RESUMO
BACKGROUND: This study aimed to determine the efficacy and safety of celecoxib for pain management after total knee arthroplasty (TKA). METHODS: PubMed, EMBASE, Web of Science, and the Cochrane Central Register of Controlled Trials (CENTRAL) were searched to identify eligible randomized controlled trials (RCTs) that compared celecoxib with a placebo in term of pain control efficacy after TKA. Primary outcomes included pain scores at 24, 48, and 72 h after TKA. Secondary outcomes included the active range of motion (ROM) at 24, 48,72 h, and 7 days postoperatively, morphine consumption over 72 h after TKA, incidence of postoperative nausea and vomiting (PONV), and total blood loss after surgery. Data analysis was conducted using RevMan version 5.3. RESULTS: Five RCTs involving 593 participants were included in the study. Compared with a placebo, celecoxib significantly reduced visual analog scale (VAS) scores at rest at 24 h [mean difference (MD) = -0.72; 95% confidence interval (CI), -1.27 to -0.17; I 2 = 82%; P = 0.01], 48 h (MD = -1.51; 95% CI, -2.07 to -0.95; I 2 = 0%; P < 0.00001), and 72 h (MD = -1.30; 95% CI, -2.07 to -0.54; I 2 = 82%; P = 0.0009) after TKA, decreased morphine consumption over postoperative 72 h (MD = -0.73; 95% CI, -0.96 to -0.51; I 2 = 96%; P < 0.00001), and increased active ROM at 48 h (MD = 13.23; 95% CI, 7.79 to 18.67; I 2 = 0%; P < 0.00001), 72 h (MD = 6.52; 95% CI, 4.95 to 8.10; I 2 = 68%; P < 0.00001), and 7 days (MD = 7.98; 95% CI, 3.64 to 12.31; I 2 = 68%; P = 0.0003) after the operation. No significant difference was found in the active ROM at 24 h (MD = 7.60; 95% CI, -6.14 to 21.34; I 2 = 94%; P = 0.28) and the incidence of PONV after surgery [risk ratio (RR) = 0.66; 95% CI, 0.40 to 1.09; I 2 = 0%; P = 0.11]. CONCLUSION: The administration of celecoxib is an effective and safe strategy for postoperative analgesia after TKA.
RESUMO
The role of inflammation response has been well documented in the development of acute lung injury (ALI). However, little is known about the functions of miRNAs in the regulation of inflammation in ALI. The aim of this study was to explore the effects of miRNAs in the regulation of inflammation in ALI and to elucidate the biomolecular mechanisms responsible for these effects. The expression profiles of miRNAs in lung tissues from lipopolysaccharide (LPS)-induced ALI mice model were analyzed using a microarray. It was observed that microRNA-221-3p (miR-221) was significantly increased in lung tissues in ALI mice. The inhibition of miR-221 attenuated lung injury including decreased lung W/D weight ratio and lung permeability and survival rates of ALI mice, as well as apoptosis, whereas its agomir-mediated upregulation exacerbated the lung injury. Concomitantly, miR-221 inhibition significantly reduced LPS-induced pulmonary inflammation, while LPS-induced pulmonary inflammation was aggravated by miR-221 upregulation. Of note, suppressor of cytokine signaling-1 (SOCS1), an effective suppressor of the NF-κB signaling pathway, was found to be a direct target of miR-221 in RAW264.7 cells. Overexpression of SOCS1 by pcDNA-SOCS1 plasmids markedly reversed the miR-221 inhibition-mediated inhibitory effects on inflammation and apoptosis in LPS-treated RAW264.7 cells. Finally, it was found that miR-221 inhibition suppressed LPS induced the activation of the NF-κB signaling pathway, as demonstrated by downregulation of phosphorylated-IκBα, p-p65 and upregulation of IκBα, whilst miR-221 overexpression had an opposite result in ALI mice. Our findings demonstrate that inhibition of miR-221 can alleviate LPS-induced inflammation via inactivation of SOCS1/NF-κB signaling pathway in ALI mice.
