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马齿苋水提物和汁对溃疡性结肠炎小鼠模型中 NLRP3 炎性小体激活的抑制作用。

Inhibitory effect of Portulaca oleracea L. aqueous extract and juice on NLRP3 inflammasome activation in an ulcerative colitis mouse model.

机构信息

National Key Laboratory of Veterinary Public Health Security, College of Veterinary Medicine, China Agricultura University, Beijing, 100193, China.

Key Biology Laboratory of Chinese Veterinary Medicine, Ministry of Agriculture and Rural Affairs, Beijing, 100193, People's Republic of China.

出版信息

Environ Sci Pollut Res Int. 2023 Aug;30(36):86380-86394. doi: 10.1007/s11356-023-28365-4. Epub 2023 Jul 5.

DOI:10.1007/s11356-023-28365-4
PMID:37402916
Abstract

Portulaca oleracea L. (PO) is an edible and medicinal plant used for treating gastrointestinal diseases. However, the effects of PO on ulcerative colitis (UC) and underlying mechanisms remain unclear. This study investigated the effects of PO aqueous extract (POE) and PO juice (PJ) on dextran sulfate sodium (DSS)-induced UC in a mouse model and attempted to unravel their underlying mechanisms. The results revealed that PJ contains more bioactive compounds and has more overlapping targets with UC than POE. Both POE and PJ effectively reduced Disease Activity Index scores and inflammatory cell infiltration in the UC mouse model, but PJ had a better effect than POE. Furthermore, PJ inhibited pyroptosis by decreasing the expression of the NLRP3 inflammasome, while also repairing the dysfunction of the intestinal barrier by upregulating the expression of tight junction proteins. Therefore, based on the study findings, we concluded that PJ can improve DSS-induced UC and may suppress pyroptosis by interfering with the activation of the NLRP3 inflammasome.

摘要

马齿苋(Portulaca oleracea L.)是一种可食用和药用植物,用于治疗胃肠道疾病。然而,马齿苋对溃疡性结肠炎(UC)的影响及其潜在机制仍不清楚。本研究探讨了马齿苋水提物(POE)和马齿苋汁(PJ)对葡聚糖硫酸钠(DSS)诱导的 UC 小鼠模型的影响,并试图阐明其潜在机制。结果表明,PJ 含有更多的生物活性化合物,与 POE 相比,与 UC 有更多的重叠靶点。POE 和 PJ 均能有效降低 UC 小鼠模型的疾病活动指数评分和炎症细胞浸润,但 PJ 的效果优于 POE。此外,PJ 通过降低 NLRP3 炎性小体的表达抑制细胞焦亡,同时通过上调紧密连接蛋白的表达修复肠道屏障功能障碍。因此,基于研究结果,我们得出结论,PJ 可以改善 DSS 诱导的 UC,并可能通过干扰 NLRP3 炎性小体的激活来抑制细胞焦亡。

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