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Berberine blocks inflammasome activation and alleviates diabetic cardiomyopathy via the miR‑18a‑3p/Gsdmd pathway
Lin Yang1, Chun-Feng Cheng1, Zhi-Fang Li1
1Shenzhen Hospital of Integrated Traditional Chinese and Western Medicine, Guangzhou University of Chinese Medicine, Shenzhen, Guangdong 518104, P.R. China.
Insights
Berberine (BBR) alleviates diabetic cardiomyopathy (DCM) by inhibiting a specific microRNA (miR-18a-3p) that controls gasdermin D (Gsdmd) expression. This research reveals BBR
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Pharmacology
Background:
- Diabetic cardiomyopathy (DCM) is a significant global cause of mortality.
- Berberine (BBR), a natural compound, shows promise in treating DCM, but its mechanisms require elucidation.
Purpose of the Study:
- Investigate the molecular mechanisms underlying BBR's anti-DCM effects.
- Determine BBR's role in regulating microRNA (miRNA) expression and its impact on pyroptosis.
Main Methods:
- Examined BBR's effect on IL-1β secretion and gasdermin D (Gsdmd) expression.
- Assessed BBR's ability to upregulate miR-18a-3p expression.
- Investigated miR-18a-3p's targeting of Gsdmd in high glucose-treated cells and a rat DCM model.
Main Results:
- BBR inhibited IL-1β secretion and Gsdmd expression at the post-transcriptional level.
- BBR upregulated miR-18a-3p expression by activating its promoter.
- miR-18a-3p targeted Gsdmd, reduced pyroptosis, and improved cardiac function markers in a DCM rat model.
Conclusions:
- BBR alleviates DCM by inhibiting miR-18a-3p-mediated Gsdmd activation.
- BBR demonstrates potential as a therapeutic agent for diabetic cardiomyopathy.
Abstract:
Diabetic cardiomyopathy (DCM) is a cardiovascular disease which has been reported as a major cause of mortality worldwide for several years. Berberine (BBR) is a natural compound extracted from a Chinese herb, with a clinically reported anti‑DCM effect; however, its molecular mechanisms have not yet been fully elucidated. The present study indicated that BBR markedly alleviated DCM by inhibiting IL‑1β secretion and the expression of gasdermin D (Gsdmd) at the post‑transcriptional level. Considering the importance of microRNAs (miRNAs/miRs) in the regulation of the post‑transcriptional process of specific genes, the ability of BBR to upregulate the expression levels of miR‑18a‑3p by activating its promoter (‑1,000/‑500) was examined. Notably, miR‑18a‑3p targeted Gsdmd and abated pyroptosis in high glucose‑treated H9C2 cells. Moreover, miR‑18a‑3p overexpression inhibited Gsdmd expression and improved biomarkers of cardiac function in a rat model of DCM. On the whole, the findings of the present study indicate that BBR alleviates DCM by inhibiting miR‑18a‑3p‑mediated Gsdmd activation; thus, BBR may be considered a potential therapeutic agent for the treatment of DCM.
