| 包装 | 价格(元) |
| 500μg | 电议 |
| 1mg | 电议 |
Cell lines | BV-2 cells |
Preparation Method | BV-2 cells were treated with recombinant murine MFG-E8 (rmMFG-E8) or/and Colivelin TFA after exposing for 4 h with oxygen glucose deprivation (OGD). |
Reaction Conditions | 50 µg/ml Colivelin for 4h |
Applications | MFG-E8 regulated OGD-induced microglial M1/M2 polarization by inhibiting p-STAT3 and SOCS3 expressions, which was reversed by STAT3 activator (Colivelin). |
Animal models | Male C57BL/6 mice |
Preparation Method | After a midline laparotomy, the cecum was exteriorized, ligated and punctured twice with a 23-G needle. The cecum was then returned into the peritoneal cavity and the abdominal incision was closed. After the procedure, mice were randomly assigned to three treatment groups: a vehicle-treated group received distilled water (200 ul/mouse) intraperitoneally (i.p.); a 100 ug colivelin-treated group received the colivelin at 100 ug/kg i.p., and a 200 ug colivelin-treated group received the colivelin at 200 ug/kg i.p. at 1 h after CLP. |
Dosage form | 100-200 ug/kg colivelin |
Applications | Colivelin as a potent synthetic humanin derivative, is a potential therapeutic compound to restore endothelial stability and improve outcomes of sepsis. |
| 产品描述 | Colivelin (CLN) is A brain-permeable neuroprotective peptide that has effective long-term effects on Aβ deposition, neuronal apoptosis and synaptic plasticity defects in neurodegenerative diseases. Colivelin is a STAT3 activator. MFG-E8 regulated OGD-induced microglial M1/M2 polarization by inhibiting p-STAT3 and SOCS3 expressions, which was reversed by STAT3 activator (Colivelin TFA)[6]. The administration of the STAT3 activator colivelin could offset the inhibitory effect of RPN2 silencing on the survival and apoptosis of NPC cells[9]. Colivelin as a potent synthetic humanin derivative, is a potential therapeutic compound to restore endothelial stability and improve outcomes of sepsis[1]. In vivo animal studies have further indicated that intracerebroventricular administration of Colivelin not only completely suppresses impairment in spatial working memory induced by repetitive intracerebroventricular injection of Abeta25-35 or Abeta1-42, but also it antagonizes neuronal loss in the CA1 region of hippocampus induced by hippocampal injection of Abeta1-42[2]. Histological analysis demonstrated increased motoneuronal survival in spinal cords of Colivelin-treated mice as compared with saline- or ADNF-treated mice, indicating that Colivelin is a promising neurotrophic peptide for treatment of ALS[3]. Colivelin blocked the alcohol-induced decline in brain weight and prevented alcohol-induced: apoptosis, activation of caspase-3 and increases of cytosolic cytochrome c, and decreases of mitochondrial cytochrome c Analysis of proteins in the upstream signaling pathway revealed that CLN down-regulated the phosphorylation of the c-Jun N-terminal kinase[4]. Colivelin administration decreased the neurological deficits and infarct lesion induced by brain ischemia. Colivelin inhibited axonal damage and neuronal death in brain tissue, which was associated with elevated anti-apoptotic gene expression in ischemic neurons as well as increased axonal growth up until two-weeks post-stroke[5]. Colivelin has strong neuroprotective effects on learning and memory behaviors in APP/PS1 mice and that this behavioral improvement is closely associated with the reduction of Aβ deposition and alleviation of LTP suppression in the hippocampus, supporting the potential of CLN for the prevention and treatment of AD[7]. Intrahippocampal injection of colivelin (0.2 nmol) effectively prevented Aβ25-35 (4 nmol)-induced deficits in spatial learning and memory of rats in Morris water maze test; the suppression of in vivo hippocampal long term potentiation (LTP) by Aβ25-35 was nearly completely prevented by CLN; in addition, CLN pretreatment also effectively inhibited Aβ25-35-induced calcium overload in primary cultured hippocampal neurons[8]. References: |
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