Objective: “Three formulas and three medicines,” namely, Jinhua Qinggan Granule, Lianhua Qingwen Capsule, Xuebijing Injection, Qingfei Paidu Decoction, HuaShi BaiDu Formula, and XuanFei BaiDu Granule, were proven to be effective for coronavirus disease 2019 (COVID-19) treatment. This study aimed to identify the active chemical constituents of this traditional Chinese medicine (TCM) and investigate their mechanisms through interleukin-6 (IL-6) integrating network pharmacological approaches.Methods: We collected the compounds from all herbal ingredients of the previously mentioned TCM, but those that could downregulate IL-6 were screened through the network pharmacology approach. Then, we modeled molecular docking to evaluate the binding affinity between compounds and IL-6. Furthermore, we analyzed the biological processes and pathways of compounds. Lastly, we screened out the core genes of compounds through the construction of the protein-protein interaction network and the excavation of gene clusters of compounds.Results: The network pharmacology research showed that TCM could decrease IL-6 using several compounds, such as quercetin, ursolic acid, luteolin, and rutin. Molecular docking results showed that the molecular binding affinity with IL-6 of all compounds except γ-aminobutyric acid was < −5.0 kJ/mol, indicating the potential of numerous active compounds in TCM to directly interact with IL-6, leading to an anti-inflammation effect. Finally, Cytoscape 3.7.2 was used to topologize the biological processes and pathways of compounds, revealing potential mechanisms for COVID-19 treatment.Conclusion: These results indicated the positive effect of TCM on the prevention and rehabilitation of COVID-19 in at-risk people. Quercetin, ursolic acid, luteolin, and rutin could inhibit COVID-19 by downregulating IL-6.

Mesenchymal stem cells (MSCs) protect the endothelial barrier complex and survival, implicated in the pathogenesis of acute lung injury (ALI) via paracrine hepatocyte growth factor (HGF). However, the mechanism of HGF in endothelial regulation remains unclear. Here, we introduced a coculture protocol of pulmonary microvascular endothelial cells (PMVECs)

This study was conducted to analyze the antibacterial effect of olive oil polyphenol extract (OOPE) against vegetative cells of Bacillus cereus isolated from raw milk and reveal the possible antibacterial mechanism. The diameter of inhibition zone, minimum inhibitory concentration, minimum bactericidal concentration, and survival counts of bacterial cells in sterile normal saline and pasteurized milk were used to evaluate the antibacterial activity of OOPE against B. cereus vegetative cells. The changes in intracellular ATP concentration, cell membrane potential, content of bacterial protein, and cell morphology were analyzed to reveal possible mechanisms of action. Our results showed the diameter of inhibition zone, minimum inhibitory concentration, and minimum bactericidal concentration of OOPE against B. cereus vegetative cells were 18.44 ± 0.55 mm, 0.625 mg/mL, and 1.25 mg/mL, respectively. Bacillus cereus GF-1 vegetative cells were decreased to undetectable levels from about 8 log cfu/ mL after treatments with 0.625 mg/mL of OOPE in normal saline at 30°C for 3 h and in pasteurized milk at 30°C for 10 h. The antibacterial mechanisms of OOPE against B. cereus GF-1 vegetative cells may be due to the reduction of intracellular ATP concentrations, cell membrane depolarization, decrease of bacterial protein content, and leakage from cytoplasm. These findings illustrated that OOPE could be used to prevent the growth of contaminating B. cereus cells in dairy products.

Background: Pulmonary arterial hypertension (PAH) is a fatal progressive disease characterized by an increased blood pressure in the pulmonary arteries. RhoA/Rho-kinase (RhoA/ROCK) signaling activation is often associated with PAH. The purpose of this study is to investigate the role and mechanisms of long non-coding RNA (lncRNA) Smooth muscle-induced lncRNA (SMILR) to activate RhoA/ROCK pathway in PAH. Methods: SMILR, microRNA-141 (miR-141) and RhoA were identified by qRT-PCR in PAH patients' serum. MTT, wound-healing assay, CCK-8 assay, and flow cytometry were performed to determine cell viability, migration, proliferation, and cell cycle in human pulmonary arterial smooth muscle cells (hPASMCs) and primary PASMCs from PAH patients. We also performed bioinformatical prediction, luciferase reporter assay and RIP to assess the interaction among SMILR, miR-141 and RhoA. RhoA/ROCK pathway and proliferation-related proteins were measured by Western blotting. Finally, we introduced the shSMILR to monocrotaline--induced PAH rat model, and used the hemodynamic measurement, qRT-PCR and immunohistochemistry to examine the therapeutic effects of shSMILR. Results: SMILR and RhoA expression were up-regulated, while miR-141 expression was down-regulated in PAH patients. SMILR directly interacted with miR-141, and negatively regulated its expression. Knockdown of SMILR suppressed PASMCs proliferation and migration induced by hypoxia. Furthermore, overexpression of miR-141 could inhibit RhoA/ROCK pathway by binding to RhoA, thereby repressing cell proliferation-related signals. Knockdown of SMILR significantly inhibited the Rho/ROCK activation and vascular remodeling in monocrotaline-induced rats. Conclusion: Knockdown of SMILR effectively elevated miR-141 expression, and in turn inhibited RhoA/ROCK pathway to regulate vascular remodeling and reduce blood pressure in PAH.