Pretreatment with Tilianin improves mitochondrial energy metabolism and oxidative stress in rats with myocardial ischemia/reperfusion injury via AMPK/SIRT1/PGC-1 alpha signaling pathway

Mar 27, 2019Journal of pharmacological sciences

Tilianin before injury may improve heart cell energy and reduce damage in rats through AMPK/SIRT1/PGC-1 alpha pathway

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Abstract

Tilianin significantly reduced myocardial infarction in a rat model of ischemia/reperfusion injury.

Treatment with Tilianin improved the pathological structure of the heart tissue.
Tilianin markedly increased ATP and NAD levels while decreasing ADP and AMP levels.
The ratio of AMP to ATP was reduced following Tilianin treatment.
Tilianin lowered levels of reactive oxygen species (ROS) and malondialdehyde (MDA), indicating reduced oxidative stress.
Enhanced activity of superoxide dismutase (SOD) was observed with Tilianin treatment.
Expression levels of AMPK, SIRT1, and PGC-1 alpha mRNA were significantly elevated by Tilianin.

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Mitochondrial energy metabolism and oxidative stress play a crucial role in ameliorating myocardial ischemia/reperfusion injury (MIRI). Tilianin has been reported to have a significant protection for mitochondrion in MIRI. However, the underlying mechanisms remain unknown. This study investigated whether Tilianin regulates mitochondrial energy metabolism and oxidative stress in MIRI via AMPK/SIRT1/PGC-1 alpha signaling pathway. The MIRI model was established by 30 min of coronary occlusion followed by 2 h of reperfusion in rats. The results revealed that Tilianin significantly reduced myocardial infarction, improved the pathological morphology of myocardium, markedly increased the contents of ATP and NAD, decreased ADP and AMP contents and the ratio of AMP/ATP, reduced the level of ROS and MDA, enhanced SOD activity, evidently increased the levels of AMPK, SIRT1 and PGC-1 alpha mRNA, up-regulated the expressions of AMPK, pAMPK, SIRT1, PGC-1alpha, NRF1, TFAM and FOXO1 proteins. However, these effects were respectively abolished by Compound C (a specific AMPK inhibitor) and EX-527 (a specific SIRT1 inhibitor). Taken together, this study found that Tilianin could attenuate MIRI by improving mitochondrial energy metabolism and reducing oxidative stress via AMPK/SIRT1/PGC-1 alpha signaling pathway. +

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Pretreatment with Tilianin improves mitochondrial energy metabolism and oxidative stress in rats with myocardial ischemia/reperfusion injury via AMPK/SIRT1/PGC-1 alpha signaling pathway

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