Decreasing angiogenesis vasa vasorum through Lp-PLA2 and H2O2 inhibition by PSP from Ganoderma lucidum in atherosclerosis: in vivo diabetes mellitus type 2

Author(s):  
Titin Andri Wihastuti ◽  
Reyhan Amiruddin ◽  
Fibe Yulinda Cesa ◽  
Amalia Istiqamah Alkaf ◽  
Meddy Setiawan ◽  
...  

AbstractBackgroundType 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.

2019 ◽  
Vol 16 (1) ◽  
pp. 26-39 ◽  
Author(s):  
Mirza Anwar Baig ◽  
Shital Sharad Panchal

Background: Diabetic complications are the major contributor in the mortality of diabetic patients despite controlling blood glucose level. In the journey of new drug discovery, animal models have to play a major role. A large number of chemical-induced and genetically modified animal models have been investigated to induce diabetic complications but none of them was found to be mimicking the pathophysiology of the human. Therefore, the search and identification of the appropriate animal model become essential. Objective: In the present review, we have made an attempt to understand the pathophysiology of diabetic complication in the neonatal streptozotocin-diabetic rat model and tried to identify the targets for therapeutic agents. The review will help the researchers to explore the animal model to induce diabetic complications, to identify targets and further to find lead molecules for treatment or prevention of diabetic complications. Methods: We have compiled the available research work from 1974 by using prominent databases, organized the available information and analyzed the data to improve the understanding of the pathophysiology of streptozotocin-induced diabetic complications in neonates of rats. Results: The neonatal streptozotocin-diabetic rat model is frequently used and well-established animal model for type 2 diabetes mellitus. We have found that this model has been used to study the pathogenesis of various micro and macrovascular diabetic complications and also investigated for its effects on the liver, thymus gland, and brain. The underlying pathophysiology for complications had a resemblance to the human. Conclusion: The neonatal streptozotocin-diabetic rat model may demonstrate symptomatic diabetic complications due to persistent hyperglycemia at the age of approximately 18-24 weeks. Critical interpretations of available research work showed that the researcher can explore split dose STZ (90- 100mg/kg b.w) model to induce Type 2 DM in neonates of rats at 2nd or 3rd postnatal day.


Author(s):  
Bushra Suhail

Introduction: Diabetes Mellitus is a common metabolic syndrome characterized by persistently elevated blood glucose levels. Canagliflozin is an SGLT-2 inhibitor that controls hyperglycemia by reducing the reabsorption of filtered glucose and excreting it in the urine. Zinc sulphate exhibits some beneficial role in diabetes mellitus but has not been compared to canagliflozin individually and in combination. Aims & Objectives: To observe the effects of treatment with canagliflozin and zinc sulphate on pancreatic histology in streptozotocin induced type-2 diabetic rat model. Place and duration of study: The study was conducted in the Department of Pharmacology, KEMU and PGMI, Lahore for the period of two months. Material & Methods: It was an animal experimental study of eight weeks duration in which 48 adult healthy albino rats of male gender were divided into six groups and were provided the high fat diet throughout the study period. Groups A and B were maintained as healthy and diseased controls respectively. Groups B, C, D, E and F were administered single I/P dose streptozotocin (35mg/kg) at day 22 for inducing diabetes. Upon confirmation of diabetes after a week the rats were further treated as per group designation orally for 4 weeks , individually or in combination with full or half doses of canagliflozin (10 mg /kg/day, 5mg/kg/day ) and zinc sulphate (30mg/kg/day, 15mg/kg/day) . All animals were euthanized at the completion of study duration. The pancreatic tissue was taken out and examined for the histopathological changes (size and number of pancreatic islets, karyolysis and ballooning degeneration). Results: There was a marked improvement in the size and number of islets as well as the inflammatory changes in the combined treatment group (with canagliflozin in full as well as half dose of zinc sulphate) as compared to the groups given zinc sulphate and canagliflozin separately. Conclusion: Combined treatment with canagliflozin and zinc sulphate has a better protective effect on the pancreatic tissue in diabetes than either of them used alone.


2013 ◽  
Vol 28 (5) ◽  
pp. 725 ◽  
Author(s):  
Sun-Ouck Kim ◽  
Hyun-Suk Lee ◽  
Kyuyoun Ahn ◽  
Kwangsung Park

2018 ◽  
Vol 4 (2) ◽  
pp. 181-188 ◽  
Author(s):  
Medhat Ahmed El-Zainy ◽  
Ahmed Mahmoud Halawa ◽  
Fatma Adel Saad

2020 ◽  
Vol 66 (Supplement) ◽  
pp. S36-S40
Author(s):  
Deni ELNOVRIZA ◽  
Hadi RIYADI ◽  
Rimbawan RIMBAWAN ◽  
Evy DAMAYANTHI ◽  
Adi WINARTO

2021 ◽  
Author(s):  
Sanaz Zamany ◽  
Aida Malek Mahdavi ◽  
Saeed Pirouzpanah ◽  
Ali Barzegar

Abstract Background: This research aimed to study the effect of coriander seed supplementation on serum glycemic indices, lipid profile and oxidative stress parameters in patients with type 2 diabetes mellitus (T2DM).Methods: In this randomized double-blinded, placebo-controlled trial, eligible 40 T2DM patients aged 30-60 years were recruited from Sina Hospital (Tabriz, Iran) and randomly assigned into two groups to receive either coriander seed powder (1000 mg/day, n=20) or placebo (1000 mg/day, n=20) for 6 weeks. Anthropometric measurements, dietary intake, and biochemical parameters including fasting blood sugar (FBS), serum insulin, Homeostatic Model Assessment for Insulin Resistance (HOMA-IR), total cholesterol (TC), triglyceride (TG), high- and low-density lipoprotein cholesterols (HDL-C and LDL-C), malondialdehyde (MDA), and total antioxidant capacity (TAC) were assessed before and after supplementation.Results: Anthropometric measurements were not significantly different between intervention and placebo groups. Coriander seed supplementation led to significant within-group reductions in FBS (156.15±23.19 to 130.30±21.15), serum insulin (17.72±0.47 to 17.12±0.76), HOMA-IR (6.82±0.95 to 5.52±0.99), TC (183.85±55.68 to 145.20±31.36), TG (152.50±37.59 to 130.40 ±27.96), LDL-C (127.35±23.45 to 111.40±25.71), and MDA (1.65±0.15 to 1.49±0.15), whereas there were significant increases observed in serum TAC (1.93±0.12 to 1.97±0.09) (P<0.05). Post-dose comparisons showed significant between-group differences for FBS, serum insulin, HOMA-IR, TC, TG, LDL-C, MDA, and TAC levels after adjusting for baseline values (P<0.05).Conclusions: Coriander seed supplementation was able to improve glycemic indices, lipid profile and oxidative stress status in T2DM and it may be useful complementary treatment in management of these patients.Trial registration: The study protocol was registered on the Iranian Registry of Clinical Trials website (IRCT20190224042821N2) on 2019/Oct/11.


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