Protective effect of atorvastatin on oxidative stress in streptozotocin‐induced diabetic rats independently their lipid‐lowering effects

2019 ◽  
Vol 33 (5) ◽  
pp. e22295 ◽  
Author(s):  
Göknur Aktay ◽  
Şule Öner Gürsoy ◽  
Umut Uyumlu ◽  
Songül Ünüvar ◽  
Nevin İlhan
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Diabetic Rats ◽  
Lipid Lowering

Testicular Injury Attenuated by Rapamycin Through Induction of Autophagy and Inhibition of Endoplasmic Reticulum Stress in Streptozotocin- Induced Diabetic Rats

2019 ◽  
Vol 19 (5) ◽  
pp. 665-675 ◽  
Author(s):  
Wenjiao Shi ◽  
Zhixin Guo ◽  
Ruixia Yuan
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Protective Effect ◽  
Er Stress ◽  
B Cell Lymphoma ◽  
Diabetic Rats ◽  
Pathological Changes ◽  
Rapamycin Treatment ◽  
Related Proteins

Background and Objective: This study investigated whether rapamycin has a protective effect on the testis of diabetic rats by regulating autophagy, endoplasmic reticulum stress, and oxidative stress. Methods: Thirty male Sprague-Dawley rats were randomly divided into three groups: control, diabetic, and diabetic treated with rapamycin, which received gavage of rapamycin (2mg.kg-1.d-1) after induction of diabetes. Diabetic rats were induced by intraperitoneal injection of streptozotocin (STZ, 65mg.Kg-1). All rats were sacrificed at the termination after 8 weeks of rapamycin treatment. The testicular pathological changes were determined by hematoxylin and eosin staining. The protein or mRNA expression of autophagy-related proteins (Beclin1, microtubule-associated protein light chain 3 (LC3), p62), ER stress marked proteins (CCAAT/enhancer-binding protein (C/EBP) homologous protein (CHOP), caspase-12), oxidative stress-related proteins (p22phox, nuclear factor erythroid2-related factor 2 (Nrf2)) and apoptosis-related proteins (Bax, B cell lymphoma-2 (Bcl-2)) were assayed by western blot or real-time fluorescence quantitative PCR. Results: There were significant pathological changes in the testes of diabetic rats. The expression of Beclin1, LC3, Nrf2, Bcl-2 were significantly decreased and p62, CHOP, caspase12, p22phox, and Bax were notably increased in the testis of diabetic rats (P <0.05). However, rapamycin treatment for 8 weeks significantly reversed the above changes in the testis of diabetic rats (P <0.05). Conclusion: Rapamycin appears to produce a protective effect on the testes of diabetic rats by inducing the expression of autophagy and inhibiting the expression of ER-stress, oxidative stress, and apoptosis.

Protective effect of rosmarinic acid against oxidative stress biomarkers in liver and kidney of strepotozotocin-induced diabetic rats

2015 ◽  
Vol 71 (4) ◽  
pp. 743-751 ◽  
Author(s):  
Nadia Mushtaq ◽  
Roberta Schmatz ◽  
Mushtaq Ahmed ◽  
Luciane Belmonte Pereira ◽  
Pauline da Costa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Rosmarinic Acid ◽  
Diabetic Rats ◽  
Oxidative Stress Biomarkers ◽  
Stress Biomarkers ◽  
Liver And Kidney

scholarly journals Adiponectin Ameliorates Lung Ischemia-Reperfusion Injury Through SIRT1-Pink1 Signaling-Mediated Mitophagy in Type 2 Diabetic Rats

2021 ◽  
Author(s):  
Tao Jiang ◽  
Tianhua Liu ◽  
Xijin Deng ◽  
Wengang Ding ◽  
Ziyong Yue ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lung Transplantation ◽  
Protective Effect ◽  
Mitochondrial Dysfunction ◽  
Small Interfering Rna ◽  
Ischemia Reperfusion ◽  
Diabetic Rats ◽  
Interfering Rna ◽  
Type 2 Diabetic

Abstract BackgroundDiabetes mellitus (DM) is a key contributing factor to the poor survival in lung transplantation recipients. Mitochondrial dysfunction is recognized as a critical mediator in the pathogenesis of diabetic lung ischemia-reperfusion (IR) injury. The protective effects of adiponectin have been demonstrated in our previously study, but the underlying mechanism remained unclear. Here we demonstrated an important role of mitophagy in the protective effect of adiponectin during diabetic lung IR injury.Methods High-fat diet-fed streptozotocin-induced type 2 diabetic rats as recipients were exposed to adiponectin with or without administration of the SIRT1 inhibitor EX527 following lung transplantation. To unravel the mechanisms underlying the action of adiponectin, rat pulmonary microvascular endothelial cells were transfected with SIRT1 small-interfering RNA or Pink1 small-interfering RNA and then subjected to in vitro diabetic lung IR injury.ResultsMitophagy was impaired in the diabetic lung subjected to IR injury, accompanied by increased oxidative stress, inflammation, apoptosis, and mitochondrial dysfunction. Adiponectin induced mitophagy and attenuated subsequent diabetic lung IR injury by improving lung functional recovery, suppressing oxidative damage, diminishing inflammation, decreasing cell apoptosis, and preserving mitochondrial function. However, both inhibitors of mitophagy and knockdown of Pink1 suppressed mitophagy, and reduced the protective action of adiponectin. Furthermore, we demonstrated that APN affected Pink1 stabilization via the SIRT1 signaling pathway, and knockdown of SIRT1 suppressed Pink1 expression and compromised the protective effect of adiponectin.ConclusionThese data demonstrated that adiponectin attenuated reperfusion-induced oxidative stress, inflammation, apoptosis and mitochondrial dysfunction via activation of SIRT1-Pink1 signaling-mediated mitophagy in diabetic lung IR injury.

