Cryptotanshinone inhibits TNF-α-induced early atherogenic events in vitro

被引:33
作者
Ahmad, Zuraini [1 ]
Ng, Chin Theng [1 ]
Fong, Lai Yen [1 ]
Abu Bakar, Nurul Ain [1 ]
Hussain, Nor Hayuti Mohd [1 ]
Ang, Kok Pian [1 ]
Ee, Gwendoline Cheng Lian [2 ]
Hakim, Muhammad Nazrul [1 ]
机构
[1] Univ Putra Malaysia, Fac Med & Hlth Sci, Dept Biomed Sci, Serdang 43400, Selangor, Malaysia
[2] Univ Putra Malaysia, Fac Sci, Dept Chem, Serdang 43400, Selangor, Malaysia
关键词
Cryptotanshinone; Nitric oxide; Soluble cellular adhesion molecule; TNF-alpha; Monocyte adhesion; Chemokine; MONOCYTE CHEMOATTRACTANT PROTEIN-1; NITRIC-OXIDE SYNTHASE; NECROSIS-FACTOR-ALPHA; SALVIA-MILTIORRHIZA; MYOCARDIAL ISCHEMIA/REPERFUSION; ADHESION MOLECULES; EXPRESSION; ATHEROSCLEROSIS; MACROPHAGE; COMPOUND;
D O I
10.1007/s12576-015-0410-7
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Endothelial dysfunction has been implicated in the pathogenesis of atherosclerosis. Salvia miltiorrhiza (danshen) is a traditional Chinese medicine that has been effectively used to treat cardiovascular disease. Cryptotanshinone (CTS), a major lipophilic compound isolated from S. miltiorrhiza, has been reported to possess cardioprotective effects. However, the anti-atherogenic effects of CTS, particularly on tumor necrosis factor-alpha (TNF-alpha)-induced endothelial cell activation, are still unclear. This study aimed to determine the effect of CTS on TNF-alpha-induced increased endothelial permeability, monocyte adhesion, soluble intercellular adhesion molecule 1 (sICAM-1), soluble vascular cell adhesion molecule 1 (sVCAM-1), monocyte chemoattractant protein 1 (MCP-1) and impaired nitric oxide production in human umbilical vein endothelial cells (HUVECs), all of which are early events occurring in atherogenesis. We showed that CTS significantly suppressed TNF-alpha-induced increased endothelial permeability, monocyte adhesion, sICAM-1, sVCAM-1 and MCP-1, and restored nitric oxide production. These observations suggest that CTS possesses anti-inflammatory properties and could be a promising treatment for the prevention of cytokine-induced early atherogenesis.
引用
收藏
页码:213 / 220
页数:8
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