Objective: Chronic nonbacterial prostatitis (CNP) has remained one of the most prevalent urological diseases, particularly in older men. Dihydroartemisinin (DHA) has been identi ed as a semi-synthetic derivative of artemisinin that exhibits broad protective effects. However, the role of DHA in inhibiting CNP in ammation and prostatic epithelial cell proliferation remains largely unknown.Materials and Methods: CNP mice model was induced by carrageenan and Haemotoxylin Eosin (HE) ,immuno uorescence and immunochemistry staining were used to con rm CNP and E2F7 expression. Human prostatic epithelial cells (HPECs) and RWPE-1 was induced by lipopolysaccharide (LPS) to mimic CNP model in vitro. Real-time quantitative PCR and Western blot were used to detect proliferation and in ammatory genes expression. Cell proliferation was determined using MTT assay.Results: DHA signi cantly alleviated the rough epithelium and inhibited multilamellar cell formation in the prostatic gland cavity and prostatic index induced by carrageenan. In addition, DHA decreased the expression of TNF-α and IL-6 in ammatory factors in prostatitis tissues and in LPS-induced epithelial cells. Upregulation of transcription factor E2F7, which expression was inhibited by DHA, was found in CNP tissues, human BPH tissues and LPS-induced epithelial cells in ammatory response. Mechanically, we found that depletion of E2F7 by shRNA inhibited epithelial cell proliferation and LPS-induced in ammation while DHA further enhance these effects. Furthermore, HIF1α was transcriptional regulated by E2F7 and involved in E2F7-inhibited CNP and cellular in ammatory response. Interestingly, we found that inhibition of HIF1α blocks E2F7-induced cell in ammatory response but does not obstruct E2F7promoted cell growth.
Conclusion:The results revealed that DHA inhibits the CNP and in ammation by blocking the E2F7/HIF1α pathway. Our ndings provide new evidence for the mechanism of DHA and its key role in CNP, which may provide an alternative solution for the prevention and treatment of CNP.
In the present study, a combined kinetic and heat transfer model was developed to study the kinetics and predict thermal runaway of vinyl chloride (VC) suspension polymerization. Reactor temperature, monomer conversion, mole of initiator, radical concentrations in the two phases (i.e., VC‐rich phase and PVC‐rich phase), and average molecular properties were mapped during non‐isothermal processes. Meanwhile, the risk of thermal runaway was evaluated using S–Z (divergence) and H–J criteria. Simulation results show that a lower jacket temperature Tj and a larger heat transfer coefficient U are able to postpone or even avoid the risk of thermal runaway. Both of the criteria serve well for the prediction of thermal runaway during non‐isothermal processes. To prevent the occurrence of thermal runaway to the greatest extent, model‐based design of strategies for an isothermal polymerization process was done. Specifically, either jacket temperature Tj or heat transfer coefficient U can be fine‐tuned to maintain a 50°C isothermal process.
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