Protective effects of tanshinone IIA on myocardial ischemia reperfusion injury by reducing oxidative stress, HMGB1 expression, and inflammatory reaction

Zhai, Chao; Qian, Gang; Gu, Aiming; Li, Jialiang; Fang, Ying; Xu, Wenbo; Jin, Dandan; Wang, Huawei; Hu, Hongsheng; Zhang, Yingqing; Tang, Guanmin

doi:10.3109/13880209.2015.1005753

Cited by 68 publications

(50 citation statements)

References 42 publications

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“…7,8 TSA has a multi-dimensional beneficial actions on the cardiovascular system through anti-atherosclerosis, anti-arrhythmia, anti-inflammation, anti-smooth muscle hyperplasia, anti-myocardial hypertrophy, and so on. [9][10][11][12] The protective effect of TSA on impairment of myocardium has been extensively reported, [13][14][15][16] and the cardioprotection is mainly related to anti-apoptosis of cardiomyocytes. [17][18][19] However, its detailed mechanism for anti-apoptosis has not been fully demonstrated.…”

Section: Introductionmentioning

confidence: 99%

Tanshinone IIA ameliorates apoptosis of cardiomyocytes induced by endoplasmic reticulum stress

Feng

Chen

2016

Exp Biol Med (Maywood)

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The fat-soluble diterpenoids tanshinone IIA (TSA) is the major active element of Danshen, which has widespread cardioprotective effect. However, the mechanism of its beneficial effect on cardiomyocytes has not been fully investigated. Here, we aim to demonstrate that TSA ameliorates apoptosis of cardiomyocytes activated by endoplasmic reticulum stress (ERS). Primary cultures of neonatal rat cardiomyocytes are used, in which ERS-mediated apoptosis is induced by tunicamycin (Tm). Apoptosis of cardiomyocytes are detected by Hoechst staining and caspase 3 activity analysis. Protein expression of ERS markers are detected by Western blot, and level of miroRNA-133 (miR-133) is detected by real-time polymerase chain reaction. Tm treatment significantly triggers the apoptosis and ERS of cardiomyocytes. TSA dramatically ameliorates apoptosis and ERS of cardiomyocytes induced by Tm. Interestingly, level of miR-133 is reduced by Tm treatment, which is reversed by TSA. The cardioprotective effect of TSA on apoptosis and ERS of cardiomyocytes is blocked by anti-miR-133. These results suggest that TSA protects cardiomyocytes through ameliorated ERS-mediated apoptosis, which may be resulted from upregulation of miR-133.

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Section: Introductionmentioning

confidence: 99%

Tanshinone IIA ameliorates apoptosis of cardiomyocytes induced by endoplasmic reticulum stress

Feng

Chen

2016

Exp Biol Med (Maywood)

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“…Consistently, tanshinone treatment at reperfusion for 15 days inhibited HMGB1 expression and NF-κB activation, protecting from neuron apoptosis in a rat MCAO model [213]. Inhibition of HMGB1 by tanshinone IIA was also found in a myocardial infarction model, coinciding with attenuated inflammation and oxidative stress [214]. Taken together, tanshinone IIA could protect against ischemia stroke injury and targets HMGB1, MMP-9 and free radicals.…”

Section: Active Compounds From Chinese Herbal Medicine For Targeting mentioning

confidence: 60%

Targeting ONOO<sup>-</sup>/HMGB1/MMP-9 Signaling Cascades: Potential for Drug Development from Chinese Medicine to Attenuate Ischemic Brain Injury and Hemorrhagic Transformation Induced by Thrombolytic Treatment

