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Updated: Jun 23, 2025
Inducing Apical Periodontitis in Mice
Published on: August 6, 2019
Milk-derived small extracellular vesicles inhibit the MAPK signaling pathway through CD36 in chronic apical
Meng Xia1, Jiayin Ding1, Saixuan Wu1
1School of Stomatology, Dalian Medical University, Liaoning 116044, China.
Background:
Small extracellular vesicles derived from milk (Milk-sEVs) have the advantages of easy availability, low cost, low toxicity, and inhibition of inflammation. CD36 mediates inflammation stress in a variety of disease states. The purpose of this study was to investigate the role of Milk-sEVs in inhibiting fibroblast inflammation through CD36 and provide reference data for the treatment of chronic apical periodontitis.
Results:
The addition of Milk-sEVs resulted in decreased expression of inflammation-related factors in L929 cells, and transcriptome sequencing screened for the DEG CD36 in the Milk-sEV treatment group under inflammation. The mouse model of apical periodontitis was successfully established, and CD36 expression increased with the development of inflammation. Transfection of si-CD36 into L929 cells reduced inflammation by inhibiting activation of the MAPK signaling pathway.
Conclusions:
CD36 expression increased with the development of apical periodontitis. In the setting of LPS-mediated inflammation, Milk-sEVs inhibited activation of the MAPK signaling pathway by decreasing the expression of CD36 in L929 cells and thereby reducing inflammation.
Insights
Milk-derived small extracellular vesicles (Milk-sEVs) reduce inflammation by targeting CD36. This study shows Milk-sEVs can inhibit fibroblast inflammation, offering potential for treating chronic apical periodontitis.
Area of Science:
- Biomedical research
- Extracellular vesicle biology
- Inflammation research
Background:
- Small extracellular vesicles derived from milk (Milk-sEVs) are readily available, cost-effective, and possess anti-inflammatory properties.
- CD36 is implicated in mediating inflammatory stress across various diseases.
- Chronic apical periodontitis is an inflammatory condition requiring novel therapeutic strategies.
Purpose of the Study:
- To investigate the mechanism by which Milk-sEVs inhibit fibroblast inflammation via CD36.
- To evaluate the therapeutic potential of Milk-sEVs for chronic apical periodontitis.
Main Methods:
- L929 fibroblast cell line treated with Milk-sEVs under inflammatory conditions.
- Transcriptome sequencing to identify differentially expressed genes (DEGs).
- Establishment of a mouse model for apical periodontitis.
- siRNA-mediated knockdown of CD36 (si-CD36) in L929 cells.
- Analysis of MAPK signaling pathway activation.
Main Results:
- Milk-sEVs treatment decreased expression of inflammation-related factors in L929 cells.
- Transcriptome analysis identified CD36 as a key DEG in Milk-sEV treated cells.
- CD36 expression was upregulated in the established mouse model of apical periodontitis.
- si-CD36 transfection reduced inflammation by inhibiting MAPK signaling pathway activation.
Conclusions:
- CD36 expression correlates with the progression of apical periodontitis.
- Milk-sEVs mitigate lipopolysaccharide (LPS)-induced inflammation in L929 cells.
- Milk-sEVs exert anti-inflammatory effects by downregulating CD36 expression and subsequently inhibiting MAPK pathway activation.
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