The well-known toxic medicine Gelsemium elegans is widely and historically used to treat bone fracture and skin ulcers by the folk people of China. Two new monoterpenoid indole alkaloids, gelselegandines D and E, together with the known analogue gelegamine A were isolated from G. elegans. Their structures were elucidated by means of spectroscopic techniques and quantum chemical calculations. All isolated compounds were tested for the effects on RANKL-induced osteoclast formation. Interestingly, gelselegandine E and gelegamine A, respectively, showed significant promoting and inhibitory activities on osteoclastogenesis, while gelselegandine D had no activity under the same concentration. This work suggested the different configurations for the carbons near the C-19/20 oxygen rings of the isolated compounds may be the key active groups on osteoclast formation and provided the evidence for the rationality as the traditional treatment for bone-related diseases of G. elegans.

Relinqing Granules (RLQ), a single-herb formulation derived from Polygonum capitatum Buch.-Ham. ex D. Don (THL), possesses diverse pharmacological properties-including antimicrobial, anti-inflammatory, and antioxidant activities-which suggest their potential utility in treating pneumonia. This study seeks to elucidate the underlying mechanisms of RLQ to support its future clinical application in managing inflammatory lung diseases. This study aimed to investigate the therapeutic effects of RLQ on pneumonia and elucidate its underlying mechanisms, with a particular focus on the phosphoinositide 3-kinase/protein kinase B/mechanistic target of rapamycin (PI3K/AKT/mTOR) signaling pathway. Pneumonia was induced in mice via lipopolysaccharide (LPS) administration, while A549 cells were similarly stimulated with LPS to establish an in vitro inflammation model. Mice received RLQ treatment by oral gavage for seven consecutive days. Subsequently, lung tissues were collected for hematoxylin-eosin (H&E) staining, enzyme-linked immunosorbent assay (ELISA), Western blotting, and quantitative real-time polymerase chain reaction (qPCR). In vitro, RLQ-treated A549 cells were evaluated through ELISA, Cell Counting Kit-8 (CCK-8), flow cytometry, Western blotting, and qPCR. To further elucidate the underlying mechanism, A549 cell models with mTOR knockdown and overexpression (OE) were constructed to assess the regulatory role of mTOR in inflammation and apoptosis. RLQ alleviated LPS-induced lung inflammation by shifting the regulatory T cell/T helper 17 cell (Treg/Th17) balance toward an immunoregulatory state and modulating pro-inflammatory cytokine expression, potentially through the PI3K/AKT/mTOR signaling pathway. In vitro, RLQ treatment reduced cytokine levels, improved cell viability, and inhibited apoptosis in LPS-injured A549 cells by regulating this pathway and its downstream apoptotic proteins. Furthermore, in mTOR knockdown and OE models, RLQ significantly mitigated LPS-induced cellular damage, enhanced cell viability, and suppressed apoptosis, which correlated with the downregulation of mTOR pathway activation. RLQ effectively protected against LPS-induced lung and alveolar epithelial cell injury by inhibiting PI3K/AKT/mTOR pathway phosphorylation, restoring the Treg/Th17 immune balance, and suppressing apoptosis. These findings provide new mechanistic insights into the therapeutic potential of RLQ in the treatment of pneumonia.

Pulmonary fibrosis (PF) is a serious interstitial disease that includes diffuse collagen deposition of lung tissue. Polygonum capitatum Buch.-Ham. ex D. Don (THL) is a traditional vaccine that has antibacterial and anti-inflammatory effects. In this research, to investigate the mechanism of action of THL in the intervention of pulmonary fibrosis by network pharmacology and molecular docking related research methods, in order to provide a theoretical basis for expanding the scope of THL medication. A total of 49 active ingredients were analyzed and screened in Cephalus cephalusis, including 35 pulmonary fibrosis targets, and 10 key targets such as ALB, EGFR were screened after software analysis. The molecular docking results showed that there were 44 binding energies less than –3 kcal·mol⁻¹ in the 60 docking results, indicating that most proteins had strong binding energies with compounds. The key targets of KEGG enrichment analysis were mainly enriched in 20 core action pathways, such as hemostasis-related pathway, regulation of kinase activity. This study shows that based on network pharmacology, the multicomponent–multitarget–multipathway effect of THL intervention in pulmonary fibrosis is discussed.