NRG1 And MicroRNA-193A-3p Inhibitors Reduce The Pro-inflammatory And Pro-fibrotic Ability Of Macrophages

Objective This study intends To explore the biological effects of NRG1 on activated macrophages,and whether the biological effects of NRG1 can be enhanced when combined with micror NA-193A-3p inhibitors,and provide experimental basis for better clinical efficacy of NRG1.Methods In this study,macrophage RAW264.7 was used as the experimental object,and LPS was used to stimulation macrophage to established inflammation model.Il-6 and TGF-β expression levels of macrophages were detected to explore whether the inflammation model was established.On the basis inflammation model,NRG1 was used to treat inflammatory models and detect the changes in the expression levels of IL-6 and TGF-β in macrophages in order to explore whether NRG1 has anti-inflammatory and anti-fibrosis effects.Microrna-193a-3p mimics or inhibitors were transfected into macrophages to regulate the expression of Erb B4,and the transfection efficiency was determined by detecting the expression level of Erb B4.Then NRG1 was used to treat macrophages which had been up-regulated by LPS-stimulated Erb B4 to explore whether more expression of Erb B4 could help NRG1 play a stronger biological effect.Results In this study,the expression levels of IL-6 and TGF-β in macrophages were significantly up-regulated after LPS stimulation,indicating successful activation of macrophages.When inflammation occurs,the NRG1 receptor Erb B4 is down-regulated.By transfecting micror NA-193A-3p inhibitors into macrophages,the expression of Erb B4 can be increased and NRG1 can play a better anti-fibrosis role.Conclusion This study verified the feasibility of optimizing the efficacy of NRG1 by up-regulating the expression of Erb B4 when the decreased expression of Erb B4 leads to the adverse effect of NRG1,and explored a new method to inhibit the fibrogenic function of macrophages.However,the efficacy of this method needs to be verified in further animal experiments.