scholarly journals Hawthorn Leaf Flavonoids Protect against Diabetes-Induced Cardiomyopathy in Rats via PKC-α Signaling Pathway

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Qing Min ◽  
Yuting Bai ◽  
Yuchen Zhang ◽  
Wei Yu ◽  
Minli Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
Blood Glucose ◽  
Protective Effect ◽  
Signaling Pathway ◽  
Morphological Changes ◽  
Cardiac Injury ◽  
Diabetic Rats ◽  
Diabetic Patients ◽  
Underlying Mechanisms

Objectives. DCM has become one of the main reasons of death in diabetic patients. In this study, we aimed to explore the hawthorn leaf flavonoids (HLF) protective effect against diabetes-induced cardiac injury and the underlying mechanisms in experimental rats. Methods. Experimental diabetic model was induced by intraperitoneal injection of streptozotocin (STZ, 40 mg/kg) in rats after feeding with high-fat diet for 8 weeks. The diabetic rats received a 16-week treatment of different doses of HLF (50, 100, and 200). The morphological changes of myocardial cells were observed by light microscope; the concentration of antioxidant indicator and TNF-α and the expression of PKC-α mRNA, PKC-α, and NF-κB proteins were assessed as well. Results. STZ-induced diabetes mellitus prompted blood glucose, cardiac injury, oxidative stress, and inflammation, accompanied with suppressed body weight. On the contrary, HLF administration improved body weight and blood glucose and attenuated myocardial structural abnormalities in diabetic rats. In addition, HLF decreased MDA level and enhanced SOD activities, inhibited TNF-α expression, and downregulated PKC-α mRNA, PKC-α, and NF-κB which were induced by diabetes. Conclusions. HLF has a protective effect against diabetic cardiomyopathy in rats. The mechanism may be involved in reducing oxidative stress and inflammation via inactivation of the PKC-α signaling pathway.

scholarly journals Simvastatin Ameliorates Diabetic Cardiomyopathy by Attenuating Oxidative Stress and Inflammation in Rats

2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Nawal M. Al-Rasheed ◽  
Nouf M. Al-Rasheed ◽  
Iman H. Hasan ◽  
Maha A. Al-Amin ◽  
Hanaa N. Al-Ajmi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
Diabetic Cardiomyopathy ◽  
Troponin I ◽  
Body Weight Loss ◽  
Diabetic Rats ◽  
Antioxidant Defenses ◽  
Lipid Lowering ◽  
Diabetic Heart ◽  
Creatine Kinase Mb

Simvastatin is a lipid-lowering agent used to treat hypercholesterolemia and to reduce the risk of heart disease. This study scrutinized the beneficial effects of simvastatin on experimental diabetic cardiomyopathy (DCM), pointing to the role of hyperglycemia-induced oxidative stress and inflammation. Diabetes was induced by intraperitoneal injection of streptozotocin and both control and diabetic rats received simvastatin for 90 days. Diabetic rats showed significant cardiac hypertrophy, body weight loss, hyperglycemia, and hyperlipidemia. Serum creatine kinase MB (CK-MB) and troponin I showed a significant increase in diabetic rats. Simvastatin significantly improved body weight, attenuated hyperglycemia and hyperlipidemia, and ameliorated CK-MB and troponin I. Simvastatin prevented histological alterations and deposition of collagen in the heart of diabetic animals. Lipid peroxidation and nitric oxide were increased in the heart of diabetic rats whereas antioxidant defenses were decreased. These alterations were significantly reversed by simvastatin. In addition, simvastatin decreased serum inflammatory mediators and expression of NF-κB in the diabetic heart. Cardiac caspase-3 was increased in the diabetic heart and decreased following treatment with simvastatin. In conclusion, our results suggest that simvastatin alleviates DCM by attenuating hyperglycemia/hyperlipidemia-induced oxidative stress, inflammation, and apoptosis.

Protective effect of macrocyclic binuclear oxovanadium complex on oxidative stress in pancreas of streptozotocin induced diabetic rats

2004 ◽  
Vol 149 (1) ◽  
pp. 9-21 ◽  
Author(s):  
Balasubramanian Ramachandran ◽  
Kasiappan Ravi ◽  
Vengidusamy Narayanan ◽  
Muthusamy Kandaswamy ◽  
Sorimuthu Subramanian
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Diabetic Rats ◽  
Oxovanadium Complex
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