Acylated ghrelin protection inhibits apoptosis in the remote myocardium post-myocardial infarction by inhibiting calcineurin and activating ARC.
Refaat A EidPublished in: Archives of physiology and biochemistry (2021)
This study investigated if acylated ghrelin (AG) could inhibit myocardial infarction (MI)-induced apoptosis in the left ventricles (LV) of male rats and tested if this protection involves modulating ARC anti-apoptotic protein. Rats ( n = 12/group) were assigned as a sham-operated, a sham + AG (100 µg/kg, 2x/d, S.C.), MI, and MI + AG. With no antioxidant activity or expression of FAS, AG inhibited caspase-3, 8, and 9 and decreased cytosolic/mitochondrial levels of cytochrome-c, Bax, Bad, and Bad-BCL-2 complex in the LVs of the sham-operated and MI-treated rats. Concomitantly, AG preserved the mitochondria structure, decreased mtPTP, and enhanced state-3 respiration in the LVs of both treated groups. These effects were associated with increased mitochondrial levels of ARC and a reduction in the activity of calcineurin. Overall, AG suppresses MI-induced ventricular apoptosis by inhibition of calcineurin, activation of ARC, and preserving mitochondria integrity.
Keyphrases
- induced apoptosis
- oxidative stress
- signaling pathway
- endoplasmic reticulum stress
- cell death
- quantum dots
- highly efficient
- heart failure
- visible light
- cell cycle arrest
- left ventricular
- diabetic rats
- pi k akt
- mass spectrometry
- endothelial cells
- clinical trial
- high glucose
- high resolution
- reactive oxygen species
- cell proliferation
- anti inflammatory
- newly diagnosed
- amino acid
- protein protein
- stress induced