| 包装 | 价格(元) |
| 5ug | 电议 |
| 1mg | 电议 |
| 5mg | 电议 |
Cell lines | Rat VSMCs |
Preparation Method | Cells were pre-treated with or without test compounds for the indicated time periods and then stimulated with or without Ang II for 30 minutes and CGRP for 60 minutes. In some experiments, CGRP 8-37 (human) or H-89 was added 30 minutes, dibutyl-cAMP 60 minutes and apocynin 2 hours before CGRP treatment. |
Reaction Conditions | CGRP 8-37 (human) (3 × 10-5 mol/L) for 30 minute |
Applications | Pre-treatment with H-89 or CGRP 8-37 (human) also blocked the CGRP inhibitory effects against Ang II-induced oxidative stress. |
Animal models | Male Sprague±Dawley rats (175±200 g) |
Preparation Method | Rts were given a spinal hemisection or a sham surgery at the T13 spinal segment. An externally accessible PE-10 intrathecal catheter that terminated at T13 was used for drug delivery. CGRP 8-37 (human) was delivered just prior to a testing session in 1, 5, 10, or 50 nM doses in artificial cerebral spinal fluid in 10 microl volumes. |
Dosage form | CGRP 8-37 (human)as1,5, 10, or 50 nM doses in artificial cerebral spinal fluid in 10 microl volume. |
Applications | CGRP 8-37 (human) is effective in abolishing mechanical and thermal allodynia produced by spinal hemisection. |
| 产品描述 | CGRP 8-37 (human)is a highly selective CGRP receptor antagonists. CGRP significantly suppressed the level of reactive oxygen species (ROS) generated by NADPH oxidase in Ang II-induced VSMCs. The Ang II-stimulated activation of both Src and the downstream transcription factor, STAT3, was abrogated by CGRP. However, the antioxidative effect of CGRP was lost following the expression of constitutively activated Src or STAT3. Pre-treatment with H-89 or CGRP 8-37 (human) also blocked the CGRP inhibitory effects against Ang II-induced oxidative stress[1]. CGRP 8-37 (human) is effective in abolishing mechanical and thermal allodynia produced by spinal hemisection[2].When explored the effects of calcitonin gene-related peptide (CGRP) and its antagonist CGRP 8-37 (human) on the latency to hindpaw withdrawal responses induced by both thermal and mechanical stimulation in rats. CGRP 8-37 (human) (5nM or 10nM) induced a significant increase in hindpay withdrawal latency[3,5].Intrathecal administration of CGRP 8-37 (human) can reversed the SP-induced decrease in latency to both withdrawal responses ,besides,it can mediated a significant increase in response latency[6].When performed to investigate the effects of intrathecal administration of CGRP 8-37 (human) on the HWL and HWT in rats with unilateral hindpaw inflammation induced by subcutaneous injection of carrageenin.Intrathecal administration of 10 nmol of CGRP8-37 induced a significant bilateral increase in the HWL and HWT in rats with experimentally induced inflammation[4]. CGRP 8-37 (human) could enhance ALI induced by LPS in the rat model, and regulate the expression levels of AQP-1 and AQP-5 by affecting inflammatory cytokines[7]. CGRP8-37 and Endomorphin-1 alone, and in combinated administration, as bolus and continues dose.Endomorphin-1and CGRP 8-37 (human) injections were able to reduce neuropathic pain after spinal cord compression injury[8]. The presence of calcitonin receptor-like receptor (CLR) and receptor activity modifying protein 1 (RAMP1) was investigated. CGRP and its receptor antagonists, olcegepant and CGRP 8-37 (human), were microinjected into the vlPAG while changes of neural responses in the trigeminocervical complex (TCC) were monitored. Inhibition of TCC responses to stimulation of dural afferents and ophthalmic cutaneous receptive fields after microinjection of bicuculline into vlPAG indicated a connection between the vlPAG and TCC neurons. CGRP facilitated these TCC responses, whereas olcegepant and CGRP 8-37 (human) decreased them[9]. References: |
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