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演題詳細

Poster

痛覚、痒み、及びその障害
Pain, Itch and Their Disorders

開催日 2014/9/13
時間 14:00 - 15:00
会場 Poster / Exhibition(Event Hall B)

マウス椎間板髄核におけるプロスタグランジン合成酵素の発現
Expression of Prostaglandin-Synthesizing Enzymes in Nucleus Pulposus of Mice

  • P3-162
  • 井上 智博 / Tomohiro Inoue:1 伊吹 京秀 / Takae Ibuki:2 伊東 雅和 / Masakazu Ito:1 松村 潔 / Kiyoshi Matsumura:1 
  • 1:大阪工業大学 / Osaka Institute of Technology, Osaka, Japan 2:京都府立医科大学麻酔科 / Dept Anesthesiol, Kyoto Prefectural University of Medicine, Kyoto, Japan 

Disk herniation is a painful pathological condition in which nucleus pulposus (NP) leaks from the disk and induces inflammation. It is not well understood how the leakage of NP induces inflammation, though some mediators are implicated in NP-induced inflammation. Prostaglandins (PGs), lipid mediators involved in inflammatory pain, are possibly involved in NP-induced inflammation. The purpose of this study is to examine the expression of enzymes responsible for PG biosynthesis in intact NP of mice. NP of adult male mice was processed for immunohistochemistry and/or western blot analysis. The immunohistochemical study revealed that cyclooxygenase-1 (COX-1)-like immunoreactivity is highly expressed in NP. The expression level was the highest among other tissues examined including the brain, spinal cord, lungs, stomach, kidneys and intestines. The western blot analysis showed a single band of approximately 72 kDa, the expected molecular weight of COX-1. No COX-1-like immunoreactivity was detected in NP of COX-1-deficient mice. Microsomal prostaglandin E synthase-1 (mPGES-1), the terminal enzyme for PGE2 synthesis, and cytosolic phospholipase A2 were also constitutively expressed in NP. These results suggest that NP cells, when leaks out, could be the source of PGE2, which induces inflammatory pain in disk herniation.

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