ArticleBMC complementary medicine and therapies2021
Taohuajing reduces oxidative stress and inflammation in diabetic cardiomyopathy through the sirtuin 1/nucleotide-binding oligomerization domain-like receptor protein 3 pathway.
Article in BMC complementary medicine and therapies, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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13 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Efficacy of traditional Chinese medicine on diabetic cardiomyopathy in animal models: a systematic review and meta-analysis.Frontiers in pharmacology · 2023Pooled it
- Chinese Herbal Medicines for Diabetic Cardio-Cerebrovascular Diseases: Key Bioactive Metabolites and Action Mechanisms.Journal of nutrition and metabolism · 2026Review
- Therapeutic potential of traditional Chinese medicine in diabetic cardiomyopathy: a review.Frontiers in endocrinology · 2025Review
- Effects of NLRP3 Inflammasome Mediated Pyroptosis on Cardiovascular Diseases and Intervention Mechanism of Chinese Medicine.Chinese journal of integrative medicine · 2024Review
- Hmgcs2 is the hub gene in diabetic cardiomyopathy and is negatively regulated by Hmgcs2, promoting high glucose-induced cardiomyocyte injury.Immunity, inflammation and disease · 2024Article
- The signaling pathways of selected traditional Chinese medicine prescriptions and their metabolites in the treatment of diabetic cardiomyopathy: a review.Frontiers in pharmacology · 2024Review
- The Radioprotective Effect of LBP on Neurogenesis and Cognition after Acute Radiation Exposure.Current radiopharmaceuticals · 2024Article
- β-Caryophyllene, a Dietary Phytocannabinoid, Alleviates Diabetic Cardiomyopathy in Mice by Inhibiting Oxidative Stress and Inflammation Activating Cannabinoid Type-2 Receptors.ACS pharmacology & translational science · 2023Article
- Activating SIRT1 deacetylates NF-κB p65 to alleviate liver inflammation and fibrosis via inhibiting NLRP3 pathway in macrophages.International journal of medical sciences · 2023Article
- Oxidative Stress Signaling Mediated Pathogenesis of Diabetic Cardiomyopathy.Oxidative medicine and cellular longevity · 2022Review
- Gpx3 and Egr1 Are Involved in Regulating the Differentiation Fate of Cardiac Fibroblasts under Pressure Overload.Oxidative medicine and cellular longevity · 2022Article
- Liraglutide ameliorates myocardial damage in experimental diabetic rats by inhibiting pyroptosis via Sirt1/AMPK signaling.Iranian journal of basic medical sciences · 2021Article
- Characterisation of the Myocardial Mitochondria Structural and Functional Phenotype in a Murine Model of Diabetic Cardiomyopathy.Frontiers in physiology · 2021Article
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8 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundOxidative stress and inflammation promote the development of diabetic cardiomyopathy (DCM). Therefore, inhibiting these processes may show beneficial effects in the treatment of patients with DCM. Taohuajing (THJ) is prepared using Persicae semen (Taoren), Polygonatum sibiricum (Huangjing), and Carthami flos (Honghua) and may have applications in the treatment of DCM. However, the protective effects of THJ have not been thoroughly assessed. Accordingly, in this study, we aimed to investigate the protective effects of THJ in a model of DCM and further clarify the potential mechanisms.
methodsA type 2 diabetes mellitus model was generated using male C57BL/6 mice. Echocardiography and histopathology were used to evaluate cardiac function. The expression levels of cytokines were measured using enzyme-linked immunosorbent assays. Western blotting and small interfering RNA were used to evaluate the targets of THJ.
resultsCompared with the control group, DCM mice showed cardiac dysfunction, metabolic disorder, fibrosis, and disorganized ultrastructure, and THJ treatment significantly inhibited these changes significantly. THJ treatment also inhibited the production of reactive oxygen species (ROS) and malondialdehyde (MDA), induced the production of glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD), decreased the levels of pro-inflammatory cytokines, and suppressed the activation of the nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome. These protective effects were abolished by sirtinol, an inhibitor of sirtuin1 (SIRT1).
conclusionsOverall, THJ protected the heart from hyperglycemia-induced oxidative stress and inflammation in DCM mice via a mechanism involving SIRT1-mediated antioxidant proteins and suppression of the NLRP3 inflammasome.
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