| Home  | About ScienceAsia  | Publication charge  | Advertise with us  | Subscription for printed version  | Contact us  
Editorial Board
Journal Policy
Instructions for Authors
Online submission
Author Login
Reviewer Login
Volume 50 Number 6
Volume 50 Number 5
Volume 50 Number 4
Volume 50 Number 3
Volume 50 Number 2
Volume 50 Number 1
Earlier issues
Volume  Number 

previous article next article

Research articles

ScienceAsia 47 (2021):ID 277-286 |doi: 10.2306/scienceasia1513-1874.2021.027


Effect of sandalwood oil on inhibition of reactive oxygen species generation and lipopolysaccharideinduced inflammation through down-regulation of the nuclear factor-κB signaling pathways


Young Min Leea, In Sook Kima, Beong Ou Lima,b,*

 
ABSTRACT:     We investigated the antioxidative and anti-inflammatory effects of sandalwood oil and attempted to elucidate its underlying mechanism of action. The antioxidant activities of sandalwood oil were assessed using various methods: 1.1-diphenyl-2-picrylhydrazyl (DPPH) and 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulphonic acid (ABTS+) radical scavenging assays, as well as DNA protection ability and reactive oxygen species (ROS) generation. The cell viability of sandalwood oil in RAW 264.7 cells (murine macrophage) was investigated by tetrazolium salt (MTT) assay. The nuclear factor kappa B (NF-κB) activation was analyzed by western blot analysis in LPS-induced RAW 264.7 cells. NF-κB nuclear translocation was evaluated by immunofluorescence staining. Furthermore, we examined ROS generation using DCF-DA in H2O2-stimulated RAW 264.7 cells. Sandalwood oil inhibited IκBα phosphorylation and NF-κB activation and its translocation into the nucleus. Sandalwood oil shows antioxidant activity in vitro, suggesting that it may inhibit the promotion of the NF-κB-mediated inflammatory signaling pathway induced by ROS.

Download PDF

137 Downloads 985 Views


a Department of Medicinal Bioscience, Division of Integrated Bioscience, College of Biomedical & Health Science, Konkuk University, Chungju 27478 Korea
b Research Institute of Inflammatory Diseases, Kunkuk University, Chungju 27478 Korea

* Corresponding author, E-mail: beongou@kku.ac.kr

Received 11 Dec 2018, Accepted 1 Dec 2020