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Background: Pulmonary hypertension (PH) is a complex disease caused by a wide range of underlying conditions, Tanshinone IIA (Tan IIA) has been widely used in PH patients. The study aimed to explore the possible molecular mechanism of Tan IIA against PH by network pharmacology and molecular docking. Methods: Tan IIA and PH-related targets were retrieved from public databases. Gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, and protein–protein interaction (PPI) network were used to investigate the protein targets and mechanism. The binding activity of core targets and Tan IIA were verified by molecular docking. Results: A total of 26 overlapping target proteins between Tan IIA and PH were screened. PPI network identified HSP90AA1, PTPN11, ATM, CA2, TERT, PRKDC, and APEX1 as key pharmacological targets. The results of GO function enrichment analysis included regulation of smooth muscle cell proliferation and migration, regulation of mitotic cell cycle, and regulation of G1/S transition of mitotic cell cycle. KEGG pathway analysis showed that nitrogen metabolism, NF-kappa B signaling pathway, cell cycle, necroptosis, apoptosis, and JAK-STAT signaling pathway were associated with Tan IIA in PH. The molecular docking results showed that Tan IIA can closely bind three core targets (HSP90AA1, PTPN11, and CA2). Conclusions: The present work initially clarified the effective therapeutic targets, biological processes, and signaling pathways of Tan IIA treatment of PH, which lay a foundation for further research on the pharmacological effects of Tan IIA.

Reperfusion therapy is the optimal therapy for acute myocardial infarction (AMI), but acute inflammatory injury and chronic heart failure (HF) after myocardial ischemia and reperfusion (MI/R) remain the leading cause of death after AMI. Pyroptosis, a newly discovered form of cell death, has been proven to play a significant role in the acute reperfusion process and the subsequent chronic process of ventricular remodeling. Current research shows that multiple stimuli activate the pyroptotic signaling pathway and contribute to cell death and nonbacterial inflammation after MI/R. These stimuli promote the assembly of the nucleotide-binding and oligomerization-like receptor pyrin domain-containing protein 3 (NLRP3) inflammasome by activating NLRP3. The mature NLRP3 inflammasome cleaves procaspase-1 to active caspase-1, which leads to mature processing of interleukin (IL)-18, IL-1ß, and gasdermin D (GSDMD) protein. That eventually results in cell lysis and generation of nonbacterial inflammation. The present review summarizes the mechanism of NLRP3 inflammasome activation after MI/R and discusses the role that NLRP3-mediated pyroptosis plays in the pathophysiology of MI/R injury and ventricular remodeling. We also discuss potential mechanisms and targeted therapy for which there is evidence supporting treatment of ischemic heart disease.

The harmful cyanobacteria blooms which usually form in spring and summer, cause global eutrophication of freshwater and coastal marine ecosystems. This study tried to utilize cyanobacteria as a raw material to produce biological poly(vinyl)alcohol-based films. Cyanobacteria was firstly modified with poly(ethylene glycol), guanidine hydrochloride, carboxymethyl cellulose and 3-glycidoxypropyltrimethoxysilane as plasticizer, modifier, toughening agent and coupling agent, respectively. And then the modified cyanobacteria was introduced to poly(vinyl)alcohol and cellulose nanofibers/poly(vinyl)alcohol matrix to improve the barrier properties of poly(vinyl)alcohol to light and water. Compared with poly(vinyl)alcohol and cellulose nanofibers/poly(vinyl)alcohol films, the obtained cyanobacteria/poly(vinyl)alcohol and the cyanobacteria/cellulose nanofibers/poly(vinyl)alcohol composites exhibit better resistance to light and water. More interestingly, we found that after adding cyanobacteria, the poly(vinyl)alcohol-based films present better barrier properties to blue-violet light and red light. In adddition, introducing cyanobacteria into poly(vinyl)alcohol or cellulose nanofibers/poly(vinyl)alcohol matrix increases the surface roughness and contact angle to water of the composites.