Tanshinone IIA sodium sulfonate attenuates inflammation by upregulating circ-Sirt1 and inhibiting the entry of NF-κB into the nucleus

Tanshinone IIA sodium sulfonate (TSS) is a water-soluble derivative of tanshinone IIA, which is the main pharmacologically active component of Salvia miltiorrhiza. This study aimed to verify the preventive and therapeutic effects of TSS and its combined therapeutic effects with magnesium isoglycyrrhizinate (MI) in D-galactosamine- (D-Gal-) induced acute liver injury (ALI) in mice. The potential regulatory mechanisms of TSS on ALI were also examined. Our results may provide a basis for the development of novel therapeutics for ALI.

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Tanshinone IIA Sodium Sulfonate Attenuates LPS-Induced Intestinal Injury in Mice

Gastroenterology Research and Practice ◽

10.1155/2018/9867150 ◽

2018 ◽

Vol 2018 ◽

pp. 1-10 ◽

Cited By ~ 2

Author(s):

Xin-Jing Yang ◽

Jin-Xian Qian ◽

Yao Wei ◽

Qiang Guo ◽

Jun Jin ◽

...

Keyword(s):

Molecular Mechanisms ◽

Intestinal Injury ◽

Beclin 1 ◽

Tanshinone Iia ◽

Inflammatory Factors ◽

Rt Pcr ◽

Intestinal Tissue ◽

Sodium Sulfonate ◽

Small Intestinal Injury ◽

Small Intestinal

Background. Tanshinone IIA sodium sulfonate (TSS) is known to possess anti-inflammatory effects and has exhibited protective effects in various inflammatory conditions; however, its role in lipopolysaccharide- (LPS-) induced intestinal injury is still unknown. Objective. The present study is designed to explore the role and possible mechanism of TSS in LPS-induced intestinal injury. Methods. Male C57BL/6J mice, challenged with intraperitoneal LPS injection, were treated with or without TSS 0.5 h prior to LPS exposure. At 1, 6, and 12 h after LPS injection, mice were sacrificed, and the small intestine was excised. The intestinal tissue injury was analyzed by HE staining. Inflammatory factors (TNF-α, IL-1β, and IL-6) in the intestinal tissue were examined by ELISA and RT-PCR. In addition, expressions of autophagy markers (microtubule-associated light chain 3 (LC3) and Beclin-1) were detected by western blot and RT-PCR. A number of autophagosomes were also observed under electron microscopy. Results. TSS treatment significantly attenuated small intestinal epithelium injury induced by LPS. LPS-induced release of inflammatory mediators, including TNF-α, IL-1β, and IL-6, were markedly inhibited by TSS. Furthermore, TSS treatment could effectively upregulate LPS-induced decrease of autophagy levels, as evidenced by the increased expression of LC3 and Beclin-1, and more autophagosomes. Conclusion. The protective effect of TSS on LPS-induced small intestinal injury may be attributed to the inhibition of inflammatory factors and promotion of autophagy levels. The present study may provide novel insight into the molecular mechanisms of TSS on the treatment of intestinal injury.

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Tanshinone IIA sodium sulfonate protects against cardiotoxicity induced by doxorubicin in vitro and in vivo

Food and Chemical Toxicology ◽

10.1016/j.fct.2009.03.038 ◽

2009 ◽

Vol 47 (7) ◽

pp. 1538-1544 ◽

Cited By ~ 42

Author(s):

Baohong Jiang ◽

Lin Zhang ◽

Yingchun Wang ◽

Ming Li ◽

Wanying Wu ◽

...

Keyword(s):

Tanshinone Iia ◽

Sodium Sulfonate

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Tanshinone IIA sodium sulfonate facilitates endocytic HMGB1 uptake

Biochemical Pharmacology ◽

10.1016/j.bcp.2012.09.015 ◽

2012 ◽

Vol 84 (11) ◽

pp. 1492-1500 ◽

Cited By ~ 38

Author(s):

Yusong Zhang ◽

Wei Li ◽

Shu Zhu ◽

Arvin Jundoria ◽

Jianhua Li ◽

...

Keyword(s):

Tanshinone Iia ◽

Sodium Sulfonate

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Tanshinone IIA Sodium sulfonate regulates antioxidant system, inflammation, and endothelial dysfunction in atherosclerosis by downregulation of CLIC1

European Journal of Pharmacology ◽

10.1016/j.ejphar.2017.09.047 ◽

2017 ◽

Vol 815 ◽

pp. 427-436 ◽

Cited By ~ 15

Author(s):

Ji Zhu ◽

Yingling Xu ◽

Guangyan Ren ◽

Xiao Hu ◽

Cui Wang ◽

...

