Cryptotanshinone inhibits TNF-α-induced LOX-1 expression by suppressing reactive oxygen species (ROS) formation in endothelial cells
The Korean Journal of Physiology and Pharmacology
; : 347-355, 2016.
Article
en En
| WPRIM
| ID: wpr-728437
Biblioteca responsable:
WPRO
ABSTRACT
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-α) 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-α 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-DCFH2-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-α induced LOX-1 expression in a dose- and time-dependent manner in endothelial cells. TNF-α induced ROS formation, phosphorylation of NF-κB p65 and ERK, and LOX-1 expression, which were suppressed by rotenone, DPI, NAC, and CPT. NF-κB inhibitor BAY11-7082 and ERK inhibitor PD98059 inhibited TNF-α-induced LOX-1 expression. CPT and NAC suppressed TNF-α-induced LOX-1 expression and phosphorylation of NF-κB p65 and ERK in rat aorta. These data suggested that TNF-α induced LOX-1 expression via ROS activated NF-κB/ERK pathway, which could be inhibited by CPT. This study provides new insights for the anti-atherosclerotic effect of CPT.
Texto completo:
1
Índice:
WPRIM
Asunto principal:
Aorta
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Fosforilación
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Rotenona
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ARN Mensajero
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Western Blotting
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Factor de Necrosis Tumoral alfa
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Especies Reactivas de Oxígeno
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Salvia miltiorrhiza
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Células Endoteliales
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Células Endoteliales de la Vena Umbilical Humana
Tipo de estudio:
Diagnostic_studies
Límite:
Animals
Idioma:
En
Revista:
The Korean Journal of Physiology and Pharmacology
Año:
2016
Tipo del documento:
Article