[Objectives] To study the anti-inflammatory activity and mechanism of salvianolic acid A(Sal A), salvianolic acid C(Sal C), and rosmarinic acid(RA) on HAECs induced by TNF-α. [Methods] VE was used as a positive contr...[Objectives] To study the anti-inflammatory activity and mechanism of salvianolic acid A(Sal A), salvianolic acid C(Sal C), and rosmarinic acid(RA) on HAECs induced by TNF-α. [Methods] VE was used as a positive control and TNF-α induced human aortic endothelial cells(HAECs) were selected as the inflammation model cells. The levels of IL-6, MCP-1 were determined using ELISA. The mRNA levels of IL-6, MCP-1, ICAM-1, P-selectin and NF-κB were analyzed by quantitative RT-PCR. The protein expression of NF-κB was determined by western blot. The adhesion of U937 to HAECs was assessed by BCECF/AM labeling assay. Immunohistochemistry detection was used for ICAM-1 and P-selectin expression levels in TNF-induced HAECs, and DHE detection for the ROS production in HAECs induced by TNF-α. [Results] TNF-α-induced over-expressions of IL-6, MCP-1, NF-κB, ICAM-1 and P-selectin in HAECs were down-regulated by Sal A, Sal C and RA both in mRNA or protein levels, respectively. Meanwhile Sal A, Sal C and RA could significantly inhibit the production of ROS and U937 cells adhesion to HAECs. [Conclusions] Phenolic acids could inhibit TNF-α-induced inflammatory responses on HAECs and the mechanism might be related to inhibition of the production of ROS and blocking NF-κB signaling pathway.展开更多
[Objectives] To study the anti-inflammatory activity and mechanism of tanshinone I,cryptotanshinone and 15,16-dihydrotanshinone I on HAECs induced by TNF-α. [Methods]Vitamin E was used as a positive control and TNF-...[Objectives] To study the anti-inflammatory activity and mechanism of tanshinone I,cryptotanshinone and 15,16-dihydrotanshinone I on HAECs induced by TNF-α. [Methods]Vitamin E was used as a positive control and TNF-α-induced human aortic endothelial cells( HAECs) were selected as the inflammation model cells. The m RNA levels of IL-6,ICAM-1,VCAM-1,and NF-κB were analyzed by quantitative RT-PCR. The protein expression of NF-κB,ICAM-1,VCAM-1 and phosphorylation of ERK1/2 were determined by Western blot. The adhesion of U937 to HAECs was assessed by BCECF/AM labeling assay. [Results] TNF-α-induced over-expression of IL-6,NF-κB,ICAM-1,and VCAM-1 in HAECs were down-regulated by tanshinone I( TAN),cryptotanshinone( CPT) and 15,16-dihydrotanshinone I( DHT) both in m RNA and protein levels,respectively. Meanwhile 15,16-dihydrotanshinone I and cryptotanshinone could inhibit phosphorylation of ERK1/2 and tanshinone I inhibited U937 adhesion to HAECs significantly. [Conclusions] Tanshinones could inhibit TNF-α induced inflammatory responses on HAECs and the mechanism might be related to inhibition of phosphorylation of ERK1/2 and blocking NF-κB signaling pathway.展开更多
基金Supported by the National Natural Science Foundation of China(81274031)
文摘[Objectives] To study the anti-inflammatory activity and mechanism of salvianolic acid A(Sal A), salvianolic acid C(Sal C), and rosmarinic acid(RA) on HAECs induced by TNF-α. [Methods] VE was used as a positive control and TNF-α induced human aortic endothelial cells(HAECs) were selected as the inflammation model cells. The levels of IL-6, MCP-1 were determined using ELISA. The mRNA levels of IL-6, MCP-1, ICAM-1, P-selectin and NF-κB were analyzed by quantitative RT-PCR. The protein expression of NF-κB was determined by western blot. The adhesion of U937 to HAECs was assessed by BCECF/AM labeling assay. Immunohistochemistry detection was used for ICAM-1 and P-selectin expression levels in TNF-induced HAECs, and DHE detection for the ROS production in HAECs induced by TNF-α. [Results] TNF-α-induced over-expressions of IL-6, MCP-1, NF-κB, ICAM-1 and P-selectin in HAECs were down-regulated by Sal A, Sal C and RA both in mRNA or protein levels, respectively. Meanwhile Sal A, Sal C and RA could significantly inhibit the production of ROS and U937 cells adhesion to HAECs. [Conclusions] Phenolic acids could inhibit TNF-α-induced inflammatory responses on HAECs and the mechanism might be related to inhibition of the production of ROS and blocking NF-κB signaling pathway.
基金Supported by the National Natural Science Foundation of China(81274031)
文摘[Objectives] To study the anti-inflammatory activity and mechanism of tanshinone I,cryptotanshinone and 15,16-dihydrotanshinone I on HAECs induced by TNF-α. [Methods]Vitamin E was used as a positive control and TNF-α-induced human aortic endothelial cells( HAECs) were selected as the inflammation model cells. The m RNA levels of IL-6,ICAM-1,VCAM-1,and NF-κB were analyzed by quantitative RT-PCR. The protein expression of NF-κB,ICAM-1,VCAM-1 and phosphorylation of ERK1/2 were determined by Western blot. The adhesion of U937 to HAECs was assessed by BCECF/AM labeling assay. [Results] TNF-α-induced over-expression of IL-6,NF-κB,ICAM-1,and VCAM-1 in HAECs were down-regulated by tanshinone I( TAN),cryptotanshinone( CPT) and 15,16-dihydrotanshinone I( DHT) both in m RNA and protein levels,respectively. Meanwhile 15,16-dihydrotanshinone I and cryptotanshinone could inhibit phosphorylation of ERK1/2 and tanshinone I inhibited U937 adhesion to HAECs significantly. [Conclusions] Tanshinones could inhibit TNF-α induced inflammatory responses on HAECs and the mechanism might be related to inhibition of phosphorylation of ERK1/2 and blocking NF-κB signaling pathway.
