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When a pathogen enters the body and reproduces, it can cause an infection, damage body cells, and cause illness symptoms that eventually lead to disease. Therefore, its prevention requires breaking the chain of infection.
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The pathophysiology of urinary tract infections (UTIs) encompasses several progressive stages, beginning with bacterial colonization and culminating in potential systemic complications if untreated. UTIs are primarily initiated by bacteria, such as Escherichia coli, which often originate from the gastrointestinal tract and migrate to the urinary system through the periurethral area. This migration can occur via several routes, including improper hygiene practices, sexual activity, or...
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基础科学和病原发生学

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

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概括

德克索鲁比化疗会引起一种称为chemobrain的神经毒性. 达帕格利弗洛辛是一种SGLT2抑制剂,通过改善大鼠的神经发生和突触完整性来保护它免受多克索鲁比诱导的化学脑膜.

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科学领域:

  • 神经科学是一个神经科学.
  • 药理学 药理学是指药理学的学科.
  • 在瘤学瘤学.

背景情况:

  • 德克索鲁比化疗可以诱导神经系统缺陷,称为化学大脑,其特点是神经发生和突触可塑性受损.
  • -葡萄糖共载体2 (SGLT2) 抑制剂,如达帕格利弗洛辛,具有独立于其降糖效果的神经保护性质.

研究的目的:

  • 为了研究达帕格利弗洛辛在多克索鲁比诱导化学大脑的老鼠模型中的潜在神经保护作用.

主要方法:

  • 成年雄性Wistar大鼠接受了多克索鲁比 (DOX) 或多克索鲁比加达帕格利弗洛辛 (DOX-DAPA) 治疗30天.
  • 对照大鼠接受了正常盐水 (NSS).
  • 对海马组织进行了神经发生和突触可塑性的分子标志物的分析.

主要成果:

  • doxorubicin 治疗导致 化学脑, 由减少的 BDNF, SOX2, DCX, NeuN 和 PSD-95 蛋白质表达体现出来, 并减少海马体的树突脊柱密度.
  • 与仅用多克索鲁比治疗的老鼠相比,达帕格利弗洛辛的联合治疗显著增加了DCX和PSD-95蛋白水平,并恢复了树突脊柱密度.

结论:

  • 多克索鲁比通过成人神经发生和突触完整性受损而诱导化学大脑.
  • 达帕格利弗洛辛表现出神经保护作用,减轻了多克索鲁比诱导的化学脑.
  • 达帕格利弗洛辛 (Dapagliflozin) 是一种潜在的治疗策略,用于管理与多克索鲁比辛相关的神经毒性.