The protective role of single bulb garlic (Allium sativum L.) towards foam cells and vascular cell adhesion molecules-1 (VCAM-1) on mice (Mus musculus) with high-fat diet

Main Authors: Chasanah, Isfatun, Ghofur, Abdul, Lestari, Sri Rahayu
Other Authors: The research was supported by Ministry of Research, Technology and Higher Education of Republic Indonesia, (Grant No. 3.4.8/UN.32.14.LT/2017).
Format: Article info application/pdf Journal
Bahasa: eng
Terbitan: Journal of the Medical Sciences (Berkala ilmu Kedokteran) , 2019
Subjects:
Online Access: https://jurnal.ugm.ac.id/bik/article/view/40848
https://jurnal.ugm.ac.id/bik/article/view/40848/pdf
https://jurnal.ugm.ac.id/bik/article/downloadSuppFile/40848/6315
Daftar Isi:
  • Atherosclerosis is initiated by inflammatory response characterized by the accumulation of lipids in the arteries, causing blockage of blood vessels. The excessive of low-density lipoprotein (LDL) in the blood is a major factor in endothelial dysfunction and results in an inflammatory process. The inflammatory process in atherosclerosis is due to the expression of adhesion molecules, vascular cell adhesion molecules-1 (VCAM-1). This research aimed to evaluate the effect of single bulb garlic oil extract (SGBOE) against VCAM-1 expression in high-fat diet mice. Thirty male mice strain Balb/C were acclimatized for one week. Mice were divided into 6 groups (n=5): normal, high-fat diet (HFD), HFD + simvastatin, and HFD + SBGOE 12.5, 25, and 50 mg/kg BW respectively. HFD was given for 45 days. The SGBOE was given for four weeks orally. The aortic VCAM-1 expression was assayed using the immunohistochemical-flouresencemethod. The result of One-Way ANOVA showed that the treatment influenced significantly (p<0.05). The foam cells increase in the high-fat diet group compared than normal mice. Dose 12,5 mg/kg BW reduces VCAM-1 expression near the normal group. Allicin and S-allyl cysteine (SAC) compounds in single bulb garlic are antioxidant compounds that act to prevent oxidative stress and prevention mechanisms against lipoprotein modification.