Eupatilin attenuates the inflammatory response induced by intracerebral hemorrhage through the TLR4/MyD88 pathway

Background: Intracranial hemorrhage (ICH) is one of the most common brain traumas, and inflammation caused by ICH seriously affects the quality of life and prognosis of patients. Eupatilin has been shown to have anti-inflammatory effects in various diseases. However, only one paper has reported that Eupatilin has a therapeutic effect on the inflammatory response caused by ICH and the underlying mechanism needs to be studied. Methods: We used erythrocyte lysis stimulation (ELS) to induce mouse microglia BV2 as the inflammation model. CCK-8 and Transwell assays were used to detect cell viability and migration. RT-PCR, western blotting, and ELISA were used to detect the secretion of inflammatory factors and the expression of related mechanism proteins. HE staining was used to detect cell edema and death. Result: We found that ELS significantly increased protein and mRNA levels and secretion of inflammatory factors IL-1 beta and TNF-alpha, which Eupatilin attenuated through the Toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88) pathway. The anti-inflammatory effect of Eupatilin was significantly attenuated after siRNA was used to reduce TLR4 expression. The experimental results and mechanism were also verified in TLR4 knockout mice in vivo. Conclusion: Eupatilin has a therapeutic effect on inflammation caused by ICH. The underlying mechanism may be related to TLR4/MyD88, which brings new hope for clinical patients to improve symptoms and prognosis.