| 저자(한글) |
Ran, Xiaoli,Zhao, Wenwen,Li, Wenping,Shi, Jingshan,Chen, Xiuping |
| 저자(영문) |
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| 소속기관 |
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| 소속기관(영문) |
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| 출판인 |
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| 간행물 번호 |
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| 발행연도 |
2016-01-01 |
| 초록 |
Cryptotanshinone (CPT) is a natural compound isolated from traditional Chinese medicine Salvia miltiorrhiza Bunge. In the present study, the regulatory effect and potential mechanisms of CPT on tumor necrosis factor alpha ( $TNF-{ alpha}$ ) induced lectin-like receptor for oxidized low density lipoprotein (LOX-1) were investigated. Human umbilical vein endothelial cells (HUVECs) were cultured and the effect of $TNF-{ alpha}$ on LOX-1 expression at mRNA and protein levels was determined by Real-time PCR and Western blotting respectively. The formation of intracellular ROS was determined with fluorescence probe $CM-DCFH_2-DA$ . The endothelial ox-LDL uptake was evaluated with DiI-ox-LDL. The effect of CPT on LOX-1 expression was also evaluated with SD rats. $TNF-{ alpha}$ induced LOX-1 expression in a dose- and time- dependent manner in endothelial cells. $TNF-{ alpha}$ induced ROS formation, phosphorylation of $NF-{ kappa}B$ p65 and ERK, and LOX-1 expression, which were suppressed by rotenone, DPI, NAC, and CPT. $NF-{ kappa}B$ inhibitor BAY11-7082 and ERK inhibitor PD98059 inhibited $TNF-{ alpha}-induced$ LOX-1 expression. CPT and NAC suppressed $TNF-{ alpha}-induced$ LOX-1 expression and phosphorylation of $NF-{ kappa}B$ p65 and ERK in rat aorta. These data suggested that $TNF-{ alpha}$ induced LOX-1 expression via ROS activated $NF-{ kappa}B/ERK$ pathway, which could be inhibited by CPT. This study provides new insights for the anti-atherosclerotic effect of CPT. |
| 원문URL |
http://click.ndsl.kr/servlet/OpenAPIDetailView?keyValue=03553784&target=NART&cn=JAKO201620340965334 |
| 첨부파일 |
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