Review Article
Antioxidative Potentials of Incretin-Based Medications: A Review of Molecular Mechanisms
Table 2
Possible molecular pathways by which incretin-based antidiabetic medications protect against oxidative damages (SOD: superoxide dismutase; CAT: catalase; GPX: glutathione peroxidase; Nrf2: nuclear factor erythroid 2-related factor 2; AGEs: advanced glycation end products; Sirt: sirtuin; MDA: malondialdehyde).
| | Molecular mechanism | Effects on oxidative stress | Ref. |
| Direct roles | Antioxidant defense system | Increase expression/activity of antioxidative elements such as SOD, CAT, and GPX at least partly via Nrf2 and Sirt signaling pathways | [60, 68, 69, 73] | Free radical generation | Reduce the free radical generation thru several pathways such as suppressing prooxidant enzymes and improving mitochondrial function | [54, 60, 86] | Indirect roles | Inflammation-induced oxidative stress | Attenuate procytokines’ expression/release leading to inflammation-induced oxidative stress | [49, 54] | Glucotoxicity | Improve insulin signaling as well as glucose homeostasis leading to lower amount of toxic byproduct as AGEs | [97, 98] | Lipotoxicity | Reduce lipid metabolites such as MDA due to promoting lipid metabolism | [106–108] |
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