Tanshinone IIA downregulates the CD40 expression and decreases MMP-2 activity on atherosclerosis induced by high fatty diet in rabbit

Fang, Zhiyuan; Lin, Rong; Yuan, Bo; Yang, Guangde; Liu, Yu; Zhang, Hui

doi:10.1016/j.jep.2007.09.025

Cited by 86 publications

(54 citation statements)

References 24 publications

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“…Tan has long been used clinically in Asian countries for the prevention and treatment of several CVDs, such as coronary heart disease, angina pectoris, and myocardial infarction (8)(9)(10). We and others have demonstrated that Tan attenuates the initiation and progression of atherosclerosis in experimental animals ( 11,12 ). More recently, we have provided evidence that Tan can stabilize "vulnerable" atherosclerotic plaques in apolipoprotein E-defi cient (ApoE Ϫ / Ϫ ) mice fed a high-cholesterol diet ( 13 ).…”

Section: Oil Red O Stainingmentioning

confidence: 99%

Tanshinone IIA suppresses cholesterol accumulation in human macrophages: role of heme oxygenase-1

Liu

Wang

Huang

et al. 2014

Journal of Lipid Research

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Section: Oil Red O Stainingmentioning

confidence: 99%

Tanshinone IIA suppresses cholesterol accumulation in human macrophages: role of heme oxygenase-1

Liu

Wang

Huang

et al. 2014

Journal of Lipid Research

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“…Tanshinone IIA(TanIIA), as the main lipophilic ingredient of Salvia miltiorrhiza, can significantly inhibit coronary artery contraction, improve coronary blood flow, exert anti-atherosclerotic actions, inhibit platelet aggregation and protect damaged endothelium [20,21,22,23,24,25,26]. Although there has been some research on the anti-inflammatory and anti-oxidative effects of TanIIA, these articles have not identificed a specific mechanism for these effects [21,27].…”

Section: Introductionmentioning

confidence: 99%

Anti-Inflammatory Effects of Tanshinone IIA on Atherosclerostic Vessels of Ovariectomized ApoE-/- Mice are Mediated by Estrogen Receptor Activation and Through the ERK Signaling Pathway

Liu¹,

Guo²,

Ma³

et al. 2015

Cell Physiol Biochem

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Aims: Estrogen plays a protective role in atherosclerosis. Our preliminary work demonstrated that the active conformation of Tanshinone IIA(TanIIA) is similar to the 17ß-estradiol and it can bind to the estrogen receptor. Here, we hypothesized that Tanshinone IIA might have anti-inflammatory and anti-oxidative effects in atherosclerosis, mediated through estrogen receptor activation. Methods: Subjects for this study were 120 apoE^-/- female mice and 20 C57/BL female mice. The apoE^-/- mice were ovariectomized (OVX) and the C57/BL mice were sham ovariectomized. The sham OVX mice were maintained on a normal diet (NOR) group. The OVX apoE^-/- mice were fed a high fat diet and randomly divided into 6 groups: Model (MOD) group which was fed a high fat diet only, E₂ group were given estrogen (E₂) 0.13mg/kg/d; E₂+ICI group were given E₂:0.13mg/kg/d and ICI182780:65mg/kg/m; TLD group (TanIIA low dose) were given TanIIA: 30mg/kg/d; THD group (TanIIA high dose) were given TanIIA:60mg/kg/d; and TLD+ICI group were given TanIIA 30mg/kg/d and ICI182780 65mg/kg/m. After three months of treatment, the aorta and the blood of the mice from each group was collected. The aorta were used for testing the lipid deposition by using hematoxylin and eosin(HE) and oil red O staining and for testing the expression of p-ERK1/2 by Western blot. The blood was used for testing the serum cholesterol, superoxide dismutase (SOD), methane dicarboxylic aldehyde (MDA), nuclear factor kappa (NF-κB), soluble intercellular cell adhesion molecule-1 (sICAM-1), activating protein-1 (AP-1), E-selectin and 17ß-estradiol in serum. Results: Tanshinone IIA significantly reduced the lipid deposition in aorta, decreased the levels of total cholesterol (TC), triglyceride (TG), low density lipoprotein (LDL), very low density lipoprotein (VLDL), MDA, NF-κB, sICAM-1, AP-1, and E-selectin in serum but increased the levels of high density lipoprotein (HDL) and SOD in serum. Tanshinone IIA also suppressed the expression of p-ERK1/2. Tanshinone IIA had no effect of level of serum 17ß-estradiol levels. All of the effects of Tanshinone IIA were similar to estrogen and were inhibited by the estrogen receptor antagonist ICI182780. Conclusion: Tanshinone IIA may play an anti-inflammatory and anti-oxidative stress role in OVX atherosclerotic apoE^-/- mice by activating the estrogen receptor through the ERK signaling pathway. Therefore, Tanshinone IIA, as a phytoestrogen, could be used for estrogen replacement therapy for cardiovascular disease of postmenopausal women.

