Liu Lei, Zhang Yu, Tang Xiao-Ren, Jia Guo-Bing, Zhou Shan, Yue Guo-Long, He Cheng-Shi
Department of Respiratory Medicine, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu Sichuan, 610000, China.
Department of Respiratory and Critical Care Medicine, Chongqing Hospital of Traditional Chinese Medicine, Jiangbei Chongqing, 400000, China.
BMC Pulm Med. 2024 Dec 2;24(1):596. doi: 10.1186/s12890-024-03406-x.
Emodin has protective effects on acute lung injury (ALI) or acute respiratory distress syndrome (ARDS). This meta-analysis intended to illustrate the efficacy of emodin on ALI/ARDS animal models.
Relevant preclinical studies were searched on PubMed, EMBASE, and Web of Science. Standardized mean differences (SMDs) with corresponding confidence intervals (CIs) were used to compare lung injury scores, lung wet-to-dry weight ratios (W/D), myeloperoxidase (MPO), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, IL-18, PaO, and PaCO between the treatment and control groups. The article quality was appraised using the SYRCLE tool.
Twenty one studies published between 2014 and 2023 were enrolled. Compared with the control group, emodin significantly reduced lung injury scores (SMD: -3.63; 95% CI: -4.36, -2.90; p < 0.00001), W/D ratios (SMD: -3.23; 95% CI: -4.29, -2.16; p < 0.00001), and MPO levels (SMD: -2.96; 95% CI: -3.92, -1.99; p < 0.00001). Furthermore, emodin downregulated TNF-α (SMD: -3.04; 95% CI: -3.62, -2.47; p < 0.00001), IL-1β (SMD: -3.76; 95% CI: -4.65, -2.87; p < 0.00001), IL-6 (SMD: -3.19; 95% CI: -3.95, -2.43; p < 0.00001), and IL-18 levels (SMD: -4.83; 95% CI: -6.10, -3.57; p < 0.00001). Emodin improved gas exchange dysfunction, increased PaO (SMD: 3.76; 95% CI: 2.41, 5.11; p < 0.00001), and decreased PaCO (SMD: -3.83; 95% CI: -4.90, -2.76; p < 0.00001). Sensitivity analyses and stratified analyses were conducted for outcome measures with heterogeneity.
Emodin treatment can effectively reduce the severity of ALI in animal models. Additional animal investigations and clinical trials involving human subjects are imperative.
大黄素对急性肺损伤(ALI)或急性呼吸窘迫综合征(ARDS)具有保护作用。本荟萃分析旨在阐明大黄素对ALI/ARDS动物模型的疗效。
在PubMed、EMBASE和Web of Science上检索相关的临床前研究。采用标准化均数差(SMD)及其相应的置信区间(CI)来比较治疗组和对照组之间的肺损伤评分、肺湿重与干重比(W/D)、髓过氧化物酶(MPO)、肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)、IL-6、IL-18、动脉血氧分压(PaO)和动脉血二氧化碳分压(PaCO)。使用SYRCLE工具评估文章质量。
纳入了2014年至2023年发表的21项研究。与对照组相比,大黄素显著降低了肺损伤评分(SMD:-3.63;95%CI:-4.36,-2.90;p<0.00001)、W/D比值(SMD:-3.23;95%CI:-4.29,-2.16;p<0.00001)和MPO水平(SMD:-2.96;95%CI:-3.92,-1.99;p<0.00001)。此外,大黄素下调了TNF-α(SMD:-3.04;95%CI:-3.62,-2.47;p<0.00001)、IL-1β(SMD:-3.76;95%CI:-4.65,-2.87;p<0.00001)、IL-6(SMD:-3.19;95%CI:-3.95,-2.43;p<0.00001)和IL-18水平(SMD:-4.83;95%CI:-6.10,-3.57;p<0.00001)。大黄素改善了气体交换功能障碍,提高了PaO(SMD:3.76;95%CI:2.41,5.11;p<0.00001),并降低了PaCO(SMD:-3.83;95%CI:-4.90,-2.76;p<0.00001)。对具有异质性的结局指标进行了敏感性分析和分层分析。
大黄素治疗可有效降低动物模型中ALI的严重程度。必须进行更多的动物研究和涉及人类受试者的临床试验。