Effect of Proteasome Inhibitor on Vascular Cell Adhesion Molecule-۱ (VCAM-۱) and Intercellular Adhesion Molecule-۱ (ICAM-۱) Expressions in Rat Model of Atherosclerosis
Publish Year: 1400
نوع سند: مقاله ژورنالی
زبان: English
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شناسه ملی سند علمی:
JR_RBMB-10-4_013
تاریخ نمایه سازی: 25 بهمن 1400
Abstract:
Background: The effect of proteasome inhibitors on atherosclerosis is known to vary depending on the atherosclerosis stage. Previous studies have shown that the highest proteasome expression in atherosclerotic lesions is at the progression stage. Adhesion molecules play a role in the progression stage of atherosclerosis, but no studies have analyzed the effect of proteasome inhibitors on the expression of adhesion molecules at this stage.
Methods: This experimental study aimed to analyze the effect of a proteasome inhibitor, namely bortezomib, on the vascular cell adhesion molecule-۱ (VCAM-۱) and intercellular adhesion molecule۱ (ICAM-۱) expressions in blood vessels of rat model of atherosclerosis at the progression stage. This study used ۱۸ male Wistar rats divided into three groups, i.e. group I that is the control group given standard feed, group II induced by atherosclerosis, and group III induced by atherosclerosis and given bortezomib. Atherosclerosis induction was performed using vitamin D۳ (۷۰۰,۰۰۰ IU/kg) orally by gastric intubation on the ۱st day and atherogenic feed given for four days. Bortezomib ۵۰ μg/kgBW/day was administered intra-peritoneally. The expression
of VCAM-۱ and ICAM-۱ molecules was measured using immunohistochemistry and analyzed quantitatively using Adobe Photoshop software.
Results: The statistical test showed differences in VCAM-۱ expression between atherosclerosis + Bortezomib group and atherosclerosis group, but there were no differences in the expression of ICAM-۱ and atherosclerotic lesions between the groups.
Conclusions: Administration of bortezomib ۵۰μg/kg for four days in progressive atherosclerosis model rats can inhibit VCAM-۱ expression, although it does not affect ICAM-۱ expression and cannot inhibit atherosclerotic lesion formation.
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Authors
Ismawati Ismawati
Department of Biochemistry, Faculty of medicine, Riau University, Pekanbaru, Indonesia.
Ilhami Romus
Department of Pathology Anatomy, Faculty of medicine, Riau University, Pekanbaru, Indonesia.
Mukhyarjon Mukhyarjon
Department of Biochemistry, Faculty of medicine, Riau University, Pekanbaru, Indonesia.
Afra Muthya
Faculty of medicine, Riau University, Pekanbaru, Indonesia.
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