Teuku Heriansyah, Titin Andri Wihastuti, Djanggan Sargowo, Mohammad Aris Widodo, Prasanti Mahesa Anjani, Triandra Devinta Suparno, Irna Nur Kharisma, Cathrine Theodora Sukotjo, Fitriani Intan Puspitasari
Atherosclerosis occurs as a result of the oxidation of low-density lipoprotein (LDL) deposits, which later form plaques. Hyperglycemia, which occurs in patients with type 2 diabetes mellitus, is a risk factor for this kind of vascular damage. Oxidative stress from hydrogen peroxide (H2O2) is increased in patients with hyperglycemia and therefore an antioxidant agent is required to prevent the destruction of the walls of blood vessels. This study aimed to show that Ganoderma lucidum polysaccharide peptide (PsP) can decrease the formation of H2O2. The study was an experimental invivo post-test with control group design. Thirty-five Wistar rats (Rattus norwegicus) were divided into five groups (a normal diet group, a hypercholesterol diet group, and hypercholesterol groups that received doses of 50mg/kg, 150mg/kg, and 300mg/kg body weight PsP). The parameters determined in this study were the level of H2O2, the lipid profile, insulin resistance, and the amounts of perivascular adipocyte tissue (PVAT), foam cells, and plaques. Each treatment group showed significant results for the administration of PsP using the one-way analysis of variance test (p<0.050) for the reduction of H2O2 (p=0.003), the lipid profile (cholesterol total and triglyceride; p=0.010, p=0.001), insulin resistance (p=0.003), the amount of PVAT (p<0.001), and plaques (p<0.001). The decrease in foam cells was insignificant (p=0.149), although an obvious pattern of reduction as a result of PsP treatment was observed. PsP from G. lucidum is a potent antioxidant and may prevent the pathophysiology of atherosclerosis in patients with type 2 diabetes mellitus. The optimum dose in patients with type 2 diabetes mellitus is 300mg/kg body weight. Further studies are required to determine the antioxidant effects of G. lucidum PsP and its benefits in the management of type 2 diabetes mellitus. © 2014.
Department of Cardiology, Faculty of Medicine, Syiah Kuala University, Aceh, Indonesia; Department of Biomedicine, Faculty of Medicine, Brawijaya University, Malang, Indonesia; Department of Cardiology, Faculty of Medicine, Brawijaya University, Malang, Indonesia; Department of Pharmacology, Faculty of Medicine, Brawijaya University, Malang, Indonesia; Bachelor Programme, Faculty of Medicine, Brawijaya University, Malang, Indonesia
