Title: P14 Hydrogen sulfide postconditioning protects isolated rat hearts against ischemia and reperfusion injury mediated by JAK2/STAT3 survival pathway
Abstract: Background JAK2/STAT3 signal pathway was an important component of the newly proposed signal pathway – Survivor Activating Factor Enhancement (SAFE) pathway. JAK–STAT pathway can transduce cellular signals from the plasma membrane to the nucleus, resulting in the regulation of gene expression. It has been shown to play an important role in multiple processes within the heart, including hypertrophy, apoptosis, ischemia–reperfusion (I/R) injury. The objective of this study was to investigate whether JAK2/STAT3 signaling pathway participated in hydrogen sulfide (H 2 S) postconditioning protecting isolated rat hearts against ischemic-reperfusion injury. Methods Eighty-four male Sprague–Dawley (SD) rats (230–270 g) were divided into 6 groups ( n = 14): time-matched perfusion (Sham) group, ischemia/reperfusion (I/R) group, H 2 S postconditioning group, H 2 S with AG-490 group, JAK2 inhibitor AG-490 (5 mmol/L) group, and the AG-490 solvent dimethylsulfoxide (DMSO) ( max ) were recorded. Myocardial infarct size was determined using triphenyltetrazolium chloride (TTC) staining. Myocardial TUNEL staining was used in situ cell death detection kit. And the percentage of TUNEL positive nuclei to all nuclei counted was used as apoptotic index (AI). The expression of phosphorylated and total forms of STAT3, bcl-2, bax was determined by Western blotting. Results No differences in baseline hemodynamics were observed among the experimental groups ( p > 0.05). After reperfusion, compared with the I/R group, H 2 S significantly improved functional recovery and largely decreased myocardial infarct size (23.3% ± 3.8% vs 41.2% ± 4.7%, p p 2 S mediated-protection was abolished by AG-490. Conclusion H 2 S postconditioning effectively protects isolated ischemia and reperfusion rat hearts via activating JAK2/STAT3 signaling pathway.
Publication Year: 2012
Publication Date: 2012-09-01
Language: en
Type: article
Indexed In: ['crossref']
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