Anesthesia is produced by drugs or other methods, and refers to the attenuation of pain via reversible suppression of neuronal transmission in the central and peripheral nervous systems, during surgery. Clinical investigations have indicated that the anesthetic action of isoflurane is efficient to alleviate pain during tumor resection clinical trials. In addition, it has been reported that isoflurane can induce caspase-3 activation and is associated with apoptosis of tumor cells. The present study investigated the anesthetic effects and molecular mechanisms underlying isoflurane-induced apoptosis in patients with hepatic carcinoma. Furthermore, the pain of patients with hepatic carcinoma was evaluated during the perioperative period according to the pain index. The apoptotic rate of hepatic carcinoma cells was analyzed in tumor tissues using TUNEL assay. The expression levels of apoptosis-associated proteins were detected in liver cancer cells following anesthesia in patients. Phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) and nuclear factor (NF)-κB signaling pathways were also analyzed in liver cancer cells following treatment with isoflurane. The results demonstrated that isoflurane inhibited growth and decreased viability of liver cancer cells in vitro and in vivo. In addition, the apoptotic rate was increased in cells obtained from isoflurane-treated patients. The results also demonstrated that isoflurane upregulated the expression levels of proapoptotic genes and downregulated anti-apoptotic mRNA expression. In addition, a molecular mechanism analysis indicated that isoflurane inhibited PI3K and AKT expression in liver cancer cells. Isoflurane also induced caspase-3 activation in liver cancer cells. Furthermore, isoflurane treatment attenuated NF-κB activity and inhibited migration and invasion of liver cancer cells. In conclusion, these findings indicated that isoflurane treatment efficiently attenuated surgical pain and inhibited tumor aggressiveness via regulation of NF-κB activity and the PI3K/AKT signaling pathway, thus suggesting that isoflurane is an efficient anesthetic drug that induces pain remission and promotes apoptosis of liver cancer cells.
What is known and objective The comparative efficacy of ancillary drugs on sevoflurane‐related emergence agitation (EA) in paediatric anaesthesia for adenotonsillectomy remains unclear. The purpose of this Bayesian network meta‐analysis was to investigate the efficacy of ancillary drugs on sevoflurane‐related EA in paediatric anaesthesia for adenotonsillectomy. Methods MEDLINE, Embase, the Cochrane Library and Web of Science databases were electronically searched to identify randomized controlled trials (RCTs) of different ancillary drugs used in adenotonsillectomy from inception to April 2019. Two reviewers independently screened the literature, extracted data and assessed the risk of bias in included studies. Subsequently, a network meta‐analysis was performed using the R software and RevMan 5.3 software. Results and discussion We included 25 RCTs, involving 2151 participants. The proportion of patients with sevoflurane‐related EA was significantly lower in the dexmedetomidine, ketamine, propofol, fentanyl, midazolam, sufentanil, remifentanil and clonidine groups than in the placebo group (P < .05). Fentanyl was superior to sufentanil (P < .05), whereas dexmedetomidine was superior to fentanyl (P < .05). Among ancillary drugs, dexmedetomidine (90.04%) showed the highest possibility of reducing the risk of EA, followed by fentanyl (87.45%), remifentanil (63.85%), ketamine (52.07%), midazolam (51.27%), clonidine (49.94%), propofol (29.89%), sufentanil (21.38%) and placebo (4.09%). What is new and conclusion Evidence suggests that the effects of dexmedetomidine in reducing the risk of sevoflurane‐related EA in paediatric anaesthesia for adenotonsillectomy were better than the effects of other drugs. However, large, high‐quality RCTs are required to further confirm this.
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