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“…Jiang et al provided evidence on the potential of Tanshinone II A as a proteictive agent against adriamycin induced cardiotoxicity ( Zhi-yuan et al, 2008). Tanshinone II A significantly inhibits adriamycin-induced cardiomyocyte apoptosis in a dose-dependent manner also has been reported (Baohong et al, 2009), and Akt-signaling pathways related with this phenomenon (Hong-Jye et al, 2012).…”

Section: Introductionmentioning

confidence: 98%

Tanshinone II A Relieves Adriamycin-induced Myocardial Injury in Rat Model

Wang¹,

Chai²,

Wang³

et al. 2015

IJC

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As an effective antineoplastic agent, adriamycin (ADR) remains a use for the treatment of cancer. However, it is limited by the serous cardiotoxicity. Tanshinone II A is the main effective component of Salvia miltiorrhiza Bunge which has been used for treatment of cardiovascular diseases. The purpose of this study is to evaluate the protective effect of Tanshinone II A on adriamycin-induced myocardial injury in rat and explore the mechanism of this effect. Male Wistar rats (200 ± 20 g) were divided into three groups, control (CON) group, adriamycin (ADR) group and ADR + Tanshinone II A (TRA) group. At the end of the 4 week treatment period, cardiac function was evaluated by transthoracic echocardiography. Molecular and cellular measurements were performed in atrial muscle to examine histopathological changes, the formation of fibrosis, Inflammation and apoptosis. Cardiac dysfunction was induced by adriamycin, as indicated by significant decreases in ventricular fractional shortening and ejection fraction. This adriamycin-induced cardiac dysfunction was prevented by the treatment of Tanshinone II A. Adriamycin induced pathological changes and fibrosis, activated apoptosis (increased TUNEL index, apoptotic DNA fragmentation,and caspase-3 activity and decreased Bcl-2/Bax ratio), inflammation and suppressed phosphorylation status (eIF2α and PERK) in atrial. All these molecular and cellular alterations induced by ADR were not found in the rats treated with Tanshinone II A. These findings demonstrate clearly that Tanshinone II A protects the cardiomyocytes against the ADR-induced cardiomyopathy by preventing the activation of cardiac fibrosis and apoptosis, and the effects are probably mediated through ERS pathway.

show abstract

Tanshinone IIA downregulates the CD40 expression and decreases MMP-2 activity on atherosclerosis induced by high fatty diet in rabbit

Cited by 86 publications

References 24 publications

Tanshinone IIA suppresses cholesterol accumulation in human macrophages: role of heme oxygenase-1

Tanshinone IIA suppresses cholesterol accumulation in human macrophages: role of heme oxygenase-1

Anti-Inflammatory Effects of Tanshinone IIA on Atherosclerostic Vessels of Ovariectomized ApoE-/- Mice are Mediated by Estrogen Receptor Activation and Through the ERK Signaling Pathway

Tanshinone II A Relieves Adriamycin-induced Myocardial Injury in Rat Model

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