Pediatric pneumonia is an infectious lung disease with high morbidity and mortality. Sinomenine, an alkaloid extracted from Caulis Sinomenii, exerts anti‐inflammatory and anti‐apoptotic activities. Lipopolysaccharide (LPS) is widely used for the establishment of an inflammatory model. This research aimed to explore the influences of sinomenine on LPS‐caused inflammatory injuries in fetal lung WI‐38 cells. WI‐38 cells were treated with LPS to establish a cellular model of pediatric pneumonia. Cell viability was evaluated using CCK‐8 assay. Apoptosis was evaluated using TUNEL staining and caspase‐3 activity assays. Inflammatory cytokines and NF‐κB p65 phosphorylation levels were measured by Enzyme‐Linked Immunosorbent Assay. Glutathione S‐transferase M1 (GSTM1) expression was detected by western blotting. Results showed that LPS reduced WI‐38 cell viability, and sinomenine protected cells against LPS‐induced viability reduction. Sinomenine concentration‐dependently attenuated LPS‐induced inflammation by reducing TNF‐α, IL‐1β and MCP‐1, and increasing IL‐10 levels. Sinomenine mitigated LPS‐induced apoptosis. GSTM1 was screened by matching the targets of sinomenine and pediatric pneumonia. GSTM1 was upregulated in LPS‐treated WI‐38 cells, and this effect was attenuated after sinomenine treatment. GSTM1 was upstream of NF‐κB pathway. Overexpression of GSTM1 reversed the suppressive functions of sinomenine on LPS‐stimulated inflammation and apoptosis. Overall, sinomenine attenuates inflammation and apoptosis in WI‐38 cells stimulated by LPS via inhibiting GSTM1 expression, indicating the therapeutic potential of sinomenine in pediatric pneumonia.

Objective: Long non-coding RNA (LncRNA) small nucleolar RNA host gene 4 (SNHG4) has been shown to be aberrantly expressed in a variety of cancers and involved in cancer development, but its role in ovarian cancer (OC) is unclear. The purpose of this study was to explore the biological function of SNHG4 in OC and reveal its potential downstream molecular targets. Methods: OC tumor tissue and normal tissue were collected; normal human ovarian epithelial cell line (IOSE80) and human ovarian cancer cell line (A2780, SKOV-3, OV-90 and CAOV3) were selected. RT-qPCR was used to detect SNHG4, miR-98-5p, and TMED5, while western blot was used to detect the protein expression levels of TMED5, Ki67, MMP-9, Bcl-2, Bax, Gsk3β, Wnt3a, and β-catenin. The subcellular localization of SNHG4 was assessed by nucleocytoplasmic separation assay. CCK-8, colony formation assay, flow cytometry, and Transwell were used to assess the biological behavior of OC cells. The targeting relationship between SNHG4, miR-98-5p and TMED5 was verified by dual luciferase reporter assay and RIP assay. Results: In OC, SNHG4 and TMED5 were highly expressed, and miR-98-5p was underexpressed. Knockdown of SNHG4 inhibited OC cell proliferation, migration and invasion, promoted apoptosis, and prevented Wnt/β-catenin pathway activation. The effect of knockdown of SNHG4 was reversed by knockdown of miR-98-5p or overexpression of TMED5. Mechanistically, SNHG4 competitively adsorbed miR-98-5p to mediate TMED5 expression, thereby activating the Wnt/β-catenin pathway. Conclusion: SNHG4 accelerates OC development via mediating the miR-98-5p/TMED5 axis and activating the Wnt/β-Catenin pathway. SNHG4 gene silencing might be a novel option for OC treatment.