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. Author manuscript; available in PMC: 2014 Jul 1.
Published in final edited form as: Mol Nutr Food Res. 2013 Mar 15;57(7):10.1002/mnfr.201200642. doi: 10.1002/mnfr.201200642

Figure 6. Schematic diagram showing wolfberry and/or its bioactive components-modulated retinoprotection in db/db mice at the early stage of diabetes.

Figure 6

Hyperglycemia and/or subsequent hypoxia in db/db diabetic mice causes inhibition of lutein and zeaxnathin metabolic gene expression and decreases in protein levels of BCO2, AMPKα2, and TFAM in mitochondria, which leads to mitochondrial dysfunction and subsequent retinal degeneration in diabetes (marked with double lines). Dietary wolfberry and/or the bioactive components (wolfberry bioactives) primarily activates AMPKα2 in mitochondria and nuclei, which then triggers increased expression of genes related to lutein and zeaxanthin metabolism (SR-BI, GSTP1, and BCO2) and mitochondrial biogenesis (PGC-1α, NRF1, and TFAM), and decreases in cell stress responses (HIF-1α, VEGF, and HSP60), resulting in attenuation of hypoxia, enhancement of mitochondrial function, and subsequent retinal neuroprotection in db/db diabetic mice (marked with single lines).