ArticleBMC cardiovascular disorders2019
Protective role of berberine in isoprenaline-induced cardiac fibrosis in rats.
Article in BMC cardiovascular disorders, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 29 citations in OpenAlex.
- 17βH-Neriifolin Improves Cardiac Remodeling Through Modulation of Calcium Handling Proteins in the Heart Failure Rat Model.Biomedicines · 2025Article
- Isoproterenol mechanisms in inducing myocardial fibrosis and its application as an experimental model for the evaluation of therapeutic potential of phytochemicals and pharmaceuticals.Animal models and experimental medicine · 2025Review
- Research on rheumatic heart disease from 2013 to early 2024: a bibliometric analysis.Journal of cardiothoracic surgery · 2024Article
- Exploring in vivo and in vitro models for heart failure with biomarker insights: a review.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2024Review
- Advances in the pharmacological mechanisms of berberine in the treatment of fibrosis.Frontiers in pharmacology · 2024Review
- Preventive and treatment efficiency of dendrosomal nano-curcumin against ISO-induced cardiac fibrosis in mouse model.PloS one · 2024Article
- Experimental research on the evaluation of left ventricular systolic function by layered speckle tracking before and after berberine treatment in a cardiac hypertrophy rat model.Cardiovascular diagnosis and therapy · 2023Article
- Gandouling Mitigates CuSOAnimals : an open access journal from MDPI · 2022Article
- Evaluation of the effects of berberine in the prevention of epidural fibrosis in rats: An experimental research.Saudi medical journal · 2022Article
- Research Progress of Traditional Chinese Medicine in Treatment of Myocardial fibrosis.Frontiers in pharmacology · 2022Review
- The effect of nutraceuticals on multiple signaling pathways in cardiac fibrosis injury and repair.Heart failure reviews · 2022Review
- A nutraceutical strategy for downregulating TGFβ signalling: prospects for prevention of fibrotic disorders, including post-COVID-19 pulmonary fibrosis.Open heart · 2021Article
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7 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundCardiac fibrosis is a crucial aspect of cardiac remodeling that can severely affect cardiac function. Cardiac fibroblasts surely influence this process. Besides, macrophage plays an essential role in cardiac remodeling after heart injury. However, whether macrophage influence fibroblasts remain a question worth exploring. This study aimed to define the role of berberine (BBR) on isoprenaline (ISO)-induced cardiac fibrosis in an in vivo rat model and try to figure out the mechanism in vitro study.
methodsThe Sprague-Dawley rats were divided into five groups: control group, ISO-treated group, and ISO + BBR (10 mg/kg/d, 30 mg/kg/d, and 60 mg/kg/d orally)-pretreatment groups. Fibrosis was induced by ISO administration (5 mg/kg/d subcutaneously) for 10 days. One day after the last injection, all of the rats were sacrificed. Using picrosirius red (PSR) straining, immunohistochemistry, immunofluorescence, flow cytometry, western blot, RT-qPCR and cell co-culture, we explored the influence of pretreatment by BBR on ISO-induced cardiac fibrosis.
resultsOur results showed that BBR pretreatment greatly limited ISO-induced cardiac fibrosis and dysfunction. Moreover, BBR administration reduced macrophage infiltration into the myocardium of ISO-treated rats and inhibited transforming growth factor (TGF)-β1/smads signaling pathways in comparison to that seen in the ISO group. Besides, in vitro study showed that BBR-pretreatment reduced ISO-induced TGF-β1 mRNA expression in macrophages and ISO stimulation of macrophages significantly increased the expression of fibrotic markers in fibroblasts, but BBR-pretreatment blocked this increase.
conclusionOur results showed that BBR may have a protective role to cardiac injury via reducing of macrophage infiltration and forbidding fibroblasts transdifferent into an 'activated' secretory phenotype, myofibroblasts.
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