Tetramethylpyrazine alleviates LPS-induced inflammatory injury in HUVECs by inhibiting Rho/ROCK pathway.

Abstract

Endothelial dysfunction plays an important role in the pathogenesis of acute lung injury (ALI). Tetramethylpyrazine (TMP) has been reported to attenuate harmful changes in ALI rats. However, the effects of TMP on endothelial cell injury and its underlying mechanisms remain unknown. In this study, human umbilical vein endothelial cells (HUVECs) induced by lipopolysaccharide (LPS) was used as an inflammatory injury model, also served as LPS group. HUVECs pretreated with TMP for 2\xa0h before induced by LPS was served as LPS\xa0+\xa0TMP group. Untreated HUVECs was served as control group. After incubation with LPS for 12\xa0h, cell viability and morphology, cell apoptosis rate, CD31-positive endothelial microparticles (EMPs) release, proinflammatory cytokines secretion, and ROCK II expression were evaluated. Compared with LPS group, TMP pretreatment improved cell viability and morphology. Besides, cell apoptosis rate, CD31-positive EMPs amount, TNF-α and IL-1β concentrates, and ROCK II mRNA and protein levels in LPS\xa0+\xa0TMP group were significantly decreased when compared with LPS group. To further confirm the mechanism, HUVECs in all the above groups were pretreated with Y27632 (ROCK II inhibitor) for 30\xa0min before grouping, then treated as above. No significant differences in cell apoptosis rate, CD31-positive EMPs amount, and ROCK II expression between Y27632\xa0+\xa0LPS group and Y27632\xa0+\xa0LPS\xa0+\xa0TMP group were found. To sum up, our study found that TMP alleviated LPS-induced inflammatory injury in HUVECs by inhibiting Rho/ROCK pathway.