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Naringin Exerts Therapeutic Effects on Mice Colitis: A Study Based on Transcriptomics Combined With Functional
Jianyi Dong1, Yuanyuan Chen1, Fang Yang1
1Comparative Medicine Department of Researching and Teaching, Dalian Medical University, Dalian, China.
Abstract:
Naringin has been shown to exert protective effects in an animal model of ulcerative colitis, but detailed mechanisms remain unclear. This study aimed to investigate function and signaling mechanisms underlying naringin-induced therapeutic effects on colitis. Two mouse models were established to mimic human Inflammatory bowel disease (IBD) by treating drinking water with dextran sodium sulphate or intra-colonic administration of 2, 4, 6-trinitrobenzene sulfonic acid. Transcriptomics combined with functional experiments were used to investigate underlying mechanisms. Colitis symptoms, including weight loss and high disease activity index were significantly reversed by naringin. The inflammatory response, oxidative reactions, and epithelial cell apoptosis that occur with colitis were also alleviated by naringin. After naringin treatment, transcriptomics results identified 753 differentially expressed mRNAs that were enriched in signaling pathways, including the neuroactive ligand-receptor interaction, calcium signaling, and peroxisome proliferator-activated receptor (PPAR) signaling. The naringin-induced alleviation of colitis was significantly inhibited by the PPAR-γ inhibitor BADGE. In IEC-6 and RAW264.7 cells incubated with lipopolysaccharide (LPS), NF-κB-p65, a downstream protein of PPAR-γ, was significantly increased. Naringin suppressed LPS-induced high expression of NF-κB-p65, which was inhibited by small interfering RNA targeting PPAR-γ. Our study clarifies detailed mechanisms underlying naringin-induced therapeutic effects on mice colitis, and PPAR-γ was found to be the main target of naringin by functional experiments both in vivo and in vitro. Our study supplies new scientific information for the use of naringin in colitis treatment.
Insights
Naringin effectively treats ulcerative colitis in mice by reducing inflammation and apoptosis. Its therapeutic action is primarily mediated through the peroxisome proliferator-activated receptor gamma (PPAR-γ) pathway.
Area of Science:
- Gastroenterology
- Pharmacology
- Molecular Biology
Background:
- Ulcerative colitis (UC) is a chronic inflammatory bowel disease (IBD) with limited treatment options.
- Naringin shows protective effects in UC animal models, but its precise mechanisms are not fully understood.
Purpose of the Study:
- To elucidate the functional and signaling mechanisms of naringin's therapeutic effects in colitis.
- To identify key molecular targets of naringin in inflammatory bowel disease.
Main Methods:
- Established dextran sodium sulfate (DSS) and 2,4,6-trinitrobenzene sulfonic acid (TNBS) induced colitis mouse models.
- Utilized transcriptomics, in vivo, and in vitro functional assays to investigate naringin's effects.
- Examined the role of peroxisome proliferator-activated receptor gamma (PPAR-γ) and NF-κB signaling pathways.
Main Results:
- Naringin significantly alleviated colitis symptoms, including weight loss and disease activity index.
- Naringin reduced inflammation, oxidative stress, and epithelial cell apoptosis in colitis models.
- Transcriptomics revealed naringin impacts pathways including neuroactive ligand-receptor interaction, calcium signaling, and PPAR signaling.
- PPAR-γ inhibition blocked naringin's therapeutic effects; naringin suppressed LPS-induced NF-κB activation via PPAR-γ.
Conclusions:
- Naringin demonstrates significant therapeutic potential for ulcerative colitis.
- Peroxisome proliferator-activated receptor gamma (PPAR-γ) is identified as a key molecular target mediating naringin's anti-colitis effects.
- This study provides novel mechanistic insights into naringin's efficacy for IBD treatment.
