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Melatonin enhances mitochondrial biogenesis and function in porcine preimplantation embryos
- 언어ENG
- URLhttps://db.koreascholar.com/Article/Detail/362160
Melatonin (N-aceyl-5-methoxytryptamine) is the major hormone of the pineal gland. Melatonin and its metabolic derivatives possess extensive free-radical scavenging abilities and played critical roles in antioxidative stress, resisting apoptotic cell death. Melatonin also could enhance mitochondrial biogenesis in rats with carbon tetrachloride-induced liver fibrosis. In addition, melatonin attenuates myocardial ischemia/reperfusion injury by reducing oxidative stress damage via activation of SIRT1 signaling in a melatonin receptor 2-dependent manner. Activation or overexpression of SIRT1 could enhance mitochondrial biogenesis and function by inducing PGC-1α expression and deacetylation. The aim of this study was to investigate if melatonin enhances mitochondrial biogenesis and function via activation of melatonin receptor 2/SIRT1/PGC1-α Pathway. The results showed that Melatonin rescued rotenone-induced impairment of porcine embryo development. Treatment with rotenone could increase oxidative stress and apoptosis. Rotenone impaired mitochondrial functions by disrupting mitochondrial membrane potential, reducing mitochondrial DNA copy number and ATP production. Melatonin could improve SIRT1 and PGC-1α expression, inducing mitochondrial biogenesis. Rotenone-induced mitochondrial dysfunction and ATP deficiency was rescued by melatonin treatment, the oxidative stress and apoptosis was significantly decreased. Inhibition of melatonin receptor 2 or Knockdown of SIRT1 abolished the protective effects of melatonin on rotenone-induced impairments. Therefore, melatonin enhanced mitochondrial biogenesis and function, protected against rotenone-induced impairments.
