柏柏林通过PPAR-γ/mTOR/HIF-1α信号通路调节巨细胞表型来缓解DSS诱导的大肠炎
Long He1, Zhuotai Zhong2, Fengbin Liu3
1The First Affiliated Hospital of Guangzhou University of Chinese Medicine, No. 16 Baiyun Road, Guangzhou 510000, China.
Journal of ethnopharmacology
|February 12, 2026
概括
柏柏林 (BBR) 通过PPAR-γ/mTOR/HIF-1α通路促进M2巨分化来缓解大肠炎. 这项研究证实BBR作为性结肠炎 (UC) 的潜在治疗方法.
科学领域:
- 免疫学 免疫学 免疫学
- 药理学 药理学是指药理学的学科.
- 胃肠病学 胃肠病学
背景情况:
- 柏柏林 (BBR) 是一种传统中医药中的,用于治疗腹和性结肠炎 (UC).
- 在治疗UC时,BBR的精确机制,特别是它对巨细胞的影响,尚未完全理解.
研究的目的:
- 为了研究BBR对大肠炎中M2巨细胞两极化的免疫调节作用.
- 阐明涉及PPAR-γ,mTOR和HIF-1α信号通路的潜在分子机制.
主要方法:
- 德克斯硫酸 (DSS) 诱导的大肠炎小鼠模型用BBR治疗.
- 流细胞计和免疫光检测用于评估结肠组织中的巨细胞表型.
- 海马分析细胞代谢,西部斑点和蛋白质表达的免疫组织化学.
- 使用RAW264.7细胞和用GW9662.2进行药理抑制的体外研究.
主要成果:
- 在体内,BBR治疗缓解了结肠炎,并将炎症性巨细胞转移到M2表型.
- BBR显著上调过氧体增殖器激活受体玛 (PPAR-γ) 表达.
- 在体外,BBR增强了M2极化,增加了RAW264.7细胞中的氧耗和ATP产生,并抑制了mTOR/HIF-1α通路.
- 用GW9662抑制PPAR-γ,取消了BBR对M2极化和mTOR/HIF-1α通路的影响.
结论:
- BBR通过PPAR-γ/mTOR/HIF-1α信号轴促进M2巨细胞的两极分化.
- 这些发现支持BBR作为性结肠炎 (UC) 的有希望的治疗剂.
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