Chen¹,

Guan²,

Shen³

2016

Integr Med Int

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Stroke is the leading cause of death and disability worldwide, and ischemic stroke accounts for more than 85% of the stroke incidence. Tissue plasminogen activator (t-PA) is the only FDA-approved drug for ischemic stroke treatment with a narrow treatment time window of 4.5 h. Hemorrhagic transformation (HT) is a severe complication of delayed t-PA treatment in ischemic stroke. Thus, it is critically important to develop combination therapies to reduce HT and extend the therapeutic time window of t-PA. Current progress suggests that peroxynitrite (ONOO^-)/high-mobility group box 1 protein (HMGB1)/matrix metalloproteinase-9 (MMP-9) signaling cascades could be important for attenuating HT during thrombolytic treatment for acute ischemic stroke. Recently, important progress has been made in seeking for natural compounds from Chinese medicine for reducing ischemic stroke injury, with some of them targeting ONOO^-/HMGB1/MMP-9 signaling cascades. Herein, we analyze the roles and interactions of these three targets in mediating HT; subsequently, we summarize the potential compounds from Chinese herbal medicine for attenuating HT and analyze the related targets. Finally, we raise the potential issues to be addressed in further development of these compounds as combination therapy.

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“…Both the hydrophilic and lipophilic constituents of SM appear to improve the I/R-induced vascular damage multifactorially and synergistically [108]. The protective function of Tan IIA on myocardial I/R injury may be through inhibiting ROS production and attenuating the expression of high mobility group box B1 protein that results in the activation of proinflammatory pathways [109]. Tan IIA can also reduce monocyte chemoattractant protein-1 expression and macrophage infiltration.…”

Section: Resultsmentioning

confidence: 99%

Oxidative Stress and Salvia miltiorrhiza in Aging‐Associated Cardiovascular Diseases

Chang

et al. 2016

Oxidative Medicine and Cellular Longevity

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Aging-associated cardiovascular diseases (CVDs) have some risk factors that are closely related to oxidative stress. Salvia miltiorrhiza (SM) has been used commonly to treat CVDs for hundreds of years in the Chinese community. We aimed to explore the effects of SM on oxidative stress in aging-associated CVDs. Through literature searches using Medicine, PubMed, EMBASE, Cochrane library, CINAHL, and Scopus databases, we found that SM not only possesses antioxidant, antiapoptotic, and anti-inflammatory effects but also exerts angiogenic and cardioprotective activities. SM may reduce the production of reactive oxygen species by inhibiting oxidases, reducing the production of superoxide, inhibiting the oxidative modification of low-density lipoproteins, and ameliorating mitochondrial oxidative stress. SM also increases the activities of catalase, manganese superoxide dismutase, glutathione peroxidase, and coupled endothelial nitric oxide synthase. In addition, SM reduces the impact of ischemia/reperfusion injury, prevents cardiac fibrosis after myocardial infarction, preserves cardiac function in coronary disease, maintains the integrity of the blood-brain barrier, and promotes self-renewal and proliferation of neural stem/progenitor cells in stroke. However, future clinical well-designed and randomized control trials will be necessary to confirm the efficacy of SM in aging-associated CVDs.

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Protective effects of tanshinone IIA on myocardial ischemia reperfusion injury by reducing oxidative stress, HMGB1 expression, and inflammatory reaction

Abstract: The protective function of TSA on myocardial ischemia reperfusion injury may be possibly exerted by inhibiting the increase of ROS caused by the reperfusion to attenuate the expression of HMGB1 and inhibit inflammation.

Cited by 68 publications

References 42 publications

Tanshinone IIA ameliorates apoptosis of cardiomyocytes induced by endoplasmic reticulum stress

Tanshinone IIA ameliorates apoptosis of cardiomyocytes induced by endoplasmic reticulum stress

Targeting ONOO<sup>-</sup>/HMGB1/MMP-9 Signaling Cascades: Potential for Drug Development from Chinese Medicine to Attenuate Ischemic Brain Injury and Hemorrhagic Transformation Induced by Thrombolytic Treatment

Oxidative Stress and Salvia miltiorrhiza in Aging‐Associated Cardiovascular Diseases

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