Effect of diabetes mellitus on cementum periodontal interface in Streptozotocin-induced diabetic rat model

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.

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Streptozotocin-Induced Diabetes Mellitus in Neonatal Rats: An Insight into its Applications to Induce Diabetic Complications

Current Diabetes Reviews ◽

10.2174/1573399815666190411115829 ◽

2019 ◽

Vol 16 (1) ◽

pp. 26-39 ◽

Cited By ~ 1

Author(s):

Mirza Anwar Baig ◽

Shital Sharad Panchal

Keyword(s):

Diabetes Mellitus ◽

Animal Model ◽

Animal Models ◽

Rat Model ◽

Diabetic Complications ◽

Research Work ◽

Diabetic Rat ◽

Diabetic Rat Model ◽

Streptozotocin Diabetic Rat

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.

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Therapeutic Effects of Canagliflozin and Zinc Sulphate Alone and in Combination on Pancreatic Histology in Type-2 Diabetic Rat Model

Proceedings of Shaikh Zayed Medical Complex Lahore - October to December ◽

10.47489/p000s343z7591-6mc ◽

2020 ◽

Vol 34 (3) ◽

pp. 35-40

Author(s):

Bushra Suhail

Keyword(s):

Diabetes Mellitus ◽

Rat Model ◽

Zinc Sulphate ◽

Combined Treatment ◽

Pancreatic Tissue ◽

Diabetic Rat ◽

Therapeutic Effects ◽

Diabetic Rat Model ◽

Type 2 Diabetic

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.

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Exploration of the Effect and Mechanism of ShenQi Compound in a Spontaneous Diabetic Rat Model

Endocrine Metabolic & Immune Disorders - Drug Targets ◽

10.2174/1871530319666190225113859 ◽

2019 ◽

Vol 19 (5) ◽

pp. 622-631 ◽

Cited By ~ 3

Author(s):

Ya Liu ◽

Jian Kang ◽

Hong Gao ◽

Xiyu Zhang ◽

Jun Chao ◽

...

Keyword(s):

Blood Glucose ◽

Signaling Pathway ◽

Rat Model ◽

Mtor Signaling ◽

Diabetic Rat ◽

Gene Microarray ◽

Mtor Signaling Pathway ◽

Glucose Fluctuation ◽

Blood Glucose Fluctuation ◽

Diabetic Rat Model

Background: Type 2 Diabetes Mellitus (T2DM) is a world-wide metabolic disease with no cure from drugs and treatment. In China, The Traditional Chinese Medicine (TCM) herbal formulations have been used to treat T2DM for centuries. Methods: In this study, we proposed a formula called ShenQi Compound (SQC), which has been used in clinical therapeutics in China for several years. We evaluated the effect of SQC in a spontaneous diabetic rat model (GK rats) by detecting a series of blood indicators and performing histological observations. Meanwhile, the gene microarray and RT-qPCR experiments were used to explore the molecular mechanism of SQC treatment. In addition, western medicine, sitagliptin was employed as a comparison. Results: The results indicated that SQC and sitagliptin could effectively improve the serum lipid (blood Total Cholesterol (TC) and blood Triglycerides (TG)), hormone levels (serum insulin (INS), Glucagon (GC) and Glucagon-Like Peptide-1 (GLP-1)), alleviated the inflammatory response (hypersensitive C-Reactive Protein (hsCRP)), blood glucose fluctuation (Mean Blood Glucose (MBG), standard deviation of blood glucose (SDBG) and Largest Amplitude of plasma Glucose Excursions (LAGE)), pancreatic tissue damage and vascular injury for T2DM. Compared with sitagliptin, SQC achieved a better effect on blood glucose fluctuation (p<0.01). Meanwhile, the gene microarray and RT-qPCR experiments indicated that SQC and sitagliptin may improve the T2DM through affecting the biological functions related to apoptosis and circadian rhythm. Moreover, SQC might be able to influence the mTOR signaling pathway by regulating Pik3r1, Ddit4 expression. Conclusion: All these results indicate that SQC is an effective therapeutic drug on T2DM. Notably, SQC presents an obvious blood glucose fluctuation-preventing ability, which might be derived from the regulation of the mTOR signaling pathway.

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