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CGRP 8-37(human)
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
CGRP 8-37(human)图片
包装与价格:
包装价格(元)
5ug电议
1mg电议
5mg电议

产品介绍

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:
[1]. Luo HM, Wu X, et,al. Calcitonin gene-related peptide inhibits angiotensin II-induced NADPH oxidase-dependent ROS via the Src/STAT3 signalling pathway. J Cell Mol Med. 2020 Jun;24(11):6426-6437. doi: 10.1111/jcmm.15288. Epub 2020 May 5. PMID: 32372557; PMCID: PMC7294141.
[2]. Bennett AD, Chastain KM, Hulsebosch CE. Alleviation of mechanical and thermal allodynia by CGRP(8-37) in a rodent model of chronic central pain. Pain. 2000 May;86(1-2):163-75. doi: 10.1016/s0304-3959(00)00242-6. PMID: 10779673.
[3]. Yu LC, Hansson P, et,al. The calcitonin gene-related peptide antagonist CGRP8-37 increases the latency to withdrawal responses in rats. Brain Res. 1994 Aug 8;653(1-2):223-30. doi: 10.1016/0006-8993(94)90393-x. Erratum in: Brain Res 1994 Dec 15;666(2):295. PMID: 7526959.
[4]. Yu LC, Hansson P, et,al. Intrathecal CGRP8-37-induced bilateral increase in hindpaw withdrawal latency in rats with unilateral inflammation. Br J Pharmacol. 1996 Jan;117(1):43-50. doi: 10.1111/j.1476-5381.1996.tb15152.x. PMID: 8825341; PMCID: PMC1909388.
[5]. LOfgren O, Yu LC, et,al. Intrathecal CGRP(8-37) results in a bilateral increase in hindpaw withdrawal latency in rats with a unilateral thermal injury. Neuropeptides. 1997 Dec;31(6):601-7. doi: 10.1016/s0143-4179(97)90006-8. PMID: 9574827.
[6]. Yu LC, Hansson P, et,al. Opioid antagonists naloxone, beta-funaltrexamine and naltrindole, but not nor-binaltorphimine, reverse the increased hindpaw withdrawal latency in rats induced by intrathecal administration of the calcitonin gene-related peptide antagonist CGRP8-37. Brain Res. 1995 Nov 6;698(1-2):23-9. doi: 10.1016/0006-8993(95)00752-c. PMID: 8581488.
[7]. Hong-Min F, Chun-Rong H, et,al.CGRP 8-37 enhances lipopolysaccharide-induced acute lung injury and regulating aquaporin 1 and 5 expressions in rats. J Physiol Biochem. 2016 Aug;73(3):381-386. doi: 10.1007/s13105-017-0563-3. Epub 2017 May 4. Erratum in: J Physiol Biochem. 2017 Oct 5;: PMID: 28470555.
[8]. Janzadeh A, Karami Z, et,al.The role of CGRP receptor antagonist (CGRP8-37) and Endomorphin-1 combination therapy on neuropathic pain alleviation and expression of Sigma-1 receptors and antioxidants in rats. J Chem Neuroanat. 2020 Jul;106:101771. doi: 10.1016/j.jchemneu.2020.101771. Epub 2020 Feb 21. PMID: 32092447.
[9].Pozo-Rosich P, Storer RJ, et,al. Periaqueductal gray calcitonin gene-related peptide modulates trigeminovascular neurons. Cephalalgia. 2015 Dec;35(14):1298-307. doi: 10.1177/0333102415576723. Epub 2015 Mar 19. PMID: 25792688.