Table 1.
Mechanisms of Nesfatin-1 Exerting Antioxidant, Anti-Inflammatory and Anti-Apoptotic Effects
| Diseases | Mechanisms | Effects | Literature |
|---|---|---|---|
| cerebral I/R | decrease the number of Iba-1-positive cells | anti-inflammatory | 34,36 |
| maintain the balance of oxidant/antioxidant systems | antioxidant | ||
| decrease Caspase-3 activity and increase Bcl-2/Bax ratio | anti-apoptotic | ||
| subarachnoid hemorrhage | inhibit neutrophil infiltration and subsequent release of inflammatory mediators | anti-inflammatory/anti-apoptotic | 38 |
| traumatic brain | inhibit NF-κB pathway | anti-inflammatory | 37 |
| lessen Caspase-3 activity | anti-apoptotic | ||
| diabetic neuropathy | inhibit intracellular ROS overproduction and reduce the apoptotic cell death | antioxidant/anti-apoptotic | 51 |
| PD (MPP+/MPTP-induced) | activate c-Raf-ERK1/2 pathway | anti-apoptotic | 45 |
| PD (rotenone-induced) | inhibit the release of cytochrome C from mitochondria, ROS production and Caspase-3 activation | antioxidant/anti-apoptotic | 44 |
| acetic acid-induced gastric ulcer | modulation of oxidant-antioxidant balance, inhibit neutrophil infiltration and proinflammatory cytokine release by a COX-dependent mechanism | antioxidant/anti-inflammatory | 57 |
| indomethacin-induced gastric ulcer | support the balance in oxidant and antioxidant systems | antioxidant | 55 |
| inhibit the generation of pro-inflammatory mediators | anti-inflammatory | ||
| chronic gastric ulcers | downregulation of SOD mRNA | antioxidant | 56 |
| stress-induced acute gastric injury | inhibit expression and release of proinflammatory cytokines | anti-inflammatory | 58 |
| myocardial infarction | activate Akt/GSK-3β pathway | anti-inflammatory/anti-apoptotic | 3 |
| cardiac I/R | inhibit the release of lactate dehydrogenase | antioxidant | 59 |
| necrotizing enterocolitis | inhibit NF-κB-65 pathway and maintain the balance of oxidant/antioxidant systems | antioxidant/anti-inflammatory | 68 |
| ulcerative colitis | suppress the free radical formation | antioxidant | 72 |
| prevent neutrophil infiltration | anti-inflammatory | ||
| testis torsion | the AKT and CREB signaling pathways | anti-inflammatory/anti-apoptotic | 77 |
| osteoarthritis | inhibit NF-κB, MAPK, and the Bax/Bcl-2 signal pathway | antioxidant/anti-inflammatory /anti-apoptotic |
90 |
| renal I/R | decrease Caspase-3 activity and increase Bcl-2/Bax ratio | anti-apoptotic | 93 |
| maintain the balance of oxidant/antioxidant systems | antioxidant | ||
| LPS-induced AMI | inhibit HMGB1/p38MAPK/NF-κB-65 pathway | antioxidant/anti-inflammatory | 4 |
| skin injury | maintain the intracellular antioxidant pools | antioxidant/anti-inflammatory | 99 |
| obstructive jaundice | decrease malondialdehyde levels | antioxidant | 105 |
| prevent neutrophil infiltration | anti-inflammatory |
Abbreviations: AMI, acute myocardial infarction; COX, cyclooxygenase; I/R, ischemia/reperfusion; LPS, lipopolysaccharide; MPP+, 1-methyl-4-phenylpyridillium ion; MPTP, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine; PD, Parkinson’s disease; ROS, reactive oxygen species; SOD, superoxide dismutase.