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Sinomenine inhibits TNF-α-induced VCAM-1 expression on human umbilical vein endothelial cells

Buyun Yu

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Abstract

AIM: To investigate whether sinomenine(SN) can decrease TNF-α-induced VCAM-1 expression in human umbilical vein endothelial cells(HUVECs).METHODS: HUVECs were isolated from freshly collected umbilical cords.Positive control samples were stimulated with TNF-α,omitting SN.Negative control samples were treated in the same way,omitting TNF-α and SN.Experiment samples were co-cultured with TNF-α and SN at different concentration(0.25,0.5,and 1.0 mol/L),or TNF-α and dexamethasone(Dex) at concentration of 1.0×10-6mol/L.Cells were harvested after cultivation with the drugs for 12 hours.VCAM-1 mRNA expression was detected by real-time quantitative PCR,and VCAM-1 expression was detected by flow cytometry(FCM).RESULTS: VCAM-1 mRNA and VCAM-1 were induced by TNF-α.Compared with the positives,the relative VCAM-1 mRNA expression decreased to varying degrees in the experiment groups(P0.05),and SN at concentration of 0.5 mol/L and 1.0 mol/L inhibited expression of VCAM-1(P0.05).SN at concentration of 1.0 mol/L decreased VCAM-1 expression by 28.8%(P0.05),and SN at concentration of 0.5 mol/L reduced VCAM-1 expression by 21.68%(P0.05).But SN at concentration of 0.25 mol/L and Dex at concentration of 1.0×10-6mol/L didn't depress expression of VCAM-1.CONCLUSION: SN may inhibit TNF-α-induced VCAM-1 expression in HUVECs in vitro.

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AIM: To investigate whether sinomenine(SN) can decrease TNF-α-induced VCAM-1 expression in human umbilical vein endothelial cells(HUVECs).METHODS: HUVECs were isolated from freshly collected umbilical cords.Positive control samples were stimulated with TNF-α,omitting SN.Negative control samples were treated in the same way,omitting TNF-α and SN.Experiment samples were co-cultured with TNF-α and SN at different concentration(0.25,0.5,and 1.0 mol/L),or TNF-α and dexamethasone(Dex) at concentration of 1.0×10-6mol/L.Cells were harvested after cultivation with the drugs for 12 hours.VCAM-1 mRNA expression was detected by real-time quantitative PCR,and VCAM-1 expression was detected by flow cytometry(FCM).RESULTS: VCAM-1 mRNA and VCAM-1 were induced by TNF-α.Compared with the positives,the relative VCAM-1 mRNA expression decreased to varying degrees in the experiment groups(P0.05),and SN at concentration of 0.5 mol/L and 1.0 mol/L inhibited expression of VCAM-1(P0.05).SN at concentration of 1.0 mol/L decreased VCAM-1 expression by 28.8%(P0.05),and SN at concentration of 0.5 mol/L reduced VCAM-1 expression by 21.68%(P0.05).But SN at concentration of 0.25 mol/L and Dex at concentration of 1.0×10-6mol/L didn't depress expression of VCAM-1.CONCLUSION: SN may inhibit TNF-α-induced VCAM-1 expression in HUVECs in vitro.

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Available abstract

AIM: To investigate whether sinomenine(SN) can decrease TNF-α-induced VCAM-1 expression in human umbilical vein endothelial cells(HUVECs).METHODS: HUVECs were isolated from freshly collected umbilical cords.Positive control samples were stimulated with TNF-α,omitting SN.Negative control samples were treated in the same way,omitting TNF-α and SN.Experiment samples were co-cultured with TNF-α and SN at different concentration(0.25,0.5,and 1.0 mol/L),or TNF-α and dexamethasone(Dex) at concentration of 1.0×10-6mol/L.Cells were harvested after cultivation with the drugs for 12 hours.VCAM-1 mRNA expression was detected by real-time quantitative PCR,and VCAM-1 expression was detected by flow cytometry(FCM).RESULTS: VCAM-1 mRNA and VCAM-1 were induced by TNF-α.Compared with the positives,the relative VCAM-1 mRNA expression decreased to varying degrees in the experiment groups(P0.05),and SN at concentration of 0.5 mol/L and 1.0 mol/L inhibited expression of VCAM-1(P0.05).SN at concentration of 1.0 mol/L decreased VCAM-1 expression by 28.8%(P0.05),and SN at concentration of 0.5 mol/L reduced VCAM-1 expression by 21.68%(P0.05).But SN at concentration of 0.25 mol/L and Dex at concentration of 1.0×10-6mol/L didn't depress expression of VCAM-1.CONCLUSION: SN may inhibit TNF-α-induced VCAM-1 expression in HUVECs in vitro.

Key concepts: Umbilical vein, Sinomenine, VCAM-1, Tumor necrosis factor alpha, Messenger RNA, Dexamethasone, Flow cytometry, Molecular biology

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