Tanshinone IIA pretreatment protects myocardium against ischaemia/reperfusion injury through the phosphatidylinositol 3‐kinase/Akt‐dependent pathway in diabetic rats

Zhang, Y.; Wei, Liping; Sun, Dongdong; Cao, Feng; Gao, Haokao; Zhao, Lin; Du, Jiazong; Li, Y.; Wang, H.

doi:10.1111/j.1463-1326.2009.01166.x

Cited by 95 publications

(58 citation statements)

References 25 publications

(30 reference statements)

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“…For instance, the pervasive effects of Tanshinone and Berberin in the prevention and cure of common cardiovascular diseases has been clarified [7,8]. In the current study, Aloeemodin (Fig.…”

Section: Introductionmentioning

confidence: 63%

Aloe-Emodin Relieves High-Fat Diet Induced QT Prolongation via MiR-1 Inhibition and IK1 Up-Regulation in Rats

Sun

Zhao

et al. 2017

Cell Physiol Biochem

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Background/Aims: High-fat diet (HFD) causes cardiac electrical remodeling and increases the risk of ventricular arrhythmias. Aloe-emodin (AE) is an anthraquinone component isolated from rhubarb and has a similar chemical structure with emodin. The protective effect of emodin against cardiac diseases has been reported in the literature. However, the cardioprotective property of AE is still unknown. The present study investigated the effect of AE on HFD-induced QT prolongation in rats. Methods: Adult male Wistar rats were randomly divided into three groups: control, HFD, and AE-treatment groups. Normal diet was given to rats in the control group, high-fat diet was given to rats in HFD and AE-treatment groups for a total of 10 weeks. First, HFD rats and AE-treatment rats were fed with high-fat diet for 4 weeks to establish the HFD model. Serum total cholesterol and triglyceride levels were measured to validate the HFD model. Afterward, AE-treatment rats were intragastrically administered with 100 mg/kg AE each day for 6 weeks. Electrocardiogram monitoring and whole-cell patch-clamp technique were applied to examine cardiac electrical activity, action potential and inward rectifier K + current (I K1 ), respectively. Neonatal rat ventricular myocytes (NRVMs) were subjected to cholesterol and/or AE. Protein expression of Kir2.1 was detected by Western blot and miR-1 level was examined by real-time PCR in vivo and in vitro, respectively. Results: In vivo, AE significantly shortened the QT interval, action potential duration at 90% repolarization (APD 90 ) and resting membrane potential (RMP), which were markedly elongated by HFD. AE increased I K1 current and Kir2.1 protein expression which were reduced in HFD rats. Furthermore, AE significantly inhibited pro-arrhythmic miR-1 in the hearts of HFD rats. In vitro, AE decreased miR-1 expression levels resulting in an increase of Kir2.1 protein levels in cholesterol-enriched NRVMs. Conclusions: AE prevents HFD-induced QT prolongation by repressing miR-1 and upregulating its target Kir2.1. These findings suggest a novel pharmacological role of AE in HFD-induced cardiac electrical remodeling.

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Section: Introductionmentioning

confidence: 63%

Aloe-Emodin Relieves High-Fat Diet Induced QT Prolongation via MiR-1 Inhibition and IK1 Up-Regulation in Rats

Sun

Zhao

et al. 2017

Cell Physiol Biochem

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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: Discussionmentioning

confidence: 99%

“…A number of studies have demonstrated that tanshinone IIA protects cardiac myocytes against oxidative stress-triggered damage and apoptosis (16), prevents myocardial hypertrophy (17), protects against sudden cardiac death (18) and attenuates myocardial ischemic (19) and reperfusion injury (20). However, the majority of studies (7,20) have focused on applying tanshinone IIA prior to ischemia, which limits its use in clinical practice. In the present study, the clinical application of tanshinone IIA was widened, as the data obtained demonstrate that when applied prior to prolonged reperfusion following sustained ischemia, tanshinone IIA at both medium and high doses, which have been used in other studies for cardioprotection, resulted in a reduction in infarct size comparable to that of ischemic postconditioning.…”

Section: Discussionmentioning

confidence: 99%

“…One previous study has also revealed that pretreatment with tanshinone IIA may inhibit mPTP opening dose-dependently, and its cardioprotective effect may be via the inhibition of pore opening during reperfusion (25). More recently, Zhang et al (20) reported that tanshinone IIA pretreatment elicits cardioprotection in diabetic rats via the PI3K/Akt-dependent pathway. The results from the present study are consistent with these previous findings.…”

Section: Discussionmentioning

confidence: 99%

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Pharmacological postconditioning with tanshinone IIA attenuates myocardial ischemia-reperfusion injury in rats by activating the phosphatidylinositol 3-kinase pathway

Yuan

Jing

et al. 2014

Experimental and Therapeutic Medicine

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Tanshinone IIA, one of the active ingredients in the Chinese medicine Danshen, is cardioprotective when applied prior to sustained myocardial ischemia. The present study aimed to investigate whether pharmacological postconditioning with tanshinone IIA attenuates myocardial ischemia-reperfusion injury when applied prior to prolonged reperfusion following a sustained ischemia. A total of 88 Sprague-Dawley rats received 30 min myocardial ischemia followed by 5 or 120 min reperfusion. Compared with the ischemia-reperfusion model group, the group that received an intravenous injection of 10 mg/kg tanshinone IIA prior to reperfusion had a reduced myocardial infarct size, higher levels of phospho-Akt and phospho-endothelial nitric oxide synthase and less reduction in the optical density of the mitochondria at 540 nm, indicating that the mitochondrial permeability transition (MPT) was attenuated. The cardioprotective effect conferred by tanshinone IIA was abolished by LY294002, a specific inhibitor of phosphatidylinositol 3-kinase (PI3K). These results demonstrate that tanshinone IIA postconditioning protects the myocardium from ischemia-reperfusion injury through the PI3K/Akt pathway, and the MPT may be also involved in this process.

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Tanshinone IIA pretreatment protects myocardium against ischaemia/reperfusion injury through the phosphatidylinositol 3‐kinase/Akt‐dependent pathway in diabetic rats

Cited by 95 publications

References 25 publications

Aloe-Emodin Relieves High-Fat Diet Induced QT Prolongation via MiR-1 Inhibition and IK1 Up-Regulation in Rats

Aloe-Emodin Relieves High-Fat Diet Induced QT Prolongation via MiR-1 Inhibition and IK1 Up-Regulation in Rats

Tanshinone IIA ameliorates apoptosis of cardiomyocytes induced by endoplasmic reticulum stress

Pharmacological postconditioning with tanshinone IIA attenuates myocardial ischemia-reperfusion injury in rats by activating the phosphatidylinositol 3-kinase pathway

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