南京中医药大学:异槲皮苷抑制肠道菌群产生尿毒症毒素
创作:Unbroken 审核:szx 2020年10月21日
  • 天然产物异槲皮苷(ISO)是一种小分子黄酮类化合物,可在不直接抑制肠道菌群生长及吲哚合成酶TnaA的表达的同时,干扰肠道菌群介导的吲哚产生;
  • 机制上,ISO通过调节肠道细菌的电子传递链,抑制H质子势的建立,从而抑制色氨酸传输,以减少吲哚的生物合成;
  • 在慢性肾病小鼠模型中,ISO可抑制吲哚和硫酸吲哚酚的产生;
  • 黄酮苷的去糖基化活性对其抑制吲哚产生的作用十分关键。
主编推荐语
szx
硫酸吲哚酚是一种典型的尿毒症毒素,在慢性肾病患者体内累积,且无法通过血液透析除去。南京中医药大学的郭建明团队与段金廒团队在Gut Microbes上发表的一项最新研究,鉴定出一种黄酮类天然产物——异槲皮苷,可通过调控电子传递链,抑制肠道菌群合成吲哚,从而抑制硫酸吲哚酚在小鼠体内的生成。该研究结果提示,靶向肠道菌群的尿毒症毒素代谢途径是抑制慢性肾病进展的潜在策略。
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Gut Microbes [IF:7.74]

Targeting the gut microbial metabolic pathway with small molecules decreases uremic toxin production

用小分子靶向肠道菌群代谢途径以减少尿毒症毒素的产生

10.1080/19490976.2020.1823800

2020-10-04, Article

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Abstract:收起
Uremic toxins are a class of toxins that accumulate in patients with chronic kidney disease (CKD). Indoxyl sulfate (IS), a typical uremic toxin, is not efficiently removed by hemodialysis. Modulation of IS production in the gut microbiota may be a promising strategy for decreasing IS concentration, thus, delaying CKD progression. In the present study, we identified isoquercitrin (ISO) as a natural product that can perturb microbiota-mediated indole production without directly inhibiting the growth of microbes or the indole-synthesizing enzyme TnaA. ISO inhibits the establishment of H proton potential by regulating the gut bacteria electron transport chain, thereby inhibiting the transport of tryptophan and further reducing indole biosynthesis. This non-microbiocidal mechanism may enable ISO to be used as a therapeutic tool, specifically against pathologies triggered by the accumulation of the microbial-produced toxin IS, as in CKD. Herein, we have shown that it is possible to inhibit gut microbial indole production using natural components. Therefore, targeting the uremic toxin metabolic pathway in gut bacteria may be a promising strategy to control host uremic toxin production.

First Authors:
Yingyi Wang,Jianping Li

Correspondence Authors:
Jianming Guo,Jinao Duan

All Authors:
Yingyi Wang,Jianping Li,Chenkai Chen,Jingbo Lu,Jingao Yu,Xuejun Xu,Yin Peng,Sen Zhang,Shu Jiang,Jianming Guo,Jinao Duan

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