Diabetic cardiomyopathy and reactive oxygen species (ROS) related parameters in male and female rats: A comparative study

Akhileshwar, Vidya; Patel, Samir P.; Katyare, Surendra S.

doi:10.1007/bf02912887

Cited by 23 publications

(12 citation statements)

References 44 publications

(45 reference statements)

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“…The formation of ROS from cardiomyocytes is a key factor in the pathogenesis of diabetic complications [43, 48, 49]. In this study, we surprisingly found that high glucose decreased mitochondrial oxidative phosphorylation efficiency, induced mitochondrial swelling, promoted mitochondrial Cyt C release and promoted ROS generation (Fig.…”

Section: Discussionsupporting

confidence: 48%

Exogenous H2S Protects Against Diabetic Cardiomyopathy by Activating Autophagy via the AMPK/mTOR Pathway

Yang

Zhang

Gao

et al. 2017

Cell Physiol Biochem

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Background/Aim: Autophagy plays an important role in cellular homeostasis through the disposal and recycling of cellular components. Hydrogen sulphide (H₂S) is the third endogenous gas that has been shown to confer cardiac protective effects. Given the regulation of autophagy in cardioprotection, this study aimed to investigate the protective effects of H₂S via autophagy during high glucose treatment. Methods: This study investigated the content of H₂S in the plasma as well as myocardial, ultrastructural changes in mitochondria and autophagosomes. This study also investigated the apoptotic rate using Hoechst/PI as well as expression of autophagy-associated proteins and mitochondrial apoptotic proteins in H9C2 cells treated with or without GYY4137. Mitochondria of cardiac tissues were isolated and RCR and ADP/O were also detected. AMPK knockdown was performed with siRNA transfection. Results: In a STZ-induced diabetic model, NaHS treatment not only increased the expression of p-AMPK in diabetic group but further activated cell autophagy. Following 48h high glucose, autophagosomes and cell viability were reduced. The present results showed that autophagy could be induced by H₂S, which was verified by autophagic ultrastructural observation and LC3-I/LC3-II conversion. In addition, the mitochondrial membrane potential (MMP) was significantly decreased. The expressions levels of autophagic-related proteins were significantly elevated. Moreover, H₂S activated the AMPK/rapamycin (mTOR) signalling pathway. Conclusions: Our findings demonstrated that H₂S decreases oxidative stress and protects against mitochondria injury, activates autophagy, and eventually leads to cardiac protection via the AMPK/mTOR pathway.

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Section: Discussionsupporting

confidence: 48%

Exogenous H2S Protects Against Diabetic Cardiomyopathy by Activating Autophagy via the AMPK/mTOR Pathway

Yang

Zhang

Gao

et al. 2017

Cell Physiol Biochem

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“…In the kidneys of diabetic rats, taurine increased the GSH/GSSG ratio via the reduction of GSSG content, which seems to result from the elevated GR activity without affecting diabetes-induced decrease in renal GSH level. ALX also significantly increased the activity of xanthine oxidase, which is another important biological source of ROS under diabetic conditions (Forbes et al 2008;Akhileshwar et al 2007). Superoxide anions derived from NADPH oxidase contributes to the development of diabetic nephropathy (Toba et al 2009;Onozato et al 2002).…”

Section: Discussionmentioning

confidence: 98%

Taurine ameliorates alloxan-induced diabetic renal injury, oxidative stress-related signaling pathways and apoptosis in rats

2012

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Hyperglycemia-induced oxidative stress plays a vital role in the progression of diabetic nephropathy. The renoprotective nature of taurine has also been reported earlier; but little is known about the mechanism of this beneficial action. The present study has, therefore, been carried out to explore in detail the mechanism of the renoprotective effect of taurine under diabetic conditions. Diabetes was induced in rats by alloxan (single i.p. dose of 120 mg/kg body weight) administration. Taurine was administered orally for 3 weeks (1% w/v in drinking water) either from the day on which alloxan was injected or after the onset of diabetes. Alloxan-induced diabetic rats showed a significant increase in plasma glucose, enhanced the levels of renal damage markers, plasma creatinine, urea nitrogen and urinary albumin. Diabetic renal injury was associated with increased kidney weight to body weight ratio and glomerular hypertrophy. Moreover, it increased the productions of reactive oxygen species, enhanced lipid peroxidation and protein carbonylation in association with decreased intracellular antioxidant defense in the kidney tissue. In addition, hyperglycemia enhanced the levels of proinflammatory cytokins (TNF-α, IL-6, IL-1β) and Na(+)--K(+)-ATPase activity with a concomitant reduction in NO content and eNOS expression in diabetic kidney. Investigation of the oxidative stress-responsive signaling cascades showed the upregulation of PKCα, PKCβ, PKCε and MAPkinases in the renal tissue of the diabetic animals. However, taurine administration decreased the elevated blood glucose and proinflammatory cytokine levels, reduced renal oxidative stress (via decrease in xanthine oxidase activity, AGEs formation and inhibition of p47phox/CYP2E1 pathways), improved renal function and protected renal tissue from alloxan-induced apoptosis via the regulation of Bcl-2 family and caspase-9/3 proteins. Taurine supplementation in regular diet could, therefore, be beneficial to regulate diabetes-associated renal complications.

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“…As heart is the major organ subjected to the vascular complications associated with diabetes we selected heart tissue for studying the peroxidation as well as antioxidant level. Akhileshwar et al [20] reported that diabetic state compromise the weak ROS defense systems in the heart thus initiating a lesion at the level of mitochondria which ultimately leads to cardiomyopathy and the effects are especially more pronounced in females. Thus we selected the female rats for our study.…”

Section: Discussionmentioning

confidence: 98%

Antioxidant and Antiglycative Potential of Ethyl Acetate Fraction of Psidium guajava Leaf Extract in Streptozotocin-Induced Diabetic Rats

Soman

Rauf

Indira

et al. 2010

Plant Foods Hum Nutr

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Hyperglycemia causes increased protein glycation and the formation of early glycation products and advanced glycation end products (AGEs) which are major factors responsible for the complications associated with diabetes. The aim of the present study was to investigate the antioxidant as well as antiglycative potential of ethyl acetate fraction of guava leaves. Oral administration of the extract at different doses showed a significant decrease in blood glucose level. It also showed an improved antioxidant potential as evidenced by decreased lipid peroxidation and a significant increase in the activity of various antioxidant enzymes such as catalase, superoxide dismutase, glutathione peroxidase and glutathione reductase. Glycated hemoglobin as well as fructosamine which are indicators of glycation was also reduced significantly in treated groups when compared to diabetic control. In vitro studies also support the antioxidant as well as antiglycative potential of guava leaves.

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Diabetic cardiomyopathy and reactive oxygen species (ROS) related parameters in male and female rats: A comparative study

Abstract: ABSTRACT

Cited by 23 publications

References 44 publications

Exogenous H2S Protects Against Diabetic Cardiomyopathy by Activating Autophagy via the AMPK/mTOR Pathway

Exogenous H2S Protects Against Diabetic Cardiomyopathy by Activating Autophagy via the AMPK/mTOR Pathway

Taurine ameliorates alloxan-induced diabetic renal injury, oxidative stress-related signaling pathways and apoptosis in rats

Antioxidant and Antiglycative Potential of Ethyl Acetate Fraction of Psidium guajava Leaf Extract in Streptozotocin-Induced Diabetic Rats

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