Objective This study utilizes network pharmacology and molecular docking techniques to explore the role of colchicine in regulating ferroptosis for the treatment of neurological injury. Methods Colchicine targets were obtained from the PubChem and Swiss Target Prediction databases, while targets related to neurological injury were retrieved from the GeneCards, OMIM, and DisGeNET databases. Ferroptosis targets were sourced from the FerrDb database, and the Venny 2.1.0 tool was accustomed to identify the intersection of these three sets. A protein-protein interaction (PPI) network was constructed based on the STRING database, and GO and KEGG pathway enrichment analyses were conducted using Metascape. Ultimately, molecular docking analyses of colchicine with the top ten targets were performed using Autodock Vina. Results There were 401 targets for colchicine, 3 367 for neurological injury, and 1 543 for ferroptosis, with 57 intersection targets. The PPI network identified TP53, IL6, EGFR, and others as major targets. KEGG analysis indicated that colchicine regulated ferroptosis through the Wnt signaling pathway to treat neurological injury. Molecular docking results showed that colchicine bound well to multiple targets. Conclusion Colchicine may regulate related genes through the Wnt signaling pathway to treat neurological injury.

Objective To evaluate the risk factors of hepatic encephalopathy in patients with cirrhosis. Methods Retrieve database both at home and abroad, collecting the relevant risk factors in patients with cirrhosis of the liver encephalopathy of case-control study, retrieval time limit are built from library to December 31, 2020, after finishing the document screening and quality evaluation software application Revman5.4 meta-analysis. Results A total of 9 papers with 1569 patients were included in this study, involving 10 risk factors, of which high heterogeneity in serum albumin and blood creatinine was not subjected to Meta-analysis.Serum ammonia, infection, upper gastrointestinal hemorrhage, ascites, serum total bilirubin, prothrombin time, urea nitrogen and serum natrium are risk factors for hepatic encephalopathy in patients with cirrhosis (P<0.05). Conclusion Elevated serum ammonia level, infected, upper gastrointestinal bleeding, ascites, serum total bilirubin level increased, prothrombin time prolonged, serum sodium level decreased and blood urea nitrogen increased are risk factors for hepatic encephalopathy in patients with cirrhosis, serum albumin levels and serum creatinine levels were uncertain.