Effect of tanshinone IIA for myocardial ischemia/reperfusion injury in animal model: preclinical evidence and possible mechanisms

Zhu, Peng-Chong; Shen, Jiayi; Renyi, Qian; Xu, Jun; Liu, Chong; Hu, Wenbiao; Zhang, Ying; Lv, Ling

doi:10.3389/fphar.2023.1165212

Cited by 5 publications

(4 citation statements)

References 50 publications

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“…Its additional cardiovascular effects include antioxidant activity ( Yan et al, 2021 ), anti-atherosclerotic effects (J. Wang et al, 2020a ; Wang et al, 2020b ), protection against myocardial I/R injury ( Li et al, 2023 ; Zhu et al, 2023 ), regulation of lipid metabolism ( Gao et al, 2021 ), anti-fibrotic effects ( Yan et al, 2022 ), vasodilation ( Fan et al, 2011 ), and potential anti-arrhythmic effects ( Shan et al, 2009 ), further demonstrating its multi-faceted role in promoting cardiovascular health.…”

Section: Discussionmentioning

confidence: 99%

Tanshinone IIA inhibits cardiomyocyte pyroptosis through TLR4/NF-κB p65 pathway after acute myocardial infarction

Chai,

Ye,

Xue

et al. 2023

Front. Cell Dev. Biol.

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Background: Tanshinone IIA, derived from Radix Salviae Miltiorrhizae (Salvia miltiorrhiza Bunge), constitutes a significant component of this traditional Chinese medicine. Numerous studies have reported positive outcomes regarding its influence on cardiac function. However, a comprehensive comprehension of the intricate mechanisms responsible for its cardioprotective effects is still lacking.Methods: A rat model of heart failure (HF) induced by acute myocardial infarction (AMI) was established via ligation of the left anterior descending coronary artery. Rats received oral administration of tanshinone IIA (1.5 mg/kg) and captopril (10 mg/kg) for 8 weeks. Cardiac function was assessed through various evaluations. Histological changes in myocardial tissue were observed using staining techniques, including Hematoxylin and Eosin (HE), Masson, and transmission electron microscopy. Tunel staining was used to detect cell apoptosis. Serum levels of NT-pro-BNP, IL-1β, and IL-18 were quantified using enzyme-linked immunosorbent assay (ELISA). Expression levels of TLR4, NF-κB p65, and pyroptosis-related proteins were determined via western blotting (WB). H9C2 cardiomyocytes underwent hypoxia-reoxygenation (H/R) to simulate ischemia-reperfusion (I/R) injury, and cell viability and apoptosis were assessed post treatment with different tanshinone IIA concentrations (0.05 μg/ml, 0.1 μg/ml). ELISA measured IL-1β, IL-18, and LDH expression in the cell supernatant, while WB analysis evaluated TLR4, NF-κB p65, and pyroptosis-related protein levels. NF-κB p65 protein nuclear translocation was observed using laser confocal microscopy.Results: Tanshinone IIA treatment exhibited enhanced cardiac function, mitigated histological cardiac tissue damage, lowered serum levels of NT-pro-BNP, IL-1β, and IL-18, and suppressed myocardial cell apoptosis. Moreover, tanshinone IIA downregulated the expression of TLR4, NF-κB p65, IL-1β, pro-IL-1β, NLRP3, Caspase-1, and GSDMD-N pyroptosis-related proteins in myocardial tissue. Additionally, it bolstered H/R H9C2 cardiomyocyte viability, curbed cardiomyocyte apoptosis, and reduced the levels of TLR4, NF-κB p65, IL-1β, pro-IL-1β, NLRP3, Caspase-1, and GSDMD-N pyroptosis-related proteins in H/R H9C2 cells. Furthermore, it hindered NF-κB p65 protein nuclear translocation.Conclusion: These findings indicate that tanshinone IIA enhances cardiac function and alleviates myocardial injury in HF rats following AMI. Moreover, tanshinone IIA demonstrates potential suppression of cardiomyocyte pyroptosis. These effects likely arise from the inhibition of the TLR4/NF-κB p65 signaling pathway, presenting a promising therapeutic target.

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Section: Discussionmentioning

confidence: 99%

Tanshinone IIA inhibits cardiomyocyte pyroptosis through TLR4/NF-κB p65 pathway after acute myocardial infarction

Chai,

Ye,

Xue

et al. 2023

Front. Cell Dev. Biol.

