FK506 protects heart function via increasing autophagy after myocardial infarction in mice
| Autor: | Zhenyu Yang, Yunle Wang, Jia Lu, Lei Yang, Rongrong Gao, Weili Cheng |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Cardiac function curve Male Cardiotonic Agents Biophysics Myocardial Infarction Infarction Inflammation Apoptosis 030204 cardiovascular system & hematology Pharmacology Biochemistry Tacrolimus 03 medical and health sciences Electrocardiography 0302 clinical medicine polycyclic compounds Autophagy Medicine Animals Myocardial infarction Phosphorylation Molecular Biology PI3K/AKT/mTOR pathway business.industry organic chemicals Myocardium TOR Serine-Threonine Kinases NF-kappa B Heart Cell Biology medicine.disease Mice Inbred C57BL Survival Rate 030104 developmental biology Immunology cardiovascular system medicine.symptom business Ligation |
| Zdroj: | Biochemical and biophysical research communications. 493(3) |
| ISSN: | 1090-2104 |
| Popis: | Objective To investigate the effect of tacrolimus (FK506) on myocardial infarction, and to further explore its function mechanism. Material and methods C57BL/6J mice were randomly divided into three groups: the sham group, the control group and the FK506 group. Anterior descending branch ligation was conducted in the control and the FK506 groups, while sham operation was conducted in the sham group. Mice in the sham and the control groups were intragastrical administration with saline, while the FK506 group were with FK506. Heart function were detected by echocardiogram at 3rd day or 21st day after MI. Hearts were harvested at 3rd day or 21st day after MI for the detection of apoptosis, autophagy, mTOR and NF-κB pathway. Results FK506 treatment increased survival rate and cardiac function in mice after MI. It decreased infarction area, inflammation reaction and apoptosis. To further study the mechanism of FK506 protection effect, we discovered it could increase autophagy via inhibit mTOR pathway. Conclusion FK506 protect heart function after MI as it improved myocardial cells autophagy process via inhibiting mTOR pathway. |
| Databáze: | OpenAIRE |
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