Auraptene Mitigates Colitis Induced by Dextran Sulfate Sodium in Mice by Regulating Specific Intestinal Flora and Repairing the Intestinal Barrier.

IF 4.5 2区 医学 Q2 CELL BIOLOGY Inflammation Pub Date : 2024-08-01 Epub Date: 2024-01-18 DOI:10.1007/s10753-023-01965-5
Tong Chen, Naizhong Jin, Qi Zhang, Zhongming Li, Qiutao Wang, Xuedong Fang
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Abstract

Auraptene (AUT) is widely known to possess both antioxidant and anti-inflammatory properties. This study attempted to evaluate the protective effects of AUT in dextran sodium sulfate (DSS)-induced colitis in mice and to determine the underlying molecular mechanisms. Our results suggest that AUT substantially minimizes the severity and worsening of DSS-induced colitis in mice, indicated by the lengthening of the colon, lower disease activity index, reduced oxidation levels, and attenuated inflammatory factors. Molecular studies revealed that AUT reduces the nuclear translocation of nuclear factor-κB (NF-κB), thereby inhibiting the expression of inflammatory factors. Additionally, AUT promotes the diversity of the intestinal flora in mice with colitis by increasing the number of beneficial bacteria such as Lactobacillaceae and lowering the number of harmful bacteria. In conclusion, AUT mitigates DSS-induced colitis by maintaining the integrity of the intestinal barrier and modulating the levels of the intestinal microbial species.

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金合欢烯通过调节特定肠道菌群和修复肠道屏障缓解硫酸葡聚糖钠诱发的小鼠结肠炎
众所周知,金合欢烯(AUT)具有抗氧化和抗炎特性。本研究试图评估 AUT 对右旋糖酐硫酸钠(DSS)诱导的小鼠结肠炎的保护作用,并确定其潜在的分子机制。我们的研究结果表明,AUT 大大降低了右旋糖酐硫酸钠诱导的小鼠结肠炎的严重程度和恶化程度,表现为结肠延长、疾病活动指数降低、氧化水平降低和炎症因子减弱。分子研究显示,AUT 可减少核因子-κB(NF-κB)的核转位,从而抑制炎症因子的表达。此外,AUT 还能增加乳酸菌等有益菌的数量,降低有害菌的数量,从而促进结肠炎小鼠肠道菌群的多样性。总之,AUT 可通过维持肠道屏障的完整性和调节肠道微生物种类的水平来缓解 DSS 引发的结肠炎。
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来源期刊
Inflammation
Inflammation 医学-免疫学
CiteScore
9.70
自引率
0.00%
发文量
168
审稿时长
3.0 months
期刊介绍: Inflammation publishes the latest international advances in experimental and clinical research on the physiology, biochemistry, cell biology, and pharmacology of inflammation. Contributions include full-length scientific reports, short definitive articles, and papers from meetings and symposia proceedings. The journal''s coverage includes acute and chronic inflammation; mediators of inflammation; mechanisms of tissue injury and cytotoxicity; pharmacology of inflammation; and clinical studies of inflammation and its modification.
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