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Published on: January 5, 2017
Therapeutic Effects of Camel Milk Exosomes and Their miR-148a-3p Cargo on DSS-Induced Colitis: Modulating Gut
Siriguleng Yu1,2, Chaoqun Liu1, Hongqiang Yao1,2
1College of Veterinary Medicine, Inner Mongolia Agricultural University, Inner Mongolia Autonomous Region, Hohhot 010011, China.
Abstract:
Camel milk contains abundant bioactive compounds, but the therapeutic potential of its exosomes as natural delivery systems for gut health remains unclear. This study investigated the therapeutic effects and underlying mechanisms of camel milk exosomes (CME) and their enriched miRNA cargo, miR-148a-3p, on dextran sodium sulfate (DSS)-induced ulcerative colitis (UC) in mice. Both CME and miR-148a-3p significantly alleviated colitis symptoms, including weight loss, colon shortening, and disease activity scores. These effects were achieved by suppressing pro-inflammatory cytokines and restoring intestinal barrier integrity through Zonula Occludens-1 (ZO-1) upregulation. Moreover, the treatments promoted M2 macrophage polarization, inhibited NF-κB signaling via silent information regulator T1 (SIRT1) upregulation and increased microbial diversity with the enrichment of beneficial taxa. Notably, the therapeutic effects of miR-148a-3p were comparable to those of CME, underscoring its role as a key functional component. These findings highlight CME as promising natural nanotherapeutics for UC, offering a novel, multitargeted strategy for managing intestinal inflammation.
Insights
Camel milk exosomes (CME) and miR-148a-3p show therapeutic potential for ulcerative colitis (UC). These natural nanotherapeutics reduce inflammation and improve gut health by targeting key molecular pathways.
Area of Science:
- Exosome biology
- Gastroenterology
- Immunology
Background:
- Camel milk exosomes (CME) contain bioactive compounds.
- Therapeutic potential of CME for gut health, specifically ulcerative colitis (UC), is largely unexplored.
- Understanding CME's mechanisms in UC is crucial for developing novel treatments.
Purpose of the Study:
- Investigate the therapeutic effects of CME and miR-148a-3p on dextran sodium sulfate (DSS)-induced UC in mice.
- Elucidate the underlying mechanisms of CME and miR-148a-3p in alleviating colitis.
- Assess the role of miR-148a-3p as a key functional component of CME.
Main Methods:
- Induction of UC in mice using DSS.
- Administration of CME and isolated miR-148a-3p.
- Assessment of clinical colitis symptoms (weight loss, colon length, disease activity score).
- Analysis of pro-inflammatory cytokines, intestinal barrier integrity (ZO-1), macrophage polarization, NF-κB signaling (SIRT1), and gut microbiota.
Main Results:
- Both CME and miR-148a-3p significantly alleviated UC symptoms.
- Treatments suppressed pro-inflammatory cytokines and enhanced intestinal barrier integrity via ZO-1 upregulation.
- Therapies promoted M2 macrophage polarization, inhibited NF-κB signaling through SIRT1 upregulation, and increased microbial diversity.
- miR-148a-3p demonstrated therapeutic effects comparable to CME.
Conclusions:
- Camel milk exosomes (CME) are promising natural nanotherapeutics for ulcerative colitis (UC).
- miR-148a-3p is a key functional component mediating CME's therapeutic effects.
- CME offer a novel, multitargeted strategy for managing intestinal inflammation and improving gut health.
