Eupatilin inhibits microglia activation and attenuates brain injury in intracerebral hemorrhage

Abstract

Inflammation serves a critical role in the pathophysiology of intracerebral hemorrhage (ICH)-induced brain injury. Eupatilin, a pharmacologically active flavone derived from Artemisia sp., has been reported to have antioxidant, anti-inflammatory, anti-allergic and antitumor activities. However, the effect of eupatilin in ICH has not been well studied. The aim of the present study was to investigate the effect of eupatilin on ICH-induced microglial inflammation. The MTT and Transwell migration assay results revealed that eupatilin significantly inhibited microglial migration. It also decreased the production of inflammatory cytokines in erythrocyte lysis-induced BV2 cells, as well as the level of intracellular reactive oxygen species. The anti-inflammatory mechanism of eupatilin was also investigated using ELISAs and western blotting and the results demonstrated that eupatilin was able to inhibit erythrocyte lysis-induced NF-κB activation in BV2 cells. Taken together, the results of the present study suggest that eupatilin serves neurological protective effects via inhibiting microglial inflammation, providing an experimental basis for the use of eupatilin as a therapeutic target for ICH.

Based on Microglial Polarization and Autophagy Activity After Intracerebral Hemorrhage Exploring the Anti-Injury-Promoting Repair Effect of Traditional Chinese Medicine Intervention Research Progress of Dual Action Mechanism

“…CaiWait [41]Using Shengdi Dahuang Decoction to interfere with collagenase induced cerebral hemorrhage in a rat model, it was found that Shengdi Dahuang Decoction could reduce the expression of microglia around the cerebral hemorrhage, thereby reducing inflammatory factors.NF-κB,TNF-alphaand IL-1betarelease and improve the inflammatory response.QiaoWait [42]The study found that Artemisia annua extract iszelanflavin can inhibit the migration of microglia and reduce the lysis-induced red blood cell lysis.BV2inflammatory cytokines in cells NF-κB production and intracellular reactive oxygen species levels. Lan Wait [16] Fibrocystin was found to reduce classically activated M1number of microglia, but did not affect theM2the number of microglia; M1relatedTNF-alpha, IL-1beta, IL-6, iNOSdown-regulation of inflammatory substances, andTLR4pathway inhibition.…”

Microglia Phenotype and Intracerebral Hemorrhage: A Balance of Yin and Yang

“…Of course, increasing the M2/M1 phenotypic proportion of microglia usually brings more satisfactory results (Wang J. et al, 2018 ; Bai et al, 2020 ), and it has become the most frequently studied therapeutic method. Relying on the aforementioned targets, experimental therapeutic studies on the precise regulation on microglia phenotype are developing rapidly, and relevant drugs are summarized in Table 3 (Hu et al, 2011 ; Ohnishi et al, 2013 , 2019 ; Yang et al, 2014a , b , 2018 ; Iniaghe et al, 2015 ; Zhao et al, 2015a , b , 2018 ; Flores et al, 2016 ; Shi et al, 2016 ; Sukumari-Ramesh and Alleyne, 2016 ; Zhang et al, 2016 ; Anan et al, 2017 ; Chen-Roetling and Regan, 2017 ; Lan et al, 2017a ; Wang J. et al, 2017 ; Wei et al, 2017 ; Xu et al, 2017 ; Zeng et al, 2017 ; Chen C. et al, 2018 ; Chen S. et al, 2018 ; Fu et al, 2018 ; Han et al, 2018 ; Li X. et al, 2018 ; Qiao et al, 2018 ; Ren et al, 2018 ; Wang et al, 2018b ; Liang et al, 2019 ; Song and Zhang, 2019 ; Xi et al, 2019 ; Zhou F. et al, 2019 ; Cheng et al, 2020 ; Ding et al, 2020 ).…”

LncRNA TCONS_00145741 Knockdown Prevents Thrombin-Induced M1 Differentiation of Microglia in Intracerebral Hemorrhage by Enhancing the Interaction Between DUSP6 and JNK

“…Microglia are widely recognized as the earliest inflammatory cells that respond to ICH ( Wang, 2010 ; Yang et al, 2015a ). Cumulative research clarifies that microglia differentiation exerts pivotal functions in the pathogenesis and progression of ICH ( Qiao et al, 2018 ; Giordano et al, 2020 ). Upon activation, microglia polarize into different phenotypes that contribute differently to neuroinflammation in brain disease models ( Walker and Lue, 2015 ).…”