RESUMO
Human umbilical vein endothelial cells (HUVECs) serve a critical role in maintaining normal vascular function. Lipopolysaccharide (LPS), which is released from pathogenic bacteria in the blood, induces HUVEC apoptosis and injury to cause vascular dysfunction and infectious vascular diseases. Procyanidin B2 (PB2) possesses numerous functions, including antioxidant, antitumor, antiinflammatory and antiapoptosis effects, but the molecular mechanism is not completely understood. The present study investigated the effects of PB2 on LPSinduced cytotoxicity and apoptosis in HUVECs, as well as the underlying mechanisms. The effects of PB2 on LPSmediated alterations to cytotoxicity, mitochondrial membrane potential, apoptosis were assessed by performing Cell Counting Kit8, JC1 fluorescence, Hoechst 33258 staining assays, respectively. IL1ß, IL6 and TNFα mRNA expression and protein levels were measured by performing reverse transcriptionquantitative PCR and ELISAs, respectively. Bcl2, Bax, cleaved caspase3, cleaved caspase7, cleaved caspase9, phosphorylated (p)IκBα, pIκBß, pNFκBp65 and total NFκB p65 protein expression levels were determined via western blotting. NFκB p65 nuclear translocation was assessed via immunofluorescence. PB2 pretreatment markedly attenuated LPSinduced cytotoxicity and apoptosis in HUVECs. PB2 also significantly downregulated the expression levels of IL1ß, IL6, TNFα, Bax, cleaved caspase3, cleaved caspase7, cleaved caspase9 and pNFκBp65, but upregulated the expression levels of Bcl2, pIκBα and pIκBß in LPSinduced HUVECs. Moreover, PB2 markedly inhibited LPSinduced NFκB p65 nuclear translocation in HUVECs. The results suggested that the potential molecular mechanism underlying PB2 was associated with the Bax/Bcl2 and NFκB signalling pathways. Therefore, PB2 may serve as a useful therapeutic for infectious vascular diseases.