Subsequent inflammation in stroke plays an important role in the damage of neurons in the perilesional area. Therapeutic intervention targeting inflammation may be a promising complementary strategy to current treatments of stroke. Here, we explored the possible beneficial effects of tyrosol, a derivative of phenethyl alcohol and natural antioxidant, playing an anti-inflammatory role in astrocyte culture and in vitro oxygen glucose deprivation (OGD) model. MTT, western blot, ELISA and EMSA assays were carried out to investigate cell viability, protein expression level, cytokine expression and NF-κB activity. We found tyrosol protected cultured astrocytes against OGD-induced cell viability loss in MTT test. Meanwhile, tyrosol attenuated the released TNF-α and IL-6 level from astrocyte via regulating Janus N-terminal kinase (JNK). The reduction of cytokines from astrocyte might be due to its inhibition of astrocyte activation and regulation of STAT3 signaling pathway since tyrosol attenuated the expression level of GFAP (glial fibrillary acidic protein) and the phosphorylation of STAT3. Additionally, we demonstrated that tyrosol prevented the degradation of IκBα and the increase of IκBα phosphorylation in astrocytes exposed to OGD, which led to the suppression of NF-κB function during ischemia. Collectively, our results showed that tyrosol may be a promising complementary treatment compound for stroke via modulating the inflammatory response in astrocytes during ischemia.

随后的中风发炎在病变周围区域神经元的损伤中起重要作用。针对炎症的治疗干预可能是当前中风治疗的有前途的补充策略。在这里，我们探讨了苯乙醇和天然抗氧化剂的衍生物酪氨醇在星形胶质细胞培养和体外起抗炎作用的可能的有益作用。氧葡萄糖剥夺（OGD）模型。进行了MTT，蛋白质印迹，ELISA和EMSA分析，以研究细胞活力，蛋白质表达水平，细胞因子表达和NF-κB活性。我们在MTT试验中发现了酪氨酸保护的星形胶质细胞免受OGD诱导的细胞活力丧失。同时，酪醇通过调节Janus N端激酶（JNK）减弱了星形胶质细胞释放的TNF-α和IL-6水平。来自星形胶质细胞的细胞因子的减少可能是由于其抑制星形胶质细胞的活化和STAT3信号通路的调节，因为酪醇降低了GFAP（胶质纤维酸性蛋白）的表达水平和STAT3的磷酸化。此外，我们证明了酪醇可防止暴露于OGD的星形胶质细胞中IκBα的降解和IκBα磷酸化的增加，导致缺血期间NF-κB功能受到抑制。总体而言，我们的结果表明，酪氨酸可能通过调节缺血过程中星形胶质细胞的炎症反应而成为中风的有希望的补充治疗化合物。