Effect of three chemical molecules on adhesion molecules expression in HMECs induced by activated complement alternative pathway
10.3969/j.issn.1001-1978.2015.10.019
- VernacularTitle:三种化学小分子对补体旁路激活致内皮细胞黏附分子表达的干预及机制研究
- Author:
Chaosheng LI
;
Qianyun SUN
- Publication Type:Journal Article
- Keywords:
complement;
complement alternative path-way ( activation );
endothelial cell;
adhesion molecule;
resveratrol;
inflammation;
cobra venom factor
- From:
Chinese Pharmacological Bulletin
2015;(10):1421-1425,1426
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate the effect of resveratrol ( Res) , PDTC and AG490 on adhesion molecules ex-pression induced by product of activated complement alternative pathway on human microvascular endothelial cells ( HMECs) and the possible mechanisms. Meth-ods HMECs were exposed to the product of comple-ment alternative pathway activation, then the superna-tant was removed to detect the concentration of malond-ialdehyde ( MDA ) with TBA method. ELISA method was used to detect the expression of soluble ICAM-1 , VCAM-1 ( and E-selectin) in the culture supernatant. Res, PDTC and AG490 with different concentrations were used to determine their effect on cell oxidation level and adhesion molecules expression. The phospho-rylation of NF-κB p65 was detected by Western blot, and the intervention of Res, PDTC and AG490 was as-sayed by the same way. Results The activation of complements alternative pathway resulted in the phos-phorylation of NF-κB p65 , and increased the concen-tration of MDA and up-regulated the expression of ICAM-1, VCAM-1 and E-selectin. Res reduced the concentration of MDA. Res, PDTC and AG490 inhibi-ted the phosphorylation of NF-κB p65 . Res and PDTC showed similar inhibition on expression of ICAM-1 and VCAM-1 , while exhibiting little effect on expression of E-selectin, and AG490 significantly inhibited the ex-pression of the above adhesion molecules. Conclusions Res, PDTC and AG490 could inhibit the expression of adhesion molecules induced by activated complement alternative pathway, the inhibition of NF-κB pathway activation was involved in their mechanism, and JAK2 may be a more important intervention target in regula-ting adhesion molecule expression.
