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Updated: Jul 30, 2025
Polarization and Characterization of M1 and M2 Human Monocyte-Derived Macrophages on Implant Surfaces
Published on: December 6, 2024
[Akt2 inhibitor promotes M2 macrophage polarization in rats with periapical inflammation by reducing miR-155-5p
1School of Stomatology/Oral Disease Research Center, Wannan Medical College, Wuhu 241000, China.
Objective:
To investigate the effect of Akt2 inhibitor on macrophage polarization in the periapical tissue in a rat model of periapical inflammation.
Methods:
Rat models of periapical inflammation were established in 28 normal SD rats by opening the pulp cavity of the mandibular first molars, followed by injection of normal saline and Akt2 inhibitor into the left and right medullary cavities, respectively. Four rats without any treatment served as the healthy control group. At 7, 14, 21 and 28 days after modeling, 7 rat models and 1 control rat were randomly selected for observation of inflammatory infiltration in the periapical tissues by X-ray and HE staining. Immunohistochemistry was used to detect the expression and localization of Akt2, macrophages and the inflammatory mediators. RT-PCR was performed to detect the mRNA expressions of Akt2, CD86, CD163, inflammatory mediators, miR-155-5p and C/EBPβ to analyze the changes in macrophage polarization.
Results:
X-ray and HE staining showed that periapical inflammation was the most obvious at 21 days after modeling in the rats. Immunohistochemistry and RT-PCR showed that compared with those in the control rats, the expressions of Akt2, CD86, CD163, miR-155-5p, C/EBPβ, and IL-10 increased significantly in the rat models at 21 days (P < 0.05). Compared with saline treatment, treatment with the Akt2 inhibitor significantly decreased the expression levels of Akt2, CD86, miR-155-5p and IL-6 and the ratio of CD86+M1/CD163+M2 macrophages (P < 0.05) and increased the expression levels of CD163, C/EBPβ and IL-10 in the rat models (P < 0.05).
Conclusion:
Inhibition of Akt2 can delay the progression of periapical inflammation in rats and promote M2 macrophage polarization in the periapical inflammatory microenvironment possibly by reducing miR-155-5p expression and activating the expression of C/EBPβ in the Akt signaling pathway.
Insights
Inhibition of Akt2 (a specific enzyme) can delay periapical inflammation in rats. This treatment promotes M2 macrophage polarization, potentially by modulating miR-155-5p and C/EBPβ within the Akt signaling pathway.
Area of Science:
- Biomedical Science
- Immunology
- Molecular Biology
Context:
- Periapical inflammation is a common dental issue.
- Macrophage polarization plays a critical role in inflammatory processes.
- The Akt signaling pathway is implicated in cellular responses to inflammation.
Purpose:
- To investigate the therapeutic effect of an Akt2 inhibitor on macrophage polarization in a rat model of periapical inflammation.
- To elucidate the molecular mechanisms underlying Akt2 inhibition's impact on periapical tissue inflammation.
Summary:
- Periapical inflammation was induced in rats, and the effects of an Akt2 inhibitor were examined.
- Akt2 inhibition significantly reduced inflammatory markers and promoted M2 macrophage polarization.
- The study suggests Akt2 inhibition influences macrophage polarization via miR-155-5p and C/EBPβ within the Akt pathway.
Impact:
- Provides insights into novel therapeutic strategies for periapical inflammation.
- Highlights the role of Akt2 and macrophage polarization in periapical disease.
- Offers potential targets for drug development in endodontic and inflammatory conditions.
