ObjectiveTo identify the active components in Maimendong decoction (MMDD) against pulmonary fibrosis (PF) and validate their molecular effects in vitro, while focusing on the role of methylophiopogonanone B in regulating fibrosis.MethodsData on MMDD components and targets were gathered from databases including BATMAN-TCM and PubMed, whereas the PF gene data were sourced from GeneCards, OMIM, and TTD. Shared targets were determined using the STRING database, and molecular docking was used to analyze the essential molecules associated with fibrosis. To simulate PF conditions, human embryonic lung fibroblasts (HPF) and A549 cells were exposed to transforming growth factor-β1 (TGF-β1). Various assays were used to determine the effects of MMDD and methylophiopogonanone B on signaling pathways, apoptosis, and epithelial–mesenchymal transition.ResultsWe identified 11 active components from MMDD extracts that targeted 511 shared proteins associated with PF, revealing 10 key targets in network analysis. Gene ontology analysis indicated that processes and pathways such as apoptosis regulation and PI3K/Akt signaling were involved. In vitro experiments revealed that MMDD downregulated the expression of α-smooth muscle actin (α-SMA), collagen type I (COL-I), and collagen type III and regulated Bcl-2/Bax signaling pathways to promote apoptosis. The flow cytometry apoptosis assay revealed that MMDD promoted the TGF-β1-induced apoptosis of myofibroblasts. The primary active ingredient in MMDD, methylophiopogonanone B, reduced α-SMA, COL-I, and PI3K/Akt/mTOR-related protein levels in TGF-β1-treated HPF cells, decreased Bcl-2 and cleaved caspase 3, and increased Bax. Moreover, methylophiopogonanone B increased E-cadherin levels and reduced α-SMA, fibronectin, N-cadherin, vimentin, and snail in TGF-β1-treated A549 cells.ConclusionMethylophiopogonanone B demonstrated the potential to treat PF by inducing myofibroblast apoptosis and inhibiting EMT. However, despite encouraging initial results, further clinical research is warranted to verify the safety and efficacy of methylophiopogonanone B in the management of PF

Objective To explore the possible role of proline-rich tyrosine kinase (Pyk2) in the pathogenesis of systemic lupus erythematosus (SLE).Methods The expression of Pyk2 in the peripheral blood mononuclear cells (PBMCs) of 50 patients with SLE and 36 healthy controls were tested with RT-PCR assay.The activation of Pyk2 was inhibited using specific inhibitor Pyk2 (TyrA9).Semi-quantitative PCR methodwas used to detect the Blys expression of PBMCs.One-way ANOVA and Pearson's correlation analysis were used for statistical analysis.Results The Pyk2 expression level (28.31 ±0.91) of SLE patients was significantly higher than that in healthy controls (33.69±0.04),the difference was statistically significant (P＜0.05).The activation of Pyk2 was stimulated and the expression levels of Blys in the PBMCs of patients with SLE was elevated.By inhibiting the activation of Pyk2,the BLyS expression levels decreased significantly.Conclusion Pyk2 may be involved in the abnormal activation of lymphocytes which lead to the pathogenesis of SLE.Pyk2 expression is associated with SLE disease activity,disease aggravation,and the Pyk2 expression levels is also increased significantly.In addition,the expression level of Pyk2 is higher in patients with renal involvement than those patients with other organ involvement.