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“…It has significant anti-inflammatory effects. It can increase coronary blood flow, improve microcirculation and protect vascular endothelial function by inhibiting inflammation ( 64 ). Xu et al ( 65 ) reported that the protective effect of baicalein on the heart is realized through its anti-inflammatory effect.…”

Section: Delaying the Development Of Cmvd By Modulating The Inflammat...mentioning

confidence: 99%

Inflammation and coronary microvascular disease: relationship, mechanism and treatment

Guo,

Yang,

Song

et al. 2024

Front. Cardiovasc. Med.

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Coronary microvascular disease (CMVD) is common in patients with cardiovascular risk factors and is linked to an elevated risk of adverse cardiovascular events. Although modern medicine has made significant strides in researching CMVD, we still lack a comprehensive understanding of its pathophysiological mechanisms due to its complex and somewhat cryptic etiology. This greatly impedes the clinical diagnosis and treatment of CMVD. The primary pathological mechanisms of CMVD are structural abnormalities and/or dysfunction of coronary microvascular endothelial cells. The development of CMVD may also involve a variety of inflammatory factors through the endothelial cell injury pathway. This paper first reviews the correlation between the inflammatory response and CMVD, then summarizes the possible mechanisms of inflammatory response in CMVD, and finally categorizes the drugs used to treat CMVD based on their effect on the inflammatory response. We hope that this paper draws attention to CMVD and provides novel ideas for potential therapeutic strategies based on the inflammatory response.

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“…While, the components that dissolve in water are salvianolic acid A, salvianolic acid B, purple oxalic acid, and rosmarinic acid. Among these two categories, the fat-soluble component, tanshinone, is highly valued due to its minimal toxicity, high effectiveness, safety, and ability to produce various pharmacological actions that are against tumors ( Jin et al, 2021 ), inflammation ( Ye et al, 2020 ), myocardial ischemia ( Zhu et al, 2023 ), oxidative stress ( Wu et al, 2021 ) and thrombosis ( Feng et al, 2021 ), inhibit left ventricular hypertrophy ( Pang et al, 2014 ), dilate blood vessels ( Lu et al, 2021 ), resist atherosclerosis ( Wen et al, 2020 ), protect brain tissue ( Wang et al, 2022 ), improve microcirculation ( Qin et al, 2023 ), significantly inhibit pulmonary fibrosis ( Feng et al, 2020 ), and activate immunity ( Chen et al, 2022 ).…”

Section: Introductionmentioning

confidence: 99%

The mechanisms of tanshinone in the treatment of tumors

Zhang,

Liu,

Wang

2023

Front. Pharmacol.

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Tanshinone is a lipophilic compound that is present in traditional Chinese medicine and is derived from the roots of Salvia miltiorrhiza (Danshen). It has been proven to be highly effective in combating tumors in various parts of the body, including liver carcinoma, gastric cancer, ovarian cancer, cervix carcinoma, breast cancer, colon cancer, and prostate cancer. Tanshinone can efficiently prevent the reproduction of cancerous cells, induce cell death, and inhibit the spread of cancerous cells, which are mainly involved in the PI3K/Akt signaling pathway, NF-κB pathway, Bcl-2 family, Caspase cascades, MicroRNA, MAPK signaling pathway, p21, STAT3 pathway, miR30b-P53-PTPN11/SHP2 axis, β-catenin, and Skp2. However, the properties and mechanisms of tanshinone’s anti-tumor effects remain unclear currently. Thus, this study aims to review the research progress on tumor prevention and mechanisms of tanshinone to gain new perspectives for further development and clinical application of tanshinone.

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Effect of tanshinone IIA for myocardial ischemia/reperfusion injury in animal model: preclinical evidence and possible mechanisms

Cited by 5 publications

References 50 publications

Tanshinone IIA inhibits cardiomyocyte pyroptosis through TLR4/NF-κB p65 pathway after acute myocardial infarction

Tanshinone IIA inhibits cardiomyocyte pyroptosis through TLR4/NF-κB p65 pathway after acute myocardial infarction

Inflammation and coronary microvascular disease: relationship, mechanism and treatment

The mechanisms of tanshinone in the treatment of tumors

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