Literature DB >> 31317389

Mechanism of Hydrogen Sulfide Preconditioning-Associated Protection Against Ischemia-Reperfusion Injury Differs in Diabetic Heart That Develops Myopathy.

Mahalakshmi Ansari1, Gino A Kurian2.   

Abstract

Hydrogen sulfide (H2S) is reported to be effective in the management of the myocardial ischemia-reperfusion (I/R) injury via PI3K/GSK3β pathway in normal rats. However, its efficacy against I/R in the presence of diabetic cardiomyopathy is relatively obscure. Thus, the present work aimed to find out H2S-mediated cardioprotection against I/R in diabetic cardiomyopathy and to evaluate its mode of action using Langendorff isolated heart perfusion system. The present work includes three groups of rat, viz. (i) normal, (ii) diabetes mellitus (DM: streptozotocin: 35 mg/kg; normal diet), and (iii) diabetes + high-fat diet (DCM) (streptozotocin: 35 mg/kg; high-fat diet). The effect of NaHS (an H2S donor; 20 µM) on cardiac function in isolated rat hearts demonstrates that H2S preconditioning (HIPC) significantly attenuated myocardial injury in both DM and DCM hearts, as evidenced by the (i) improvement in hemodynamics, which includes rate pressure product [(in mmHg × 103 × bpm) DM: 40 to 56; DCM: 21 to 58] and left ventricular developed pressure [(in mmHg) DM: 53 to 74; DCM: 28 to 74), (ii) reduction in infarct size (25% to 8%) and attenuated caspase activity, compared to their respective I/R controls. Also, the observed positive recovery of mitochondrial function during HIPC treatment reinforces the cardioprotection by HIPC in DCM heart against I/R injury. However, HIPC could not repair I/R-induced oxidative stress in DCM rat heart. Further, to study the H2S mode of action, the experimental rats were exposed to a PI3K inhibitor (Wortmannin) and GSK3β inhibitor (SB216763) before HIPC protocol, whose results suggest that unlike in normal and DM, HIPC mediates its cardioprotective effect independent of PI3K/GSK3β pathway. To conclude, HIPC ameliorates I/R injury in DCM rat via an alternative pathway other than existing PI3K pathway, which is required to be probed under disease conditions.

Entities:  

Keywords:  Diabetic cardiomyopathy; Hydrogen sulfide preconditioning; Ischemia–reperfusion injury; Mitochondria; Oxidative stress

Year:  2020        PMID: 31317389     DOI: 10.1007/s12012-019-09542-9

Source DB:  PubMed          Journal:  Cardiovasc Toxicol        ISSN: 1530-7905            Impact factor:   3.231


  2 in total

Review 1.  Implications of Oxidative and Nitrosative Post-Translational Modifications in Therapeutic Strategies against Reperfusion Damage.

Authors:  Mabel Buelna-Chontal; Wylly R García-Niño; Alejandro Silva-Palacios; Cristina Enríquez-Cortina; Cecilia Zazueta
Journal:  Antioxidants (Basel)       Date:  2021-05-08

2.  Inhibition of PI3K/mTOR/KATP channel blunts sodium thiosulphate preconditioning mediated cardioprotection against ischemia-reperfusion injury.

Authors:  Sri Rahavi Boovarahan; Harini Venkatasubramanian; Nidhi Sharma; Sushma Venkatesh; Priyanka Prem; Gino A Kurian
Journal:  Arch Pharm Res       Date:  2021-06-25       Impact factor: 4.946

  2 in total

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