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Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes
Published on: September 18, 2017
Exogenous hydrogen sulphide ameliorates diabetic cardiomyopathy in rats by reversing disordered calcium-handling
Yu-Si Cheng1, De-Zai Dai2, Yin Dai2
1Institute of Nephrology, Zhong Da Hospital, Medical School of Southeast University, Nanjing, China.
Insights
Hydrogen sulphide (H2S) administration improved diabetic cardiomyopathy by restoring the sarcoplasmic reticulum
Area of Science:
- Cardiovascular Science
- Endocrinology
- Molecular Biology
Background:
- Hydrogen sulphide (H2S) is implicated in cardiovascular diseases, but its precise role remains unclear.
- Diabetic cardiomyopathy is a significant complication of diabetes mellitus, characterized by cardiac dysfunction.
- Disordered calcium handling in the sarcoplasmic reticulum (SR) is a key feature of cardiac pathology.
Purpose of the Study:
- To investigate the therapeutic potential of sodium hydrogen sulphide (NaHS), an H2S donor, in diabetic cardiomyopathy.
- To determine if NaHS can ameliorate diabetic cardiomyopathy by correcting calcium-handling abnormalities in the SR.
- To elucidate the molecular mechanisms underlying the protective effects of H2S in this condition.
Main Methods:
- A diabetic rat model was established using streptozotocin (STZ) injection.
- Rats were treated with aminoguanidine (AG) or sodium hydrogen sulphide (NaHS).
- Cardiac function, myocardial hypertrophy, oxidative stress markers, and the expression of key proteins involved in calcium handling and signaling pathways were assessed.
Main Results:
- Diabetic rats exhibited cardiac dysfunction, myocardial hypertrophy, increased reactive oxygen species (ROS), and altered expression of endothelin A receptor (ETA) and protein kinase Cε (PKCε).
- Expressions of SR calcium-handling proteins, including FKBP12.6, SERCA2a, and CASQ2, were downregulated in diabetic hearts, leading to calcium leak.
- NaHS treatment significantly attenuated these pathological changes and improved cardiac function.
Conclusions:
- Exogenous hydrogen sulphide (H2S) exerts a protective effect against diabetic cardiomyopathy.
- H2S normalizes the SR calcium-handling system and inhibits the ET-NADPH oxidase-PKCε pathway.
- NaHS represents a potential therapeutic agent for managing diabetic cardiomyopathy.
Objectives:
Hydrogen sulphide (H2 S) has been found to be involved in cardiovascular diseases, but the exact mechanism has not been clarified. The purpose of this study was to investigate whether sodium hydrogen sulphide (NaHS), the donor of H2 S, can improve diabetic cardiomyopathy by reversing disordered calcium-handling system in sarcoplasmic reticulum (SR).
Methods:
Sprague Dawley rats were injected with streptozotocin (STZ, 60 mg/kg, i.p.) to build diabetic model. Treatment groups included: aminoguanidine group (AG, 100 mg/kg, p.o.) and NaHS group (5 mg/kg per day, s.c.).
Key Findings:
Cardiac dysfunction and myocardial hypertrophy were found in diabetic model (DM) group, along with increased ROS levels and upregulated mRNA and protein expressions of NADPH p22(phox) , endothelin A receptor (ETA ) and protein kinase Cε (PKCε). Expressions of calcium-handling proteins in SR including FK506-binding proteins (FKBP12.6), sarcoplasmic reticulum Ca(2+) ATPase (SERCA2a) and calsequestrin 2 (CASQ2) were downregulated in DM group, accompanied by elevated concentration of diastolic free calcium in high glucose-incubated cardiomyocytes, indicating of calcium leak. After treated by NaHS, these abnormalities were attenuated significantly.
Conclusions:
Exogenous H2 S played a protective role in diabetic cardiomyopathy by inhibiting abnormal calcium-handling system in SR and ET-NADPH oxidase-PKCε pathway.
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