实验结果表明，二甲双胍通过修复肠道屏障并重塑肠道菌群，显著缓解了小鼠的结肠炎症状。进一步的研究揭示，二甲双胍通过下调乙酰辅酶A水平抑制STAT3信号通路的过度激活，从代谢层面调控蛋白翻译后修饰，发挥抗炎作用（见机制示意图）。这一发现不仅为二甲双胍在UC治疗中的“老药新用”提供了理论依据，也为代谢通路在UC发病机制中的研究提供了新的方向。该研究得到国家自然科学基金面上项目资助。

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