Protection of curcumin against tumor necrotic factor-alpha-mediated inflammatory injury of vascular endothelial cells / 中国组织工程研究

ABSTRACT

BACKGROUND:Previous studies have shown that, curcumin plays a crucial role on the inflammation in cells caused by oxidative stress. OBJECTIVE:To elucidate the biological effect and mechanism of curcumin in the pathological inflammation reaction in vascular endothelial cells. METHODHuman vascular endothelial cells were taken as the cellmodels. Tumor necrosis factor (10μg/L) treatment was used to induce the inflammation of cells. Curcumin (0, 50, 100μg/L) treatment for 24 hours was used to intervene the cells. The intercellular hyperpermeability of the vascular endothelial cellmonolayers was examined by HRP-conjugated bovine serum albumin, and intercellular filamentous actin stress fiber formation was examined by rhodamin-phal oidin staining. ELISA assay was used to detect the secretion of interleukin-1βin vascular endothelial cells. Immunoflurensece staining was applied to investigate the expression and translocalization of nuclear factor-κB. Western blot analysis reflected the expression of NRLP3 and caspase-1. RESULTS AND CONCLUSION:HRP-bovine serum albumin detection results showed that, curcumin inhibited the intercellular hyperpermeability of the vascular endothelial cellmonolayers and the formation of robust intercellular filamentous actin in a dose-dependent manner. ELISA assay showed that curcumin protected vascular endothelial cells against tumor necrotic factor-α-induced interleukin-1βsecretion in a dose-dependent manner. Meanwhile, the nuclear factor-κB expression was increased and the translocation of nuclear factor-κB into the nuclei was obviously seen in vascular endothelial cells induced by tumor necrosis factor-α, but the translocation was not changed in 100μg/L curcumin-treated cells. Furthermore, western blot analysis revealed that the expression of NRLP3 and caspase-1 were inhibited in curcumin-treated cells. Curcumin can inhibit tumor necrosis factor-α-induced activation of inflammasome and secretion of interleukin-1βin vascular endothelial cells by down-regulating the expression of nuclear factor-κB, thus prevent pathological inflammatory injury in cells.