Glycine Protects against Hypoxic-Ischemic Brain Injury by Regulating Mitochondria-Mediated Autophagy via the AMPK Pathway

<div>Glycine eliminated mitochondria-mediated autophagy via regulation of the AMPK pathway. (a) Protein expression level of p-AMPK<i><sub>α</sub></i> in the cortex from ipsilateral sides of each group and analysis of p-AMPK<i><sub>α</sub></i> (of AMPK<i><sub>α</sub></i>), p-mTOR (of GAPDH). (b) Protein expression level of p-AMPK<i><sub>α</sub></i> on the hippocampus from ipsilateral sides of each group and analysis. (c) Protein expressions of p-mTOR, p-AMPK<i><sub>α</sub></i>, AMPK<i><sub>α</sub></i>, Mfn-2, p62, parkin, PINK1, Bnip3, LC3 II, and LC3 I from the cortex. (d) Analyses of protein expressions above. (e) Protein expressions of p-mTOR, p-AMPK<i><sub>α</sub></i>, AMPK<i><sub>α</sub></i>, Mfn-2, p62, parkin, PINK1, Bnip3, LC3 II, and LC3 I from the cortex. 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Oxidative Medicine and Cellular Longevity

fig3

Figure 3

Figure 3: Glycine Protects against Hypoxic-Ischemic Brain Injury by Regulating Mitochondria-Mediated Autophagy via the AMPK Pathway 