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Triptolide inhibits proinflammatory factor-induced over-expression of class II MHC and B7 molecules in renal tubular epithelial cells.

  
@article{APS7744,
	author = {Heng LI and Zhi-Hong LIU and Chun-Ssun DAI and Dong LIU and Lei-Shi LI},
	title = {Triptolide inhibits proinflammatory factor-induced over-expression of class II MHC and B7 molecules in renal tubular epithelial cells.},
	journal = {Acta Pharmacologica Sinica},
	volume = {23},
	number = {9},
	year = {2016},
	keywords = {},
	abstract = {AIM: To investigate the effects of triptolide on proinflammatory factor-induced
over-expression of class II major histocompatibility complex (class II MHC),
B7-1, B7-2, and intercellular adhesion molecule-1 (ICAM-1) in human proximal
tubular epithelial (HKC) cells.
METHODS: HKC cells were exposed to both interferon gamma (IFN-gamma, 200
microg/L) and tumor necrosis factor alpha (TNF-alpha, 20 microg/L) and cultured
in media containing different concentrations of triptolide for 24 h. Class II
MHC, B7-1, B7-2, and ICAM-1 levels in HKC cells were evaluated by flow cytometry.
ICAM-1 mRNA level was measured by semi-quantitative RT-PCR method.
RESULTS: HKC cells expressed quite high level of ICAM-1 and very low levels of
class II MHC, B7-1, and B7-2 molecules. Class II MHC, B7-1, B7-2, and ICAM-1
levels in HKC cells were significantly increased by the costimulation of
IFN-gamma and TNF-alpha. Triptolide inhibited the over-expression of class II
MHC, B7-1, and B7-2 molecules in a concentration-dependent manner. The
up-regulations of ICAM-1 molecules and ICAM-1 mRNA level were not altered by
triptolide.
CONCLUSION: Triptolide can significantly inhibit proinflammatory factors induced 
over-expression of class II MHC, B7-1, and B7-2 costimulatory factors in tubular 
epithelial cells. These results may contribute to the therapeutic effects of
triptolide in some renal diseases.},
	issn = {1745-7254},	url = {http://www.chinaphar.com/article/view/7744}
}