Meta-analysis of the efficacy of budesonide and ambroxol hydrochloride inhalation in children with pneumonia and their effects on inflammatory response.

Childhood pneumonia, often caused by acute upper respiratory tract infections or bronchitis, is one of the leading causes of mortality in children. Nebulized inhalation, as a low-risk treatment method, has garnered significant attention. However, its effectiveness and safety remain controversial. In this study, a systematic review of relevant literature on the use of budesonide (BUD) and ambroxol hydrochloride (AMB) inhalation in the treatment of childhood pneumonia was conducted, and a total of 10 articles were included. The meta-analysis revealed an odds ratio (OR) of 1.61 and an I2 value of 0.00 % for the effectiveness of combined BUD and AMB inhalation therapy in children with pneumonia, indicating no heterogeneity among the studies in terms of effectiveness. The OR values for BUD or AMB inhalation in alleviating cough, lung auscultation abnormalities, respiratory distress, body temperature, and cyanosis of the lips in children with pneumonia all favored the combined BUD therapy, showing significant relief of the aforementioned symptoms. However, due to variations in drug dosage and administration methods, high heterogeneity was observed. This study suggested that combined BUD and AMB inhalation therapy has better efficacy in treating childhood pneumonia, and BUD combined with AMB inhalation is more effective in alleviating symptoms such as cough, lung auscultation abnormalities, respiratory distress, normalizing body temperature, and reducing cyanosis of the lips. Nevertheless, further validation is required due to the limited sample size and substantial heterogeneity in the included studies. To sum up, this study provides the first analysis of the efficacy and inflammatory response of BUD and AMB inhalation in children with pneumonia. Future research should aim to verify and clarify these findings, considering the limitations of the existing studies in terms of sample size and heterogeneity.

The Expression Profile of miRNA in Glioma and the Role of miR-339-5p in Glioma.

Objective: To reveal the expression profile of miRNA in glioma and the effects of microRNA-339-5p (miR-339-5p) on glioma. Methods: The glioma and normal tissues were randomly selected for miRNA gene chip detection and qRT-PCR verification. The U87 cells were separated into miR-NC, miR-339-5p mimic, and miR-339-5p suppressor group. Clonogenesis test, flow cell technique, Transwell, and cell scratch assay were utilized to verify the roles of miR-339-5p in cell proliferation, cell apoptosis, cell invasion, and cell migration. The epithelial-meso-transformation-associated proteins was verified by Western blot. Results: A total of 49 miRNAs (16 upregulated and 33 downregulated) were differentially expressed in glioma tissues, and miR-339-5p was the most downregulated. The clone number, invasion number, and healing rate of cells in miR-339-5p mimic group were decreased compared with miR-NC group (P < 0.05); the clone quantity, invasion number, and healing rate of cells in miR-339-5p inhibitor group were increased compared with miR-NC group (P < 0.05). The apoptosis rate of human glioma U87 cells in miR-339-5P mimic group was compared with miR-NC group (P < 0.05); the apoptosis rate of human glioma U87 cells in miR-339-5p suppressor group decreased compared with miR-NC group (P < 0.05). Compared with miR-NC group, the protein expression of Twist, Snsnail, N-cadherin, and Vimentin in miR-339-5p mimic group was considerably decreased, whereas E-cadherin was elevated (P < 0.05). Compared with miR-NC group, the protein expression of Twist, Snsnail, N-cadherin, and Vimentin in miR-339-5p suppressor group was considerably increased, whereas E-cadherin was considerably decreased (P < 0.05). Conclusion: Forty-nine glioma-related miRNAs were screened out, and miRNA expression was significantly different between glioma and normal tissues. The downregulated miR-339-5p in glioma can regulate the proliferative, apoptotic, invasive, and migratory abilities of glioma U87 cells and might suppress the occurrence and development of glioma.

Inhibitory Effect of miR-339-5p on Glioma through PTP4A1/HMGB1 Pathway.

Objective: Finding miR-339-5p inhibitory functions in glioma through PTP4A1/HMGB1 pathway. Methods: From May 2020 to August 2021, 20 glioblastoma and para cancer tissues were chosen for qRT-PCR analysis. The miR-NC, miR-con, miR-339-5PMIMIC, and miR-con + groups were transfected into human glioma U251 cells. The capacity of cell vascular-like structure construction was found by simulating angiogenesis, and the ability of cell movement was examined by cell scratching. The twofold luciferase reporter gene method determined that miR-339-5p targets PTP4A1, and the protein expression levels of PTP4A1 and HMGB1 were examined using Western blot. Results: MiR-339-5P expression was substantially lower in cancer samples than noncancer samples (P < 0.05). PTP4A1 expression in cancer samples was higher than in healthy controls (P < 0.05). The miR-339-5p group produced significantly less vascular-like structures than the NC and miR-con groups (P < 0.05). The miR-339-5p group lowered the invasive index and migratory rate of U251 cells (P < 0.05). PTP4A1 inhibited the luciferase activity of the pTP4A1-WT reporter gene (P < 0.05) but not the PTP4A1-MUT (P > 0.05). The miR-339-5p group had lower protein levels of PTP4A1 and HMGB1 than the NC and miR-con groups (P < 0.05). The development of vascular-like structures was substantially more significant in the miR-con +PTP4A1 group than in the miR-con and miR-339-5p +PTP4A1 groups (P < 0.05). In terms of migration and invasion index, there was a substantial difference between the miR-339-5p +PTP4A1 and the miR-con +PTP4A1 groups (P < 0.05). The miR-con +PTP4A1 group had a greater migration rate and invasive index than the miR-con and miR-339-5p +PTP4A1 groups (P < 0.05). Conclusion: MiR-339-5P inhibits angiogenic mimicry, migration, and invasion of brain glioma U251 cells by inhibiting the PTP4A1/HMGB1 signal pathway.