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Published on: January 5, 2017
Aurantii Fructus extract alleviates DSS-induced colitis in mice via regulating NF-κB and Nrf2/HO-1 signaling pathways
JunBao Yu1, WenYa Mei1, JiaYuan Zhu1
1School of Pharmacy, Hunan University of Chinese Medicine, Changsha, Hunan, China.
Background:
Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by progressive loss of intestinal function, highlighting an urgent need for effective therapeutics. This study aimed to investigate the protective effects of Aurantii Fructus extract (AFE) on dextran sulfate sodium (DSS)-induced UC in mice and its impact on the gut microbiota.
Methods:
The chemical components of AFE were identified using high-performance liquid chromatography (HPLC). A murine model of DSS-induced colitis was established, and the therapeutic efficacy of AFE was assessed through the disease activity index (DAI), colon length measurement, and histopathological examination. Inflammatory status and oxidative stress markers were evaluated by enzyme-linked immunosorbent assay (ELISA) and western blotting, while the expression of tight junction proteins was analyzed via immunohistochemistry. Additionally, cecal contents were subjected to 16S rRNA gene sequencing to analyze changes in the intestinal microbiota.
Results:
AFE treatment significantly alleviated the severity of colitis, as evidenced by reduced DAI scores, attenuated colon shortening, and improved histopathological damage. It restored the expression of the tight junction protein ZO-1 in the colon. AFE also markedly reduced the levels of pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β) and suppressed the activation of the NF-κB pathway. Concurrently, AFE enhanced antioxidant capacity by increasing glutathione (GSH) levels, decreasing malondialdehyde (MDA), and activating the Nrf2/HO-1 signaling pathway. Furthermore, AFE treatment inhibited the proliferation of pathogenic bacteria and restored the homeostasis of the gut microbiota.
Conclusion:
The findings demonstrate that AFE confers a protective effect against DSS-induced UC. The underlying mechanism is associated with the inhibition of the NF-κB pathway, activation of the Nrf2/HO-1 antioxidant pathway, enhancement of the intestinal barrier, and restoration of gut microbiota homeostasis.
Insights
Aurantii Fructus extract (AFE) shows protective effects against ulcerative colitis (UC) in mice by reducing inflammation and oxidative stress. AFE also improves gut barrier function and restores gut microbiota balance, offering a potential therapeutic strategy for UC.
Area of Science:
- Pharmacology
- Gastroenterology
- Microbiology
Background:
- Ulcerative colitis (UC) is a chronic inflammatory bowel disease requiring novel therapeutic interventions.
- Intestinal dysfunction in UC necessitates effective treatments to improve patient outcomes.
Purpose of the Study:
- To investigate the protective effects of Aurantii Fructus extract (AFE) on dextran sulfate sodium (DSS)-induced UC in a mouse model.
- To elucidate the impact of AFE on gut microbiota composition and function in the context of colitis.
Main Methods:
- Chemical profiling of AFE using HPLC.
- Induction of UC in mice using DSS and assessment of therapeutic efficacy via DAI, colon length, and histopathology.
- Evaluation of inflammatory markers, oxidative stress, tight junction proteins, and gut microbiota composition (16S rRNA sequencing).
Main Results:
- AFE treatment significantly reduced colitis severity, improved colon histology, and restored tight junction protein expression (ZO-1).
- AFE suppressed inflammatory cytokines (TNF-α, IL-6, IL-1β) via NF-κB pathway inhibition and enhanced antioxidant capacity through Nrf2/HO-1 activation.
- AFE modulated gut microbiota, inhibiting pathogenic bacteria and promoting homeostasis.
Conclusions:
- AFE demonstrates significant protective effects against DSS-induced UC in mice.
- Mechanisms include NF-κB inhibition, Nrf2/HO-1 antioxidant pathway activation, intestinal barrier enhancement, and gut microbiota restoration.
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