[Cinnamaldehyde attenuates lipopolysaccharide induced inflammation and apoptosis in human umbilical vein endothelial cells].

Objective: To investigate the effect of cinnamaldehyde (CIN) on the inflammation and apoptosis on human umbilical vein endothelial cells (HUVECs) induced by lipopolysaccharide (LPS), and to explore the potential mechanisms. Methods: HUVECs were divided in to 8 groups: blank control group, LPS group, LPS+(low, medium, high) dose CIN groups and (low, medium, high) CIN groups. Cell cytotoxicity was determined by trypan blue staining, mRNA expression of the inflammatory factors was determined by RT-PCR,apoptosis was determined by TUNEL staining,the signal pathway was determined by Western blot. Results: (1) Cell viability:compared with the control group,cell survival rate was significantly lower in the LPS group (P<0.01), while the survival rates were all significantly higher in the 3 LPS+CIN groups than in the LPS group (all P<0.01) in a concentration-dependent manner. (2) The mRNA expression of the inflammation factors: compared with the control group, mRNA expression of the inflammation factors were all increased in the LPS group (all P<0.01),while the effect of LPS could be significantly reversed by cotreatment with CIN in a concentration-dependent manner (all P<0.01). Compared with control group, the mRNA expression of the inflammation factors in the LPS group were all enhanced in a time-dependent manner (0,6,12,24 h),which could be significantly downregulated by cotreatment with LPS+CIN (high dose) in a time-dependent manner. (3) Cell apoptosis: compared with the control group, the apoptosis rate was significantly higher in the LPS group (P<0.01), while this effect could be significantly reversed by the cotreatment with CIN (high dose) (P<0.01). (4) Signaling pathway: compared with the control group, the phosphorylation of iκBα, p65 in HUVECs treated with LPS were rapidly up-regulated compared with their corresponding total proteins and the expression of TLR4 (all P<0.01), while the degree of p-iκBα/iκBα, p-p65/p65 and TLR4 could be significantly suppressed by cotreatment with CIN (high dose) (all P<0.01). Conclusion: CIN can attenuate LPS induced inflammation and apoptosis in HUVECs, possibly by inhibiting the activation of NF-κB signaling pathway.