BackgroundType 2 diabetes mellitus (T2DM) is a major risk factor of atherosclerosis. Hyperglycemia in T2DM causes advanced formation of glycation end products (AGE) which leads to oxidative stress and chronic inflammation. Oxidative stress occurs due to increased levels of reactive oxygen species (ROS) such as H2O2. On the other hand, lipoprotein-associated phospholipase (Lp-PLA2) has pro-inflammatory effects, which cause instability of atherosclerosis plaques. This condition causes hypoxemic cells to stimulate HIFα induced vasa vasorum angiogenesis. This study aims to understand the potential of PSP as an anti-angiogenic agent through decreased levels of H2O2 and Lp-PLA2 leading to the decline of vasa vasorum angiogenesis in diabetic rat model. In addition, this study also measured the lipid profile of diabetic rat model in relation to vasa vasorum angiogenesis.MethodsTrue laboratory experiment with randomized post-test control of group design using 25 wistar rats (Rattus norvegicus) were divided into five groups; one normal group and four group with High Fat Diet (HFD) and low dose streptozotocin (30 mg/kgBW) injection sc, treated with placebo and three various doses of PSP 50, 150, 300 mg/kgBW.ResultsANOVA test (p < 0.05) shows that there is a significant influence of polysaccharide peptide (PSP) feeding on the decreased amount of vasa vasorum angiogenesis (p = 0.00), lipid profile (cholesterol total and triglyceride; p = 0.01, p = 0.001), and amount of H202 (p = 0.003). The amount of Lp-PLA2 declined to (p = 0.184). This result indicates that PSP prevents inflammation in atherosclerosis.ConclusionsPSP of Ganoderma lucidum is an anti-angiogenic agent in T2DM.
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.
Dyslipidemia is one of risk factors for atherosclerosis induced by high fat diet. In atherosclerosis, an angiogenesis of immature and fragile vasa vasorum leads to atherosclerotic plaque destabilization. Angiogenesis of vasa vasorum is influence by oxidative stress and inflammation. Polysaccharide peptide (PsP) from Ganoderma lucidum (GL) contains bioactive compounds that possess antioxidant and anti-inflammatory properties which might become anti-angiogenesis agent in atherosclerosis. The aim of this study is to determine whether administration of PsP GL is able to decrease the number of vasa vasorum, H2O2 and Lp-PLA2 in atherosclerosis mouse model with dyslipidemia. True Experimental research design was conducted with Randomized Post Test Only Controlled Group Design. Twenty five Wistar strain Rattus novergicus were divided into 5 groups (n=5). Negative control group was administered with normal diet, positive control group was given high fat diet (HFD), and 3 treatment groups received HFD and PsP administration of 50mg/kgBW, 150 mg/kgBW, and 300mg/kgBW. Vasa vasorum measurement was performed using histopathological section of mouse aorta and measured using Scan Dot Slide Olyvia with 400x magnification. Serum Lp-PLA2 and H2O2 were measured using ELISA method. One way ANOVA analysis demonstrates that PsP GL significantly reduced vasa vasorum count (p<0,05) in mouse model of atherosclerosis with dyslipidemia. Duncan Post Hoc analysis indicates a significant difference in vasa vasorum count in 50mg/kgBW PsP treated group compared to other doses. The conclusions of this study is Polysaccharid peptide G. lucidum extract significantly reduces vasa vasorum count in Wistar strain Rattus novergicus with HFD administration.
Dyslipidemia is a risk factor for cardiovascular disease through atherogenesis induction. The productive age of early adulthood today has different eating habits in relation to increasing culinary lifestyles and food hunter habits. In general, dyslipidemia rarely causes early phase symptoms. We suspect that there is an increase in the group with impaired lipid profiles related to dietary habits that do not pay attention to the essential needs of eating. The collected serum was carried out using a venous puncture procedure on 45 early adult subjects (men n = 9; women n = 36) aged 19-27 years in Malang City. The lipids were analysed for lipid profiles including TC, TG, HDL-c, and LDL-c. The results of men respondents showed higher differences in the lipid profiles of TC (p = 0.000), TG (p = 0.001), and LDL (p = 0.000) than women while HDL-c levels (p = 0.010) in women had higher differences than men. Dumpling (contains noodles and beef) has positive correlation with TG, TC, and LDL. At least in this study, we found that men in early adult had a higher lipid profile compared to women. This is of course related to diet have an impact on increasing lipid levels. For this reason, it is advisable to maintain a more productive eating habits to reduce the risk of dyslipidemia.
Gangguan tidur atau insomnia yang muncul pada pasien hipertensi dapat disebabkan oleh efek samping obat-obat antara lain golongan Angiotensin Converting Enzyme Inhibitor (ACEI) dan Calcium Channel Blocker (CCB), namun besarnya pengaruh masing-masing golongan belum banyak diperbandingkan. Oleh karena itu, dilakukan penelitian dengan menggunakan rancangan case control untuk menilai risiko penggunaan ACEI dan CCB terhadap angka kejadian insomnia. Data demografi dan status insomnia dikumpulkan melalui Lembar Pengumpul Data (LPD) dan kuesioner Athens Insomnia Scale (AIS), kemudian dilakukan analisis univariat, bivariat, dan multivariat. Hasil analisis menunjukkan bahwa pada kelompok usia 56-60 tahun, pasien yang menjalani pengobatan dengan ACEI memiliki risiko insomnia lebih kecil yaitu sekitar 0,38 kali (p=0,026, 95% CI=0,15-0,94) dibandingkan dengan pasien lain yang menggunakan CCB, sedangkan pada kelompok kategorial yang lain tidak ditemukan hubungan yang signifikan. Dengan demikian, pemantauan efek samping insomnia menjadi penting untuk dilakukan oleh tenaga kesehatan terutama pada pasien yang menjalani pengobatan dengan CCB pada usia 56-60 tahun.
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