SIRT3 激活剂 红 抑制 Th17 细胞分化并缓解结肠炎
Xiaotian Chen1,2, Mingming Zhang3, Fan Zhou4
1Department of Clinical Nutrition, Nanjing Drum Tower Hospital Clinical College of Nanjing Medical University, Nanjing 210008, P.R. China.
红 (HKL) 提取物从马格诺利亚树皮减少T辅助17细胞分化,通过激活SIRT3和抑制STAT3/RORγt通路,提供潜在的保护对结肠炎.
科学领域:
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
- 药理学 药理学是指药理学的学科.
背景情况:
- 辅助性T细胞17 (Th17) 参与了诸如性结肠炎 (UC) 等炎性肠道疾病的发病.
- 红醇 (HKL) 是一种天然的马格诺利亚树皮提取物,可激活Sirtuin-3 (SIRT3),并被认为具有抗炎性质.
研究的目的:
- 在结肠炎的背景下,研究霍诺基 (HKL) 对Th17细胞分化的抑制作用.
- 探索涉及SIRT3和STAT3/RORγt信号通路的潜在分子机制.
主要方法:
- 在UC患者和健康对照中分析血清细胞因子,T细胞子集,SIRT3和p-STAT3/RORγt.
- 在实验室中对T细胞的分化和从小鼠和人类样本中获得的Th17细胞的两极分化,用HKL治疗.
- 在体内研究使用硫酸 (DSS) 诱导的大肠炎和IL-10缺乏的小鼠治疗HKL.
主要成果:
- 与对照组相比,UC患者的IL-17和Th17比例较高,IL-10和SIRT3水平较低.
- 在实验室中,HKL降低了IL-17和Th17细胞比率,独立于STAT3激活.
- 在体内,HKL治疗改善了结肠炎参数,减少了Th17细胞种群,增加了SIRT3表达,并抑制了STAT3酸化和RORγt表达.
结论:
- 红醇 (HKL) 通过通过SIRT3激活调节Th17细胞分化,显示出对大肠炎的保护作用.
- 抑制STAT3/RORγt信号通路是HKL发挥抗炎作用的关键机制.
- 在炎症性肠病研究中,HKL是潜在的治疗候选者.
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