LQVTDSGLYRCVIYHPP (LP17) TFA is a triggering receptor expressed on myeloid cells (TREM-1) inhibitory peptide. LQVTDSGLYRCVIYHPP TFA substantially alleviates ischemia-induced infarction and neuronal injury. LQVTDSGLYRCVIYHPP TFA can get access into brain and block TREM-1[1].
LQVTDSGLYRCVIYHPP (LP17) (1 or 10 μM; 24 h) substantially decreases mRNA levels of pro-inflammatory cytokines and chemokines after reoxygenation and remarkably attenuates extracellular protein levels of IL-1β and IL-18 in a microglia oxygen-glucose deprivation (OGD) model[1].
LQVTDSGLYRCVIYHPP (LP17) (10 μM; 24 h) interacts with microglial SYK[1].
RT-PCR[1]
| Cell Line: | Primary microglia |
| Concentration: | 1 or 10 μM |
| Incubation Time: | 24 h |
| Result: | Decreased mRNA levels of NLRP3, IL-1β, IL-18, IL-6, CD16, CD32, iNOS, MCP-1, CXCL-1, and CXCL-2 after reoxygenation. |
Western Blot Analysis[1]
| Cell Line: | Primary microglia |
| Concentration: | 10 μM |
| Incubation Time: | 24 h |
| Result: | Suppressed ischemia/reperfusion-induced increments in CARD9, p-p65 in CARD9/NF-κB signaling and NLRP3, ASC, cleaved caspase-1, mature IL-1β, and mature IL-18 in NLRP3/caspase-1 signaling in a microglia oxygen-glucose deprivation (OGD) model. |
LQVTDSGLYRCVIYHPP (LP17) (0.5 or 1 mg/kg; intranasal; daily for 3 days) alleviates ischemia-induced infarction and neuronal injury in mice[1].
| Animal Model: | Adult male C57BL/6J mice (20-25 g), mice cerebral ischemia/reperfusion (I/R) model induced by middle cerebral artery occlusion (MCAO)[1] |
| Dosage: | 0.5 mg/kg or 1 mg/kg |
| Administration: | Intranasal administration, once daily for 3 consecutive days after MCAO |
| Result: | Abolished ischemia-induced TREM-1 elevation at 1 mg/kg. Significantly reduced infarct volume by 27.3%, induced a markedly reduction in TUNEL positive cells and FJC positive neurons at 1 mg/kg. Rescued neurological deficits and cognitive dysfunction of MCAO mice. Inhibited microglial M1 polarization and neutrophil infiltration. |