA‑335 and microRNA‑383
- Wei Wang
- Kang Wang
- Xing Zhong
Affiliations: Department of Anesthesiology, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong 510632, P.R. China, Office of Construction, Sun Yat‑Sen University, Guangzhou, Guangdong 510000, P.R. China, Department of Ultrasound, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong 510632, P.R. China
- Published online on: February 28, 2023 https://doi.org/10.3892/mmr.2023.12970
Copyright: © Wang
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Intubation for general anaesthesia is a life‑threatening risk because it can cause haemodynamic changes. Electroacupuncture (EA) has been reported to alleviate the risk of intubation. In the present study, haemodynamic changes were measured at different time points before and after EA. Reverse transcription‑quantitative PCR was performed to measure the expression of micro (mi)RNAs and endothelial NO synthase (eNOS) mRNA. Western blotting was performed to evaluate the expression of eNOS protein. A luciferase assay was used to explore the inhibitory role of miRNAs in eNOS expression. The transfection of miRNA precursors and antagomirs was performed to assess their effect on eNOS expression. The systolic blood pressure, diastolic blood pressure and mean arterial pressure of patients were significantly decreased by EA, while the heart rate of patients was markedly increased. The expression of micro RNA (miR)‑155, miR‑335 and miR‑383 was effectively inhibited by EA in the plasma and peripheral blood monocytes of patients, whereas eNOS expression and NOS production were markedly elevated by EA. The luciferase activity of the eNOS vector was significantly inhibited by miR‑155, miR‑335 and miR‑383 mimics but activated by miR‑155, miR‑335 and miR‑383 antagomirs. miR‑155, miR‑335 and miR‑383 precursors suppressed the expression of eNOS, while miR‑155, miR‑335 and miR‑383 antagomirs enhanced the expression of eNOS. The present study demonstrated that EA may exert a vasodilative effect during intubation for general anaesthesia by promoting NO production and upregulating eNOS expression. The effect of EA on upregulating eNOS expression may be mediated by its inhibitory effect on the expression of miRNA‑155, miRNA‑335 and miRNA‑383.