ArticleCurrent medical science2024
Jianpi Qinghua Formula Alleviates Diabetic Myocardial Injury Through Inhibiting JunB/c-Fos Expression.
Article in Current medical science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 2 citations in OpenAlex.
- Analysis of Allele-Specific Expression Highlights Novel Participants of Empagliflozin-Driven Effects on T2DM-Associated Regulatory Pathways.International journal of molecular sciences · 2026Article
- Knockdown of JunB alleviates LPS-induced H9C2 cardiomyocyte injury and sepsis-induced myocardial injury by activating the PI3K/Akt/mTOR signaling pathway.BMC cardiovascular disorders · 2025Article
- Jianpi-Qinghua Formula alleviates liver dysfunction by suppression of HBV replication in HepG2.2.15 cells.International journal of molecular and cellular medicine · 2025Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveDiabetic cardiomyopathy (DCM) represents a substantial risk factor for heart failure and increased mortality in individuals afflicted with diabetes mellitus (DM). DCM typically manifests as myocardial fibrosis, myocardial hypertrophy, and impaired left ventricular diastolic function. While the clinical utility of the Jianpi Qinghua (JPQH) formula has been established in treating diabetes and insulin resistance, its potential efficacy in alleviating diabetic cardiomyopathy remains uncertain. This study aims to investigate the impact and underlying molecular mechanisms of the JPQH formula (JPQHF) in ameliorating myocardial injury in nonobese diabetic rats, specifically focusing on apoptosis and inflammation.
methodsWistar rats were assigned as the normal control group (CON), while Goto-Kakizaki (GK) rats were randomly divided into three groups: DM, DM treated with the JPQHF, and DM treated with metformin (MET). Following a 4-week treatment regimen, various biochemical markers related to glucose metabolism, cardiac function, cardiac morphology, and myocardial ultrastructure in GK rats were assessed. RNA sequencing was utilized to analyze differential gene expression and identify potential therapeutic targets. In vitro experiments involved high glucose to induce apoptosis and inflammation in H9c2 cells. Cell viability was evaluated using CCK-8 assay, apoptosis was monitored via flow cytometry, and the production of inflammatory cytokines was measured using quantitative real-time PCR (qPCR) and ELISA. Protein expression levels were determined by Western blotting analysis. The investigation also incorporated the use of MAPK inhibitors to further elucidate the mechanism at both the transcriptional and protein levels.
resultsThe JPQHF group exhibited significant reductions in interventricular septal thickness at end-systole (IVSs) and left ventricular internal diameter at end-systole and end-diastole (LVIDs and LVIDd). JPQHF effectively suppressed high glucose-induced activation of IL-1β and caspase 3 in cardiomyocytes. Furthermore, JPQHF downregulated the expression of myocardial JunB/c-Fos, which was upregulated in both diabetic rats and high glucose-treated H9c2 cells.
conclusionThe JPQH formula holds promise in mitigating diabetic myocardial apoptosis and inflammation in cardiomyocytes by inhibiting JunB/c-Fos expression through suppressing the MAPK (p38 and ERK1/2) pathway.
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