| biological activity | N-Acetyl lysyltyrosylcysteine amide is an effective, reversible, specific and non-toxic myeloperoxidase (MPO) tripeptide inhibitor. N-Acetyl lysyltyrosylcysteine amide can effectively inhibit MPO from producing toxic oxidants in vivo. N-Acetyl lysyltyrosylcysteine amide attenuates neuronal damage in the brain after stroke and preserves brain tissue and neural function. N-Acetyl lysyltyrosylcysteine amide inhibits MPO-dependent hypochlorous acid (HOCl) production, protein nitration, and LDL oxidation. |
| in vivo study | N-Acetyl lysyltyrosylcysteine amide (KYC) significantly decreases infarct size, blood-brain barrier leakage, infiltration of myeloid cells, loss of neurons, and apoptosis in the brains of middle cerebral occlusion (MCAO) mice. N-Acetyl lysyltyrosylcysteine amide (10 mg/kg; I.p.; Daily for 3-7 days) significantly reduces neurological severity scores and infarct size in MCAO mice. N-Acetyl lysyltyrosylcysteine amide (10 mg/kg; I.p.; daily 7 days) significantly protects BBB function and decreased neutrophil infiltration. N-Acetyl lysyltyrosylcysteine amide (10 mg/kg; I.p.; daily 7 days) significantly reduces microglia/macrophage activation and neuron loss in MCAO mice. N-Acetyl lysyltyrosylcysteine amide (10 mg/kg; I.p.; Daily for 3-7 days) decreases apoptosis and cell injury in the brains of MCAO mice. N-Acetyl lysyltyrosylcysteine amide reduced MPO in the brains of MCAO mice. N-Acetyl lysyltyrosylcysteine amide reduces NO2Tyrand 4-HNE in MCAO mice. Animal Model: 8-10 weeks old c57bl/6j mice (middle cerebral object occlusion (mcao) mode) dosage: 10 mg/kg Administration: I.p.; Daily for 3-7 days result: Significantly reduced neurological deficit and brain infarct size in ice subjected to mcao. |
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Animal Model:
| 8-10 weeks old C57BL/6J mice (middle cerebral artery occlusion (MCAO) mode) |
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Dosage:
| 10 mg/kg |
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Administration:
| I .p.; daily for 3-7 days |
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Result:
| Significantly reduced neurological deficit and brain infarct size in mice subjected to MCAO. |
