由高脂肪饮食诱导的细胞外基质变化的对胆囊平滑肌肉功能障碍的影响
Xingguo Zhong1,2, Feiyang Wu2,3, Weicheng Gao2,3
1Department of General Surgery, The First Affiliated Hospital of Anhui Medical University, 230022 Hefei, Anhui, China.
Frontiers in bioscience (Landmark edition)
|December 30, 2024
概括
高脂肪饮食通过改变其细胞外基质来改变胆囊光滑肌肉,导致收缩性降低,并可能导致胆结石形成. 这影响了胆囊功能,并提供了新的治疗点.
科学领域:
- 消化系统生理学 消化系统生理学
- 细胞生物学 细胞生物学
- 生物化学 生物化学
背景情况:
- 胆结石形成是一个普遍的消化系统问题,原因不完全理解.
- 胆囊光滑肌肉 (GSM) 功能障碍,特别是在高脂肪饮食 (HFD) 条件下,与胆结石的发病有关.
- 通过HFD影响GSM及其通过细胞外基质 (ECM) 改变的收缩性的确切机制尚不清楚.
研究的目的:
- 调查HFD对GSM结构和功能的影响.
- 阐明HFD引起的ECM变化如何影响GSM收缩性.
- 为了确定参与HFD介导的胆囊功能障碍的分子途径.
主要方法:
- 使用海豚和小鼠食HFD或正常饮食 (ND) 的比较研究.
- 用于体外分析的几内亚猪胆囊光滑肌细胞 (GSMCs) 的初级培养.
- 利用组织学染色,RNA测序,生物信息学,3D组织培养,PCR,西部斑点,原子力显微镜和肌肉张力测量.
主要成果:
- HFD诱导了胆囊肌肉层的结构变化,并增加了ECM原沉积.
- 在HFD养的动物中观察到原蛋白,整蛋白,矩阵金属蛋白酶 (MMP) 和PI3K-Akt信号通路的高表达.
- 在HFD组中,发现ECM刚度增加和GSM收缩性降低,较高的原度促进了合成GSMC表型.
结论:
- HFD显著改变了胆囊肌肉ECM的组成.
- 整合素/PI3K-Akt/MMP信号通路被HFD激活,影响GSMC表型和收缩性.
- 这些发现为胆结石形成机制提供了新的见解,并建议胆囊功能障碍的潜在治疗点.
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