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首页> 外文期刊>Life sciences >The proteinase/proteinase-activated receptor-2/transient receptor potential vanilloid-1 cascade impacts pancreatic pain in mice.
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The proteinase/proteinase-activated receptor-2/transient receptor potential vanilloid-1 cascade impacts pancreatic pain in mice.

机译：蛋白酶/蛋白酶激活的受体2 /瞬时受体电位香草酸1级联会影响小鼠的胰腺疼痛。

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AIMS: Proteinase-activated receptor-2 (PAR2) and transient receptor potential vanilloid-1 (TRPV1) are co-localized in the primary afferents, and the trans-activation of TRPV1 by PAR2 activation is involved in processing of somatic pain. Given evidence for contribution of PAR2 to pancreatic pain, the present study aimed at clarifying the involvement of TRPV1 in processing of pancreatic pain by the proteinase/PAR2 pathway in mice. MAIN METHODS: Acute pancreatitis was created by repeated administration of cerulein in conscious mice, and the referred allodynia/hyperalgesia was assessed using von Frey filaments. Injection of PAR2 agonists into the pancreatic duct was achieved in anesthetized mice, and expression of Fos in the spinal cord was determined by immunohistochemistry. KEY FINDINGS: The established referred allodynia/hyperalgesia following cerulein treatment was abolished by post-treatment with nafamostat mesilate, a proteinase inhibitor, and with capsazepine, a TRPV1 antagonist, in mice. Injection of trypsin, an endogenous PAR2 agonist, or SLIGRL-NH(2), a PAR2-activating peptide, into the pancreatic duct caused expression of Fos protein in the spinal superficial layers at T8-T10 levels in the mice. The spinal Fos expression caused by trypsin and by SLIGRL-NH(2) was partially blocked by capsazepine, the former effect abolished by nafamostat mesilate. SIGNIFICANCE: Our data thus suggest that the proteinase/PAR2/TRPV1 cascade might impact pancreatic pain, in addition to somatic pain, and play a role in the maintenance of pancreatitis-related pain in mice.
机译：目的：蛋白酶激活受体2（PAR2）和瞬时受体电位香草酸-1（TRPV1）共同定位在初级传入者中，并且通过PAR2激活对TRPV1的反式激活涉及躯体疼痛的处理。给定PAR2对胰腺疼痛的贡献的证据，本研究旨在阐明TRPV1在小鼠中通过蛋白酶/ PAR2途径参与胰腺疼痛的处理。主要方法：反复向有意识的小鼠中施用铜蓝蛋白可引起急性胰腺炎，并使用von Frey细丝评估所提及的异常性疼痛/痛觉过敏。在麻醉的小鼠中将PAR2激动剂注射到胰管中，并通过免疫组织化学测定了脊髓中Fos的表达。主要发现：通过用蛋白酶抑制剂甲磺酸萘法莫他和TRPV1拮抗剂Capsazepine进行小鼠后处理，取消了对小脑蛋白治疗后已建立的相关性异常性疼痛/痛觉过敏。将胰蛋白酶（一种内源性PAR2激动剂，或SLIGRL-NH（2），一种PAR2激活肽）注射入胰管中，会导致Fos蛋白在小鼠T8-T10水平在脊髓浅表层表达。胰蛋白酶和SLIGRL-NH（2）引起的脊柱Fos表达被卡萨平部分阻断，卡那西平被甲磺酸萘法莫他所废除。意义：因此，我们的数据表明蛋白酶/ PAR2 / TRPV1级联除可能会影响躯体疼痛外，还可能影响胰腺疼痛，并在维持小鼠胰腺炎相关疼痛中发挥作用。

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