Effects of parasternal intercostal block on surgical site wound infection and pain in patients undergoing cardiac surgery: A meta-analysis.

This study aimed to assess the effect of parasternal intercostal block on postoperative wound infection, pain, and length of hospital stay in patients undergoing cardiac surgery. PubMed, Embase, Cochrane Library, China National Knowledge Infrastructure, VIP, and Wanfang databases were extensively queried using a computer, and randomised controlled studies (RCTs) from the inception of each database to July 2023 were sought using keywords in English and Chinese language. Literature quality was assessed using Cochrane-recommended tools, and the included data were collated and analysed using Stata 17.0 software for meta-analysis. Ultimately, eight RCTs were included. Meta-analysis revealed that utilising parasternal intercostal block during cardiac surgery significantly reduced postoperative wound pain (standardised mean difference [SMD] = -1.01, 95% confidence intervals [CI]: -1.70 to -0.31, p = 0.005) and significantly shortened hospital stay (SMD = -0.40, 95% CI: -0.77 to -0.04, p = 0.029), though it may increase the risk of wound infection (OR = 5.03, 95% CI:0.58-44.02, p = 0.144); however, the difference was not statistically significant. The application of parasternal intercostal block during cardiac surgery can significantly reduce postoperative pain and shorten hospital stay. This approach is worth considering for clinical implementation. Decisions regarding its adoption should be made in conjunction with the relevant clinical indices and surgeon's experience.

Dexmedetomidine attenuates acute lung injury induced by lipopolysaccharide in mouse through inhibition of MAPK pathway.

Dexmedetomidine (Dex) is widely used for sedation in intensive care units and can be used as an adjunct to anesthetics. Previous studies have demonstrated that Dex has anti-inflammatory property. In this study, we aim to explore the potential therapeutic effects and mechanisms of Dex on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. To induce ALI, mice were intraperitoneally injected with LPS, while Dex was treated 1 h before LPS injection. The inflammation of lung tissues was evaluated by HE stain, and bronchoalveolar lavage fluid (BALF) was obtained after 6 h to measure protein concentrations. We also used an enzyme-linked immunosorbent assay to detect the secretion levels of proinflammatory cytokines in the serum. Western blotting method was adopted to observe changes in mitogen-activated protein kinases and downstream nuclear transcription factors. The results showed that pretreatment with Dex considerably reduced neutrophil infiltration and pulmonary edema, and significantly reduced protein concentrations in the BALF, as well as suppressed LPS-induced elevation of proinflammatory cytokines (TNF-α and IL-1ß) in the serum. In addition, we observed that the molecular mechanism of Dex-mediated anti-inflammation is associated with decreasing phosphorylation of MKK4, MMK3/6, ERK1/2, p38MAPK, and JNK, and diminishing activation of Elk-1, c-Jun, and ATF-2. Dex could attenuate ALI induced by LPS in mice, and this effect may be mediated through the inhibition of MAPK pathway.

Protective effects of protocatechuic acid on acute lung injury induced by lipopolysaccharide in mice via p38MAPK and NF-κB signal pathways.

The study aims to investigate the effects of protocatechuic acid (PCA) separated from Chinese herbs, on acute lung injury (ALI) induced by lipopolysaccharide (LPS) in mice. The mouse model was induced by intraperitoneal injection of LPS at the dose of 5mg/kg body weight. Three doses of PCA (30, 15, 5 mg/kg) were administered to mice with intraperitoneal injection one hour prior to LPS exposure. Six hours later after LPS administration, the effect of PCA on ALI mice was assessed via histopathological examination by HE staining, inflammatory cytokine production by ELISA assay and RT-PCR, p38MAPK and NF-κB activation by Western blot analysis. We found that PCA administration significantly ameliorated lung histopathological changes and decreased protein concentration in the bronchoalveolar lavage fluid. Furthermore, the overproduction of tumor necrosis factor-α (TNF-α) and interleukin-1ß (IL-1ß) was reduced by PCA. Additionally, PCA at the dose of 30 mg/kg could block the activation of p38MAPK and NF-κB signal pathways induced by LPS. In conclusion, our findings demonstrate that PCA possesses a protective effect on LPS-induced ALI in mice via suppression of p38MAPK and NF-κB signal pathways. Therefore, PCA may be useful in the therapy of lung inflammatory diseases, especially for ALI.