Fructose 1,6-diphosphate alleviates myocardial ischemia reperfusion injury in rats through JAK2/STAT3 pathway
- Author:
Ju-Fei WANG
1
;
Cheng JIANG
1
Author Information
- Publication Type:Journal Article
- Keywords: 6-diphosphate; Apoptosis; Janus kinase 2; Fructose 1; Myocardial ischemia reperfusion; Signal transducer Activator of transcription 3
- From: Asian Pacific Journal of Tropical Medicine 2018;11(2):147-150
- CountryChina
- Language:Chinese
- Abstract: Objective: To study the effect of fructose 1,6-diphosphate (FDP) on myocardial ischemia reperfusion injury in rats and its molecular mechanism. Methods: Male SPF SD rats were selected as experimental animals and randomly divided into four groups. Sham group received sham operation, I/R group were made into myocardial ischemia reperfusion injury models, FDP group were made into myocardial ischemia reperfusion injury models and then were given FDP intervention, and FDP+AG490 group were made into myocardial ischemia reperfusion injury models and then were given FDP and JAK2 inhibitor AG490 intervention. Results: CK, CK-MB, cTnI and LDH contents in serum as well as Bax and Caspase-3 protein expression in myocardial tissue of I/R group were significantly higher than those of Sham group whereas Bcl-2, p-JAK2 and p-STAT3 protein expression in myocardial tissues were significantly lower than those of Sham group; CK, CK-MB, cTnI and LDH contents in serum as well as Bax and Caspase-3 protein expression in myocardial tissue of FDP group were significantly lower than those of I/R group whereas Bcl-2, p-JAK2 and p-STAT3 protein expression in myocardial tissue were significantly higher than those of I/R group; CK, CK-MB, cTnI and LDH contents in serum as well as Bax and Caspase-3 protein expression in myocardial tissue of FDP+AG490 group were significantly higher than those of FDP group whereas Bcl-2 protein expression in myocardial tissue was significantly lower than that of FDP group. Conclusion: FDP could reduce the myocardial ischemia reperfusion injury in rats by activating the JAK2/STAT3 pathway.
