ArticleChinese medicine2021
Tanshinone I exerts cardiovascular protective effects in vivo and in vitro through inhibiting necroptosis via Akt/Nrf2 signaling pathway.
Article in Chinese medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- Different traditional Chinese medicine injections combined with conventional therapy for sepsis-induced myocardial dysfunction: a systematic review and network meta-analysis.Frontiers in pharmacology · 2025Pooled it
- A Review of the Effects of Herbal Medicines on the Conductance of Ion Channels.Physiological research · 2026Review
- Traditional Chinese Medicine Treatment for Coronary Heart Disease: Pathological Mechanisms of Modulating Cell Death Pathways.Journal of inflammation research · 2026Review
- Multitarget mechanisms and clinical integration of traditional Chinese medicine in cardiac rehabilitation: a narrative review.Frontiers in cardiovascular medicine · 2026Review
- Advances in pharmacological research on myocardial remodeling agents: A decade in review.Medicine · 2025Review
- Advances in Chinese herbal medicine in modulating mitochondria to treat myocardial ischemia-reperfusion injury: a narrative review.Cardiovascular diagnosis and therapy · 2025Review
- Mitochondria and myocardial ischemia/reperfusion injury: Effects of Chinese herbal medicine and the underlying mechanisms.Journal of pharmaceutical analysis · 2025Review
- Mongolian medicine Wulanwendusu-11 alleviates myocardial ischemia-reperfusion injury by modulating the intestinal microbiota and associated metabolic pathways.Frontiers in microbiology · 2025Article
- Biosynthesis and signal transduction of plant growth regulators and their effects on bioactive compound production in Salvia miltiorrhiza (Danshen).Chinese medicine · 2024Review
- Dexmedetomidine ameliorates high glucose-induced epithelial-mesenchymal transformation in HK-2 cells through the Cdk5/Drp1/ROS pathway.Acta biochimica et biophysica Sinica · 2024Article
- Article
- Simvastatin-Loaded Nanoniosome Protects H9c2 Cells from Oxygen-Glucose Deprivation/ Reperfusion Injury by Downregulating Inflammation.Iranian biomedical journal · 2024Article
- Sugarcane leaf polysaccharide exerts a therapeutic effect on cardiovascular diseases through necroptosis.Heliyon · 2023Article
- Pharmaceutical Therapies for Necroptosis in Myocardial Ischemia-Reperfusion Injury.Journal of cardiovascular development and disease · 2023Review
- Screening and identification of effective components from modified Taohong Siwu decoction for protecting H9c2 cells from damage.In vitro cellular & developmental biology. Animal · 2023Article
- Paricalcitol Ameliorates Acute Kidney Injury in Mice by Suppressing Oxidative Stress and Inflammation via Nrf2/HO-1 Signaling.International journal of molecular sciences · 2023Article
- A Pharmacological Review of Tanshinones, Naturally Occurring Monomers fromOxidative medicine and cellular longevity · 2023Review
- Protective effects of Chinese herbal monomers against ischemia-reperfusion injury.American journal of translational research · 2023Review
- Necroptosis: A Pathogenic Negotiator in Human Diseases.International journal of molecular sciences · 2022Review
- The regulation of necroptosis and perspectives for the development of new drugs preventing ischemic/reperfusion of cardiac injury.Apoptosis : an international journal on programmed cell death · 2022Review
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundTanshinone I (TI) is a primary component of Salvia miltiorrhiza Bunge (Danshen), which confers a favorable role in a variety of pharmacological activities including cardiovascular protection. However, the exact mechanism of the cardiovascular protection activity of TI remains to be illustrated. In this study, the cardiovascular protective effect and its mechanism of TI were investigated.
methodsIn this study, tert-butyl hydroperoxide (t-BHP)-stimulated H9c2 cells model was employed to investigate the protective effect in vitro. The cell viability was determined by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide (MTT) assay and lactate dehydrogenase (LDH) kit. The reactive-oxygen-species (ROS) level and mitochondrial membrane potential (MMP) were investigated by the flow cytometry and JC-1 assay, respectively. While in vivo experiment, the cardiovascular protective effect of TI was determined by using myocardial ischemia-reperfusion (MI/R) model including hematoxylin-eosin (H&E) staining assay and determination of superoxide dismutase (SOD) and malondialdehyde (MDA). Tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) release were detected by Enzyme-linked immunosorbent assay (ELISA). Receptor interacting protein kinase 1 (RIP1), receptor interacting protein kinase 3 (RIP3), receptor interacting protein kinase 3 (MLKL), protein kinase B (Akt), Nuclear factor erythroid 2 related factor 2 (Nrf2), Heme oxygenase-1 (HO-1) and NAD(P)H: quinone oxidoreductase-1 (NQO-1) were determined by western blotting.
resultsOur data demonstrated that TI pretreatment attenuated t-BHP and MI/R injury-induced necroptosis by inhibiting the expression of p-RIP1, p-RIP3, and p-MLKL. TI activated the Akt/Nrf2 pathway to promote the expression of antioxidant-related proteins such as phosphorylation of Akt, nuclear factor erythroid 2 related factor 2 (Nrf2), quinone oxidoreductase-1 (NQO-1) and heme oxygenase-1 (HO-1) expression in t-BHP-stimulated H9c2 cells. TI relieved oxidative stress by mitigating ROS generation and reversing MMP loss. In vivo experiment, TI made electrocardiograph (ECG) recovery better and lessened the degree of myocardial tissue damage. The counts of white blood cell (WBC), neutrophil (Neu), lymphocyte (Lym), and the release of TNF-α and IL-6 were reversed by TI treatment. SOD level was increased, while MDA level was decreased by TI treatment.
conclusionCollectively, our findings indicated that TI exerted cardiovascular protective activities in vitro and in vivo through suppressing RIP1/RIP3/MLKL and activating Akt/Nrf2 signaling pathways, which could be developed into a cardiovascular protective agent.
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