Introduction: The aim of this study was to evaluate the efficacy and safety of azithromycin (AZI) combined with glucocorticoid (GC) in the treatment of children with refractory Mycoplasma pneumoniae. Methods: Computer search for PubMed, EMbase, Cochrane Library, China Biomedical Literature Database (CBMdisc), China Knowledge Network (CNKI), Wanfang, VIP (VIP), and a randomized controlled trial (RCT) of AZI combined with GC in the treatment of children with refractory Mycoplasma pneumoniae pneumonia test (RCT), the search time limit is built until March 20, 2019. Two researchers independently performed literature screening, data extraction, and literature risk bias, and meta-analysis was performed using RevMan 5.3 software. Results: A total of 12 RCTs were included, including 1130 patients. Meta-analysis showed that AZI combined with GC therapy significantly improved the total effective rate of the disease compared with the conventional treatment group (odds ratio [OR] = 6.37; 95% confidence interval [CI] 4.03, 10.07; P < .00001; I ² = 0%), effectively shortened the antipyretic time (SMD = −2.29; 95% CI −2.70, −1.88; P < .0001); promoted lung inflammation absorption (SMD = −1.89; 95% CI −2.38, −1.40; P < .0001), reduced cough time (SMD = −2.39; 95% CI −2.80, −1.99; P < .0001); shortened hospital stay (SMD = −2.19; 95% CI −3.21, −1.17; P < .0001); improved imaging findings (OR = 5.38; 95% CI 1.09, 26.51, P = .04); reduced inflammation index (SMD = −3.15; 95% CI −4.93, −1.36; P = .004); improved immune function (SMD = 1.29; 95% CI −0.02, 2.60; P < .0001); had no significant adverse reactions (OR = 1.18; 95% CI 0.71, 1.98; P = .53). Conclusions: According to the current limited research evidence, the addition of GCs to the conventional treatment of refractory Mycoplasma pneumoniae in children can improve the clinical efficacy to a certain extent, and the safety is better. However, due to the quality and quantity of the included literature, the conclusions of this study need to be confirmed by more high-quality studies.

Objective(s): Chemerin is associated with insulin resistance, obesity, and metabolic syndrome. alpha-lipoic acid (alpha-LA) is a potent antioxidant involved in the reduction of diabetic symptoms. This study aimed to investigate the relationship between chemerin and P38 MAPK in the progression of diabetic nephropathy (DN) and examine the effects of alpha-LA on chemerin-treated human mesangial cells (HMCs). Materials and Methods: HMCs were transfected with a chemerin-overexpressing plasmid. HMCs were also treated with high-glucose, chemerin, alpha-LA, PDTC (pyrrolidine dithiocarbamate ammonium, NF Kappa B p65 inhibitor), and/or SB203580 (P38 MAPK inhibitor). Cell proliferation was tested using the Cell Counting Kit-8 assay. Collagen type IV and laminin were tested by ELISA. Chemerin expression was detected by qRT-PCR. The chemerin receptor was detected by immunohistochemistry. Interleukin-6 (IL-6), tumor necrosis factor-a (TNF-alpha), nuclear factor-Kappa Bp-p65 (NF-Kappa B p-p65), transforming growth factor-beta (TGF-beta), and p-P38 mitogen-activated protein kinase (p-P38 MAPK) were evaluated by western blot. Results: High-glucose culture increased the expression of the chemerin receptor. alpha-LA inhibited HMC proliferation. Chemerin overexpression increased collagen type IV and laminin expression. P38 MAPK signaling was activated by chemerin, resulting in up-regulation of IL-6, TNF-alpha, NF-Kappa B p-p65, and TGF-beta. SB203580, PDTC, and alpha-LA reversed the effects of chemerin, reducing IL-6, TNF-alpha, NF-Kappa B p-p65, and TGF-beta expression. Conclusion: Chemerin might be involved in the occurrence and development of DN. alpha-LA might prevent the effects of chemerin on the progression of DN, possibly via the P38 MAPK pathway.