Curcumin inhibits TNFα-induced lectin-like oxidised LDL receptor-1 (LOX-1) expression and suppresses the inflammatory response in human umbilical vein endothelial cells (HUVECs) by an antioxidant mechanism

Abstract

In this study, the anti-oxidative activities of 70% ethanol extract from Curcuma aromatica Salisb. (CAS) and curcumin (CUR) were studied. The CAS extracts and CUR were both found to have a potent scavenging activity against the reactive species tested, as well as an inhibitory effect on LDL oxidation. Cultured human umbilical vein endothelial cells (HUVECs) were stimulated with tumour necrosis factor alpha (TNFalpha), expression of intracellular reactive oxygen species (ROS), nitric oxide (NO), endothelial nitric oxide synthase (eNOS), lectin-like oxidised LDL receptor-1 (LOX-1), adhesion molecules, inhibitory kappa Balpha (IkappaBalpha) and nuclear factor kappa B (NFkappaB) were measured. In HUVECs stimulated with TNFalpha, CUR significantly suppressed expression of the intracellular ROS, LOX-1 and adhesion molecules, degradation of IkappaBalpha and translocation of NFkappaB, while inducing production of NO by phosphorylation of eNOS (p <0.05). In conclusion, CAS and CUR may modulate lipoprotein composition and attenuate oxidative stress by elevated antioxidant processes.

Sulforaphane Inhibits TNF-α-Induced Adhesion Molecule Expression Through the Rho A/ROCK/NF-κB Signaling Pathway

“…47 Curcumin also decreased the intracellular ROS levels, phosphorylation of JNK, p38, and STAT3, and the expression of ICAM-1, MCP-1, IL-8, and lectin-like oxidized LDL receptor-1 (LOX-1) in TNF-a-stimulated HUVECs. 48,49 In the present study, pretreatment with SFN inhibited significantly NF-jB-induced IL-1, IL-6, IL8, and ICAM expressions, indicating that SFN has similar antiinflammatory and vasoprotective properties.…”

Involvement of ROS in Curcumin-induced Autophagic Cell Death

“…There have been several mechanisms to explain the antioxidant, antiinflammatory and anticancer effect of curcumin [25][26][27][28][29]. Autophagy which is designated as type II programmed cell death has also been reported to be an anticancer mechanism of curumin, resulting in the growth inhibition of a variety of malignant of cells such as chronic myeloid leukemia cells, malignant glioma cells, and oesophageal cancer cells [30][31][32].…”

Vasoprotection by Dietary Supplements and Exercise: Role of TNFαSignaling

“…Curcumin effectively blocked TNF α -induced downregulation of TM and endothelial protein C receptor (EPCR) at both mRNA and protein levels in several human endothelial cells [47]. Curcumin also reduced the intracellular reactive oxygen species (ROS) levels, phosphorylation of c-Jun N-terminal kinases (JNK), p38 mitogen-activated protein kinases (p38), and signal transducer and activator of transcription-3 (STAT3), and the expression of ICAM-1, MCP-1, interleukin-8 (IL-8), and lectin-like oxidised LDL receptor-1 (LOX-1) in TNF α -stimulated HUVECs [48, 49]. …”