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基础科学和病原发生学

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

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概括

慢性高脂肪饮食和LPS通过损害神经生成诱导类似抑郁的行为. P2X7抑制剂和米诺环林恢复了神经发生和减轻了肥胖大鼠的抑郁行为,表明了治疗潜力.

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科学领域:

  • 神经科学是一个神经科学.
  • 免疫学 免疫学 免疫学
  • 代谢过程中的代谢.

背景情况:

  • 慢性高脂肪饮食 (HFD) 和脂多糖 (LPS) 管理促进神经炎症和类似抑郁的行为.
  • 通过纯能受体P2X7的微细胞激活与LPS诱导的炎症和ATP产生有关.
  • 在免疫挑战下,P2X7抑制剂对饮食诱导的肥胖症的神经发生和行为的影响尚不清楚.

研究的目的:

  • 为了研究P2X7抑制对体重,内脏脂肪,脏体重,神经发生和类似抑郁的行为的影响.
  • 评估P2X7抑制剂在LPS.挑战的肥胖大鼠中的治疗潜力.

主要方法:

  • 威斯塔大鼠被食正常饮食 (ND) 或HFD12周.
  • 在注射LPS之前,老鼠接受了盐水,米诺环素或P2X7抑制剂 (JNJ-55308942).
  • 使用强迫游泳测试来评估类似抑郁症的行为,并在牙状中评估神经发生.

主要成果:

  • HFD增加了身体和内脏脂肪的体重. 敏环和P2X7抑制剂都降低了HFD养大鼠的脏重量,表明了抗炎作用.
  • 通过SOX2阳性细胞评估的神经发生在HFD养的老鼠中减少,但通过米诺环林或P2X7抑制剂恢复.
  • 通过增加结时间和延迟来表明类似抑郁的行为,在HFD养的老鼠中,这两种治疗都减弱了.

结论:

  • 抑制P2X7和米诺环林在接受免疫挑战的肥胖大鼠中显示出抗炎作用.
  • 这两种治疗都有效地恢复了神经发生,并改善了HFD养大鼠的抑郁类行为.
  • 准P2X7为饮食诱导的与肥胖有关的抑郁症提供了潜在的治疗策略.