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Abstract <p>This study investigates the roles and interactions of spinalhistone deacetylase 2 (HDAC2) and glutamate metabotropic receptor2 (mGluR2) in chronic pancreatitis (CP)-related pain. A CP rat model wasinduced using dibutyltin dichloride (DBTC). Pain sensitivity wasassessed using mechanical and thermal pain tests. HDAC2 and mGluR2expression levels in the spinal cord were measured using Westernblot and qPCR. The effects of HDAC2 inhibition and mGluR2 activationon inflammatory markers and pain sensitivity were also evaluated.Cell co-culture experiments explored regulatory mechanisms involvingcholecystokinin (CCK)-stimulated pancreatic acinar cells (AR42J)and neuron-like cells (F11). In this study, HDAC2 was highly expressedand mGluR2 expression was down-regulated in the spinal cords ofrats modelling CP. HDAC2 inhibition increased mGluR2 expression,decreased inflammatory cytokines (IL-1β, IL-6, TNF-α, CCL-2) inpancreatic tissue, and reduced pain sensitivity. Activation of mGluR2similarly alleviated inflammation and pain. Co-culture experimentsshowed that CCK-stimulated AR42J cells modulated HDAC2 and mGluR2expression in F11 cells via inflammatory factors. HDAC2 was foundto bind and modify the mGluR2 promoter, regulating its expression.In conclusion, HDAC2 and mGluR2 play critical roles in CP-relatedpain. Modulating their activity effectively reduces pain, providingnew insights into CP pain mechanisms and potential therapeutic targets.Further research should explore the specific interactions betweenHDAC2 and mGluR2 to develop more effective treatments.</p>

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Spinal HDAC2 Influences the Development of Chronic Pancreatitis-Related Pain through mGluR2

  • 期刊论文

  • 发表日期：

    2025年1月1日

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  • Xiang-tian Zeng,
  • Ding-wen Zhong,
  • Wen-hui Chen,
  • Qi-xin Dai,
  • Xianyu Huang,
  • Yong He,
  • Rong-qiang Ye,
  • Xiu-lin Xiao,
  • Yong-hui Liao

摘要

Abstract

This study investigates the roles and interactions of spinalhistone deacetylase 2 (HDAC2) and glutamate metabotropic receptor2 (mGluR2) in chronic pancreatitis (CP)-related pain. A CP rat model wasinduced using dibutyltin dichloride (DBTC). Pain sensitivity wasassessed using mechanical and thermal pain tests. HDAC2 and mGluR2expression levels in the spinal cord were measured using Westernblot and qPCR. The effects of HDAC2 inhibition and mGluR2 activationon inflammatory markers and pain sensitivity were also evaluated.Cell co-culture experiments explored regulatory mechanisms involvingcholecystokinin (CCK)-stimulated pancreatic acinar cells (AR42J)and neuron-like cells (F11). In this study, HDAC2 was highly expressedand mGluR2 expression was down-regulated in the spinal cords ofrats modelling CP. HDAC2 inhibition increased mGluR2 expression,decreased inflammatory cytokines (IL-1β, IL-6, TNF-α, CCL-2) inpancreatic tissue, and reduced pain sensitivity. Activation of mGluR2similarly alleviated inflammation and pain. Co-culture experimentsshowed that CCK-stimulated AR42J cells modulated HDAC2 and mGluR2expression in F11 cells via inflammatory factors. HDAC2 was foundto bind and modify the mGluR2 promoter, regulating its expression.In conclusion, HDAC2 and mGluR2 play critical roles in CP-relatedpain. Modulating their activity effectively reduces pain, providingnew insights into CP pain mechanisms and potential therapeutic targets.Further research should explore the specific interactions betweenHDAC2 and mGluR2 to develop more effective treatments.