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用S-adenosylmethionine的治疗改善了小鼠体内因氨基酸诱导的肠道屏障功能障碍和肠道微生物疾病

Lin Xiao¹, Weidong Dou¹, Yajie Wang¹

¹Department of General Surgery, Peking University First Hospital, No. 8 Xishiku Street, Beijing 100034, China.

Biochemical pharmacology

|August 27, 2023

概括

通过改善肠道屏障功能和恢复肠道微生物群平衡,S-adenosylmethionine (SAM) 保护免受 irinotekan 诱导的腹. 此外,SAM还减少了活性氧物种,并保持了结肠细胞中紧密结合蛋白.

科学领域:

胃肠病学胃肠病学
药理学药理学是指药理学的学科.
微生物学微生物学

背景情况:

化疗可以引起严重的胃肠道副作用,包括腹和肠道屏障功能障碍.
皮肤上皮质的完整性和肠道微生物组的变化是依赖于氨酸诱导的肠道毒性的确切机制.
S-adenosylmethionine (SAM) 是一种天然存在的化合物,具有已知的细胞保护性质.

研究的目的:

为了研究SAM对因虹素诱导的肠道屏障损伤的保护作用.
为了评估SAM对肠道微生物失调造成的SAM的影响.
阐明涉及SAM保护作用的分子通路.

主要方法:

使用人类结肠细胞系 (Caco-2) 接受了SN-38 (氨基酸氨基酸的活性代谢物) 的治疗.
采用了一种因氨基酸诱导的腹小鼠模型.
评估了肠道透性,紧结蛋白表达 (ZO-1,奥克卢丁,克劳丁-1),反应性氧物种 (ROS) 水平和肠道微生物群组成.

主要成果:

在小鼠中,SAM前期治疗显著降低了因虹素诱导的体重减轻和腹.
在小鼠和Caco-2细胞中,SAM抑制了肠道透性的增加,并恢复了紧结蛋白的表达.
萨姆逆转了氨酸诱导的蛋白细菌的过度生长,并降低了Caco-2细胞中的ROS水平.
通过抑制p38 MAPK/p65 NF-κB/MLCK/MLC通路,SAM保护了Caco-2屏障的功能.

结论:

萨姆显示显著的保护性作用,对排尿素诱导的肠壁功能障碍和腹.
萨姆减轻了肠道微生物失调症,并减少了与虹素治疗相关的氧化应激.
SAM的机制涉及抑制关键的炎症和障碍破坏信号通路.
萨姆显示出作为治疗剂的潜力,以管理与氨酸相关的胃肠道毒性.

关键词:

化疗化疗是一种化学疗法.我们的肠道微生物群.氨酸是一种氨酸.P38 MAPK/p65 NF-κB/MLCK/MLC 信号通路的使用情况萨姆·萨姆·萨姆·萨姆是什么意思紧密结合蛋白质是紧密结合的蛋白质.

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