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AimThis review was performed to investigate the effect of ondansetron on the prevention of propofol injection pain.MethodsPubMed, Cochrane Library, and China National Knowledge Infrastructure (CNKI) were searched for randomized controlled trials (RCTs) of ondansetron in preventing the pain on injection of propofol. Then, RevMan 5.2 was adopted to conduct a meta-analysis on propofol injection pain.ResultsTen RCTs, totaling 782 patients, were included in this analysis. The meta-analysis showed that: 1) compared with the control group, the ondansetron group was related to a decreasing incidence of propofol injection pain, and it was statistically significant (risk ratio [RR] = 0.41, 95% confidence interval [CI, 0.34, 0.49], P < 0.00001); 2) compared with the incidence of propofol injection pain in the lidocaine group, there was no difference and no statistical significance (RR = 1.28, 95% CI [0.85, 1.93], P = 0.25); 3) no statistically significant differences were found between the ondansetron and magnesium sulfate groups in the incidence of propofol injection pain (RR = 1.20, 95% CI [0.87, 1.66], P = 0.27); and 4) the incidence of ondansetron group igniting moderate pain (RR = 0.37, 95% CI [0.26, 0.52], P < 0.00001) and severe pain (RR = 0.27, 95% CI [0.17, 0.43] P < 0.00001) was less likely to occur during the injection of propofol compared with the control group, but there was no difference between the ondansetron and control groups in the incidence of mild propofol injection pain (RR = 0.83, 95% CI [0.63, 1.10], P = 0.20).ConclusionOndansetron can effectively prevent propofol injection pain, and the effect is similar to that of magnesium sulfate and lidocaine.

Ventilator-induced lung injury (VILI) is one of the most common complications of mechanical ventilation and can severely affect health. VILI appears to involve excessive inflammatory responses, but its pathogenesis has not yet been clarified. Since interleukin-17 (IL-17) plays a critical role in the immune system and the development of infectious and inflammatory diseases, we investigated here whether it plays a role in VILI. In a mouse model of VILI, mechanical ventilation with high tidal volume promoted the accumulation of lung neutrophils, leading to increased IL-17 levels in the lung, which in turn upregulated macrophage chemoattractant protein-1 via p38 mitogen-activated protein kinase. Depletion of neutrophils decreases the production IL-17 in mice and inhibition of IL-17 significantly reduced HTV-induced lung injury and inflammatory response. These results were confirmed in vitro using RAW264.7 macrophage cultures. Our results suggest that IL-17 plays a pro-inflammatory role in VILI and could serve as a new target for its treatment.

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Lung ischemia-reperfusion injury (LIRI) is a severe multifaceted pathological condition that can lead to poor patient outcome where oxidative stress and the resulting inflammatory response can trigger and exacerbate tissue damage in LIRI patients. Sirtuin3 (SIRT3), a member of the sirtuin family, protects against oxidative stress-related diseases. However, it remains unclear if and how SIRT3 alleviates lung injury induced by ischemia/reperfusion (I/R). Our previous study showed that lung tissue structures were severely damaged at 6 h after lung I/R in mice, however, repair of the injured lung tissue was significant at 24 h. In this study, we found that both SIRT3 mRNA and protein levels were markedly increased at 24 h after lung I/R in vivo. Meanwhile, inhibition of SIRT3 aggravated lung injury and inflammation, augmented mitochondrial fission and oxidative stress and increased Hypoxia-inducible factor-1α (HIF-1α) expression in vivo. The results suggest that SIRT3 may be an upstream regulator of HIF-1α expression. Knockdown of SIRT3 resulted in excessive mitochondrial fission and increased oxidative stress in vitro, and we found that knocking down the expression of HIF-1α alleviated these changes. This suggests that the SIRT3-HIF-1α signaling pathway is involved in regulating mitochondrial function and oxidative stress. Furthermore, inhibition of dynamin-related protein 1 (Drp-1) by the inhibitor of mitophagy, Mdivi-1, blocked mitochondrial fission and alleviated oxidative stress in vitro. Taken together, our results demonstrated that downregulation of SIRT3 aggravates LIRI by increasing mitochondrial fission and oxidative stress. Activation of SIRT3 inhibits mitochondrial fission and this mechanism may serve as a new therapeutic strategy to treat LIRI.