IntroductionThe increasing blood glucose level due to insulin resistance which occurs in diabetes mellitus (DM) may cause vascular damage. This study aims to prove the effect of the polysaccharide peptide (PsP) Ganoderma lucidum on improving vascular damage through an increase of circulating endothelial cells and circulating endothelial cells (CEC) ratio, decreased H2O2, triglyceride (TG), total cholesterol (TC) and insulin resistance in type 2 DM.MethodsOur study is a true experimental study with randomized posttest control group design that used 35 Wistar rats divided into five groups: normal, control (+) and three groups of different variant PsP doses 50, 150 and 300 mg/kg BW (n=7).ResultsBy using one-way ANOVA and post-hoc Duncan test, the results show a significant increase of endothelial progenitor cell (EPC) concentration (p=0.000) and ratio EPC:CEC (0.000) by dose-dependent fashion and also reduced CEC concentration (p=0.001), H2O2 (p=0.03), TG (p=0.001), TC (p=0.01) and insulin resistance (p=0.003).ConclusionIn this study, PsP induced endothelial repairing process and reduced the risk factor with 300 mg/kg BW as optimum dose. However, further research on EPC and CEC detection markers is important. Further research on PsP and clinical trial for commercial uses is also needed.

BACKGROUND: High-fat diet (HFD) is associated with dyslipidemia which is a risk factor for atherosclerosis. Dyslipidemia causes oxidative stress which induces vascular cell adhesion molecule-1 (VCAM-1). Oxidative stress also triggers the thickening of tunica intima-media (IMT) and Perivascular Adipose Tissue (PVAT). Xanthone compound in ethanolic extract of Mangosteen pericarp (EEMP) has an antioxidant property to overcome the oxidative stress. AIM: The objective of this study is to investigate the effect of dietary EEMP administration on the expression of VCAM-1 and thickness of PVAT and IMT in atherosclerotic rat model fed with HFD. METHODS: This experimental laboratory study uses 25 Wistar strain Rattus norvegicus which were divided into 5 study groups. Negative Control group (GT1) was given a normal diet, Positive Control group (GT2) was treated with HFD, and three treatment groups were each treated with HFD with Mangosteen pericarp extract of 200 mg/kg BW (GT3), 400 mg/kg BW (GT4), and 800 mg/kg BW (GT5). Measurements of VCAM-1 expression were performed using immunofluorescence. PVAT and IMT measurements were performed on rat aortic preparations. RESULTS: One-way ANOVA test showed the addition of dietary EEMP significantly (p < 0.05) decreased the expression of VCAM-1 and decreased the thickness of PVAT and IMT in treatment groups as compared with both negative and positive controls. Tukey HSD test showed a dose of 800 mg/kg BW was the most effective dose for decreasing VCAM-1 level, PVAT and IMT. CONCLUSION: Dietary EEMP significantly decreases the expression of VCAM-1, as well as the thickness of PVAT and IMT in Wistar strain Rattus norvegicus treated with HFD.

PurposeThe aim of this study is to prove that type 2 diabetes mellitus can induce increasing inflammation marker in renal and that the provision of darapladib as Lp-LA2 Inhibitor agents can inhibit inflammation that were measured from the expression of IL-1B and IL-6- type cytokine in renal. This study also discusses the correlation between IL-1B and IL-6- type cytokine expression in renal.MethodsThirty Sprague-Dawley (SD) rats were divided into three main groups; those are negative control group (NC), Type 2 Diabetes Mellitus group (T2DM) given high fat diet (HFD) with streptozotocin intraperitoneal injection (35mg/kg BW) and diabetes mellitus + darapladib group (DM + DP). Each group was treated within two serial treatment time: 8 weeks and 16 weeks. Expressions of IL-1B and IL-6- type cytokine in renal were the markers that we measured by immunofluorosense method.ResultsThe administration of darapladib can significantly decrease the expression of IL-1B- type cytokine (p ANOVA = 0.029, p < 0.005) measured in rats’ renal both at weeks 8 and 16 in the T2DM group. The Expression of IL-6- type cytokine also showed a significant difference after treated with darapladib both at weeks 8 and 16 in T2DM group with p-value of ANOVA = 0.033, p < 0.005. The Pearson correlation showed a strong correlation (linear regression value was r2 = 0.743).ConclusionOur results show that atherosclerosis caused by inflammation in renal T2DM SD rats could be inhibited by the administration of darapladib.

INTRODUCTION Endothelial Progenitor Cells (EPCs) are part of hematopoietic stem cells that differentiate into endothelial cells during their blood vessels’ maturation process. The role of EPCs is widely known to contribute to repair of the vascular wall when endothelial dysfunction occurs. However, various risk factors for cardiovascular disease (CVD) influence EPC performance, leading to endothelial dysfunction. One EPC dysfunction is decreased amount of EPC mobilization to the injured tissue. EPC dysfunction reduces the angiogenetic function of EPCs. The vital maturation process that the EPCs must pass is the late phase. The dysfunction of late EPCs is known as senescence. This study aimed to identify and compare senescence of late EPCs, through CD62E and CD41 markers, in non-smokers and smokers as a risk factor for CVD. METHODS EPC collection was from peripheral mononuclear cells (PBMCs) in non-smokers (n=30) and smokers (n=31). The EPCs were then marked by CD62E/CD41 and senescence β-galactosidase assay using FACS. Identification of senescence cells was based on fluorescence with DAPI. RESULTS Positive percentage of late EPCs in non-smokers was not significantly different from that in smokers (p=0.014). The number of senescent late EPCs in smokers was higher than in non-smokers (p<0.0001). CONCLUSIONS Endothelial progenitor cells that experienced senescence in the smokers showed EPC dysfunction, which resulted in decreased cell angiogenic function. Further research is needed to explain the mechanism of re-endothelialization failure in EPC dysfunction due to smoking.

Cardiovascular disease is a major cause of heart failure and premature deaths worldwide. It contributes substantially to the increase in health care costs. 1 The previous study showed 48% of deaths in the world were caused by cardiovascular disease. A cohort study at the Harapan Kita National Heart Center and 5 hospitals in Indonesia suggested that the death rate due to heart disease in the hospital was around 6-12% and the re-hospitalization rate was 29%. 2 Hidayat et al. reported that the total cost of INA-CBG claim for in-patient services for 18 months was Rp 42.4 triliun. 3 Up to now, the therapy for stable coronary artery disease was medical treatment in accordance with the recommendation, because it was proven to improve symptoms and prognosis unless progression of worsening occurred should be sent for revascularization. Revascularization either with percutaneous coronary intervention (PCI) or coronary artery bypass graft (CABG) is more effective in treating angina, reducing of anti-angina drugs need, improving exercise capacity, and quality of life, compared to medical treatment strategies alone. 4 After revascularization procedures, the coronary artery disease (CAD) patients recommended to perform in hospital base followed by community based cardiac rehabilitation.