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基礎科学と病態生理

Titikorn Chunchai1,2, Hiranya Pintana1,2, Patcharapong Pantiya1,2

  • 1Neurophysiology Unit, Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.

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まとめ

慢性的な高脂肪食とLPSは、神経発生を損なうことによってうつ病様行動を誘発する。P2X7阻害剤とミノサイクリンは、肥満ラットの神経発生を回復させ、うつ病様行動を軽減し、治療の可能性を示唆した。

キーワード:
神経炎症神経発生うつ病肥満P2X7受容体ミノサイクリン高脂肪食ラット動物モデル

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科学分野:

  • 神経科学
  • 免疫学
  • 代謝

背景:

  • 慢性的な高脂肪食（HFD）とリポ多糖（LPS）の投与は、神経炎症とうつ病様行動を促進する。
  • プリン作動性受容体P2X7を介したミクログリアの活性化は、LPS誘発性の炎症とATP産生に関与している。
  • 免疫チェックポイント下の食事誘発性肥満における神経発生とうつ病様行動に対するP2X7阻害剤の影響は、よく理解されていない。

研究 の 目的:

  • 体重、内臓脂肪、脾臓重量、神経発生、およびうつ病様行動に対するP2X7阻害の影響を調査すること。
  • LPSで挑戦された肥満ラットにおけるP2X7阻害剤の治療可能性を評価すること。

主な方法:

  • Wistarラットを12週間、通常の食事（ND）またはHFDで飼育した。
  • ラットは、LPS注射の前に生理食塩水、ミノサイクリン、またはP2X7阻害剤（JNJ-55308942）を投与された。
  • うつ病様行動は強制水泳試験で評価され、神経発生は海馬歯状回で評価された。

主要な成果:

  • HFDは体重と内臓脂肪の重量を増加させた。ミノサイクリンとP2X7阻害剤の両方が、HFD食ラットの脾臓重量を減少させ、抗炎症効果を示唆した。; SOX2陽性細胞で評価された神経発生は、HFD食ラットで減少したが、ミノサイクリンまたはP2X7阻害剤によって回復した。; 凍結時間と潜時の増加によって示されるうつ病様行動は、HFD食ラットの両方の治療によって軽減された。

結論:

  • P2X7阻害とミノサイクリンは、免疫チェックポイントにさらされた肥満ラットにおいて抗炎症効果を示した。
  • 両方の治療は、HFD食ラットにおいて神経発生を効果的に回復させ、うつ病様行動を改善した。
  • P2X7を標的とすることは、食事誘発性肥満関連うつ病の潜在的な治療戦略を提供する。