Objective. To explore the active compounds and targets of cinobufotalin (huachansu) compared with the osteosarcoma genes to obtain the potential therapeutic targets and pharmacological mechanisms of action of cinobufotalin on osteosarcoma through network pharmacology. Methods. The composition of cinobufotalin was searched by literature retrieval, and the target was selected from the CTD and TCMSP databases. The osteosarcoma genes, found from the GeneCards, OMIM, and other databases, were compared with the cinobufotalin targets to obtain potential therapeutic targets. The protein-protein interaction (PPI) network of potential therapeutic targets, constructed through the STRING database, was inputted into Cytoscape software to calculate the hub genes, using the NetworkAnalyzer. The hub genes were inputted into the Kaplan-Meier Plotter online database for exploring the survival curve. Functional enrichment analysis was identified using the DAVID database. Results. 28 main active compounds of cinobufotalin were explored, including bufalin, adenosine, oleic acid, and cinobufagin. 128 potential therapeutic targets on osteosarcoma are confirmed among 184 therapeutic targets form cinobufotalin. The hub genes included TP53, ACTB, AKT1, MYC, CASP3, JUN, TNF, VEGFA, HSP90AA1, and STAT3. Among the hub genes, TP53, ACTB, MYC, TNF, VEGFA, and STAT3 affect the patient survival prognosis of sarcoma. Through function enrichment analysis, it is found that the main mechanisms of cinobufotalin on osteosarcoma include promoting sarcoma apoptosis, regulating the cell cycle, and inhibiting proliferation and differentiation. Conclusion. The possible mechanisms of cinobufotalin against osteosarcoma are preliminarily predicted through network pharmacology, and further experiments are needed to prove these predictions.

Objective. Hip fractures are quite common worldwide, especially among the elderly, and are associated with a high incidence of postoperative delirium, which worsens functional results and increases death. The causes of postoperative delirium in patients with hip fractures are unknown, and a separate pathobiology has been hypothesized. Substance P is a neuropeptide that has been linked to a number of immune-inflammatory and neurological conditions. The purpose of this study was to see if serum substance P levels could predict postoperative delirium in a group of hip fracture patients. Methods. A total of 148 hip fracture patients were enrolled in the study, all of whom had no substantial pre-existing medical or cognitive issues. Demographic and regular laboratory data were gathered as a starting point. ELISA was used to examine substance P levels before and after surgery (after 1 day). Patients were then divided into two groups: “postoperative delirium” and “no postoperative delirium.” Intergroup comparisons, study of delirium prevalence rates in postoperative serum substance P quartile categories, and binary logistic regression for postoperative delirium category as outcome were all done. Results. Except for serum low-density lipoprotein (LDL) levels, there were no statistically significant variations in preoperative substance P levels or other baseline characteristics between the two groups. The “postoperative delirium” group had significantly higher postoperative substance P levels than the “no postoperative delirium” group (46.36.1 versus 31.94.7 pg/ml). There was a significant difference in postoperative delirium rates between the quartile categories of postoperative substance P, with the fourth quartile having the highest rate. Regression analysis revealed that postoperative substance P levels were related with a significantly increased OR (1.265, CI: 1.172-1.283) of postoperative delirium. Conclusion. In the current sample of hip fracture patients, a higher postoperative serum substance P level was linked to a higher risk of postoperative delirium. Further research into the utility of early postoperative serum substance P as a delirium indicator in hip fracture patients is needed.