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Effects of electroacupuncture on microglia phenotype and epigenetic modulation of C/EBPβ in SAMP8 mice
Li Wang1, Weixian Li2, Wenhui Wu3
1College of Acupuncture and Orthopedics, Hubei University of Chinese Medicine, Wuhan, Hubei, China; Hubei Shizhen Laboratory, Wuhan, Hubei, China.
Background:
Alzheimer's disease (AD), an age-progressive neurodegenerative disease, is featured by a relentless deterioration of cognitive abilities. In parallel with the hypotheses of Aβ and tau, microglia-mediated neuroinflammation is a core pathological hallmark of AD. Promoting the transition of microglia from M1 to M2 phenotype and inhibition of neuroinflammatory response provide new insights into the treatment of AD. And substantial studies have confirmed that overexpression of C/EBPβ accelerates the progression of AD pathology. Acupuncture is renowned for its unique advantages including safety and effectiveness, which has gained wide application in geriatric diseases, and thoroughly exploring the mechanism for its treatment of AD will provide scientific basis for its clinical application.
Methods:
In this study, SAMP8 mice were employed and EA therapy was performed as the main intervention. The combination of behavioural experiments (including water maze and novel objective recognition), Immunofluorescence, Western blot, and Chip-qPCR assay were performed to compare between different groups.
Results:
EA therapy facilitates the polarization of microglia from M1 to M2 phenotype, reduces pro-inflammatory cytokines (IL-6, IL-1β and TNF-α) and promotes the expression of anti-inflammatory factors (IL-4 and IL-10), as well as attenuates neuroinflammation. Simultaneously, EA also inhibits the enrichment of H3K9ac at C/EBPβ promoter region and expression of C/EBPβ. Thus, it was evident that EA had a favorable effect on ameliorating cognitive decline in SAMP8 mice.
Conclusion:
EA therapy may ameliorate cognitive deficits in AD via facilitating microglia shift from M1 to M2 phenotype and epigenetically regulating C/EBPβ. And further studies are required to better understand how the mechanism between microglia and epigenetic modulation of C/EBPβ are effective in reversing AD.
Insights
Electroacupuncture (EA) therapy may improve cognitive function in Alzheimer's disease (AD) by shifting microglia to an anti-inflammatory state and epigenetically regulating C/EBPβ. This approach offers a potential new avenue for AD treatment.
Area of Science:
- Neuroscience
- Immunology
- Genetics
Background:
- Alzheimer's disease (AD) is characterized by cognitive decline and neuroinflammation, with microglia playing a key role.
- Overexpression of C/EBPβ is linked to accelerated AD pathology.
- Acupuncture, particularly electroacupuncture (EA), shows promise in treating geriatric diseases, including potential applications in AD.
Purpose of the Study:
- To investigate the therapeutic potential of EA in ameliorating cognitive deficits in a mouse model of AD.
- To explore the underlying mechanisms, focusing on microglia polarization and epigenetic regulation of C/EBPβ.
Main Methods:
- Utilized SAMP8 mice as an AD model.
- Administered EA therapy as the primary intervention.
- Employed behavioral tests (water maze, novel object recognition), immunofluorescence, Western blot, and ChIP-qPCR assays for analysis.
Main Results:
- EA therapy promoted microglia polarization from M1 to M2 phenotype, reducing pro-inflammatory cytokines and increasing anti-inflammatory factors.
- EA therapy attenuated neuroinflammation and inhibited H3K9ac enrichment at the C/EBPβ promoter region, thereby reducing C/EBPβ expression.
- EA therapy demonstrated a favorable effect on improving cognitive decline in SAMP8 mice.
Conclusions:
- EA therapy may ameliorate cognitive deficits in AD by facilitating microglia M1-to-M2 phenotype shift and epigenetically regulating C/EBPβ.
- Further research is needed to elucidate the intricate mechanisms linking microglia modulation and epigenetic regulation of C/EBPβ in reversing AD pathology.
