Aim.To explore the pharmacological mechanism of Xiaoyao powder (XYP) on anovulatory infertility by a network pharmacology approach.Method.Collect XYP’s active compounds by traditional Chinese medicine (TCM) databases, and input them into PharmMapper to get their targets. Then note these targets by Kyoto Encyclopedia of Genes and Genomes (KEGG) and filter out targets that can be noted by human signal pathway. Get the information of modern pharmacology of active compounds and recipe’s traditional effects through databases. Acquire infertility targets by Therapeutic Target Database (TTD). Collect the interactions of all the targets and other human proteins via String and INACT. Put all the targets into the Database for Annotation, Visualization, and Integrated Discovery (DAVID) to do GO enrichment analysis. Finally, draw the network by Cytoscape by the information above.Result.Six network pictures and two GO enrichment analysis pictures are visualized.Conclusion.According to this network pharmacology approach some signal pathways of XYP acting on infertility are found for the first time. Some biological processes can also be identified as XYP’s effects on anovulatory infertility. We believe that evaluating the efficacy of TCM recipes and uncovering the pharmacological mechanism on a systematic level will be a significant method for future studies.

Premature ovarian failure (POF) affects 1-3.5% of women under 40 years of age, characterized by irreversible depletion of the follicular pool and decline in oocyte quality, with its pathogenesis remaining incompletely understood. Current mainstream therapies, such as hormone replacement therapy, only alleviate symptoms, fail to reverse the underlying functional decline, and carry long-term risks, necessitating the exploration of novel strategies targeting the etiology. This review systematically dissects the central role of epigenetic regulation in POF. First, DNA methylation governs female reproductive lifespan by reprogramming the dormant-activation balance of primordial follicles and maintaining epigenetic memory in oocytes. Second, histone modification homeostasis determines ovarian endocrine function by influencing granulosa cell senescence and steroid hormone synthesis. Additionally, non-coding RNAs form regulatory hubs by constructing competing endogenous RNA networks that integrate oxidative stress and developmental signaling pathways. These mechanisms provide new insights into the pathological basis of POF, identify potential biomarkers, and offer a theoretical framework for deciphering targeted intervention strategies and developing precision epigenetic therapies to delay POF progression.

Ferroptosis and immunogenic cell death, as two unique forms of cell death, have attracted extensive attention in the biomedical field. Recent studies have shown the synergistic effect of ICD and ferroptosis in the tumor microenvironment, where tumor cells undergo immunogenic cell death and release immunogenic molecules, such as DAMPs, to recruit and activate immune cells and promote adaptive immune responses. At the same time, molecules such as lipid peroxides produced by ferroptosis may also enhance the anti-tumor activity of immune cells. In addition, the synergistic use of ferroptosis and ICD in combination with novel protocols such as biomaterials and nanotechnology has demonstrated promising anti-tumor effects. This article reviews the cross-regulatory mechanism of ferroptosis and ICD in the tumor microenvironment, and explores the related biological effects between immune cells and ferroptosis, and the potential application of the two in the treatment of cancer. At the same time, we put forward insights into the solution of the existing problems in the combination of ferroptosis and ICD, as well as new ideas and development directions for future cancer treatment.

Objective. To explore the effect of Jiawei Buguzhi Pills (JWBGZP) on the TGF-β-Smad pathway in postmenopausal osteoporosis (PMO) based on integrated pharmacological strategy. Method. The ETCM database was used to collect JWBGZP. GeneCards and OMIM databases were utilized to obtain PMO-related genes. Cytoscape was used for network construction and analysis, and DAVID was used for GO and KEGG enrichment analysis of key targets. Animal experiments and cell experiments were conducted to further explore the mechanism. The bone mass density was detected by dual-energy X-ray bone densitometer. The TGF-β1 and Smad4 mRNA in bone tissue were detected by RT-qPCR. The TGF-β1 and Smad4 protein in bone tissue were detected by the western blot. The TGF-β1 and Smad4 protein in osteoblasts were determined by immunohistochemistry. Result. A total of 721 JWBGZP potential targets and 385 PMO-related genes were obtained. The enrichment analysis showed that JWBGZP may regulate the TGF-beta signaling pathway, oxidation-reduction process, aging, response to hypoxia, response to ethanol, negative regulation of cell proliferation, PI3K-Akt, HIF-1, and other signaling pathways. The animal experiments showed that compared with the model group, the femoral bone mineral density and lumbar bone mineral density of the JWBGZP group increased (P<0.05); the expression levels of TGF-β1 and Smad mRNA and proteins in the JWBGZP group were significantly higher (P<0.05). The cell experiment results showed a large number of osteoblast stained blue-purple and orange-red calcified nodules. The expression levels of TGF-β1 and Smad proteins in the JWBGZP group were significantly higher than those in the blank control group and the sham operation group, and the protein expression levels in the model group were the lowest (P<0.05). Conclusion. JWBGZP may be involved in PI3K-Akt, HIF-1, estrogen, prolactin, and other signaling pathways and regulate MAPK1, AKT1, PIK3CA, JAK2, and other gene targets, regulate bone metabolism, and thereby treat PMO.