Compared with the DMIS group, the expression of LC3 II/I and BNIP3 in the DMIS + IPOC group was significantly higher ( P < 0.05), and the expression of p62 showed a decreasing trend, suggesting that IPOC can promote mitochondrial autophagy ( Figure 3B ).
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Ischemic postconditioning ameliorates diabetic cerebral ischemia via activating the brain-derived neurotrophic factor-tropomyosin receptor kinase B-hypoxia-inducible factor 1α-Bcl-2/adenovirus E1B 19-kDa-interacting protein 3 pathway to induce microglial mitophagy and suppress A1 astrocyte-mediated neuroinflammation.
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