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Representative left ventricular developed pressure (LVDP) tracings showed that a 20-minute perfusion with GLP-1(2836) (6 nM) improved recovery of LVDP following IRI as compared with buffer- and scramble-treated (6 nM) controls (Figure 1E)
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To date, studies in animals and humans suggest that GLP-1 may improve hepatic lipid accumulation through signal transduction of the AMP-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) pathway [33]
Although initial studies suggested that GSH depletion was only a byproduct of oxidative stress generated during cell death, recent discoveries suggest that GSH depletion and post-translational modifications of proteins through glutathionylation are critical regulators of apoptosis
Previous studies in preterm infants have linked increases in pulmonary oxidative stress and glutathione metabolism to the development of BPD
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