The chemical biology of low side effects compound in anti-fever drugs, which is derived from the analysis about fatal function by diclofenac.

为了阐明双氯芬酸诱导流感脑炎的机制，我们研究了流感病毒和双氯芬酸对体外培养的人血管内皮细胞紧密连接（TJ）的破坏作用。在这项研究中，我们发现，流感病毒诱导TJ蛋白，如ZO 1的降解，导致其中断。另一方面，双氯芬酸本身抑制TJ蛋白的合成，从而加速血管内皮细胞中流感病毒感染诱导的TJ破坏。

To clarify the mechanisms of influenza encephalitis induced by diclofenac, we examined the effect of influenza virus and diclofenac on the disruption of tight junction (TJ) in human vascular endothelial cells in vitro. In this study, we found that influenza virus induced the degradation of TJ proteins, such as ZO1, leading to its disruption. On the other hands, diclofenac by itself inhibited the synthesis of TJ proteins, consequently accelerating the disruption of TJ induced by influenza infection in vascular endothelial cells.