Keyword(s):

Endothelial Dysfunction ◽

Antioxidant System ◽

Tanshinone Iia ◽

Sodium Sulfonate

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Tanshinone IIA attenuates elastase-induced AAA in rats via inhibition of MyD88-dependent TLR-4 signaling

VASA ◽

10.1024/0301-1526/a000326 ◽

2014 ◽

Vol 43 (1) ◽

pp. 39-46 ◽

Cited By ~ 16

Author(s):

Tao Shang ◽

Feng Ran ◽

Qian Qiao ◽

Zhao Liu ◽

Chang-Jian Liu

Keyword(s):

Nuclear Factor Κb ◽

Tanshinone Iia ◽

Myeloid Differentiation ◽

Aortic Tissue ◽

Toll Like Receptor ◽

Sprague Dawley ◽

Toll Like Receptor 4 ◽

Tissue Samples ◽

Myeloid Differentiation Factor ◽

And Control

Background: The purpose of this study was to determine whether myeloid differentiation factor88-dependent Toll-Like Receptor-4 (TLR-4) signaling contributed to the inhibition of abdominal aortic aneurysm (AAA) by Tanshinone IIA (Tan IIA). Materials and methods: Male Sprague-Dawley rats (n = 12 / group) were randomly distributed into three groups: Tan IIA, control, and sham. The rats from Tan IIA and control groups under-went intra-aortic elastase perfusion to induce AAAs, and those in the sham group were perfused with saline. Only the Tan IIA group received Tan IIA (2 mg / rat / d). Aortic tissue samples were harvested at 24 d after perfusion and evaluated using reverse transcriptase-polymerase chain reaction, Western blot, immunohistochemistry and immunofluorescence. Results: The over-expression of Toll-Like Receptor-4 (TLR-4), Myeloid Differentiation factor 88 (MyD88), Phosphorylated Nuclear Factor κB (pNF-κB) and Phosphorylated IκBα (pIκBα) induced by elastase perfusion were significantly decreased by Tan IIA treatment. Conclusions: Tan IIA attenuates elastase-induced AAA in rats possibly via the inhibition of MyD88-dependent TLR-4 signaling, which may be one potential explanation of why Tan IIA inhibits AAA development through multiple effects.

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Tanshinone IIA Promotes Macrophage Cholesterol Efflux and Attenuates Atherosclerosis of apoE-/- Mice by Omentin-1/ABCA1 Pathway

Current Pharmaceutical Biotechnology ◽

10.2174/1389201020666190404125213 ◽

2019 ◽

Vol 20 (5) ◽

pp. 422-432 ◽

Cited By ~ 3

Author(s):

Yu-lin Tan ◽

Han-xiao Ou ◽

Min Zhang ◽

Duo Gong ◽

Zhen-wang Zhao ◽

...

Keyword(s):

Atherosclerotic Plaque ◽

Lipid Content ◽

Plasma Levels ◽

Cholesterol Efflux ◽

Density Lipoprotein ◽

Tanshinone Iia ◽

Lipoprotein Cholesterol ◽

Mrna Levels ◽

Cellular Lipid ◽

Oil Red O

Background: Tanshinone IIA (Tan IIA) and Omentin-1 have a protective role in the cardiovascular system. However, if and how Tan IIA and Omentin-1 regulate cholesterol metabolism in macrophages has not been fully elucidated. Objective: To investigate the possible mechanisms of Tan IIA and Omentin-1 on preventing macrophage cholesterol accumulation and atherosclerosis development. Methods: The effect of Tan IIA on the protein and mRNA levels of Omentin-1 and ATP-binding cassette transporter A1 (ABCA1) in macrophages was examined by Western blot and qRT-PCR assay, respectively. Cholesterol efflux was assessed by liquid scintillation counting (LSC). Cellular lipid droplet was measured by Oil Red O staining, and intracellular lipid content was detected by high performance liquid chromatography (HPLC). In addition, the serum lipid profile of apoE−/− mice was measured by enzymatic method. The size of atherosclerotic lesion areas and content of lipids and collagen in the aortic of apoE−/− mice were examined by Sudan IV, Oil-red O, and Masson staining, respectively. Results: Tan IIA up-regulated expression of Omentin-1 and ABCA1 in THP-1 macrophages, promoting ABCA1-mediated cholesterol efflux and consequently decreasing cellular lipid content. Consistently, Tan IIA increased reverse cholesterol transport in apoE−/− mice. Plasma levels of high-density lipoprotein cholesterol (HDL-C), ABCA1 expression and atherosclerotic plaque collagen content were increased while plasma levels of low-density lipoprotein cholesterol (LDL-C) and atherosclerotic plaque sizes were reduced in Tan IIA-treated apoE−/− mice. These beneficial effects were, however, essentially blocked by knockdown of Omentin-1. Conclusion: Our results revealed that Tan IIA promotes cholesterol efflux and ameliorates lipid accumulation in macrophages most likely via the Omentin-1/ABCA1 pathway, reducing the development of aortic atherosclerosis.

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Simultaneous Determination of Six Components in Jingzhiguanxin Tablet by High-Performance Liquid Chromatography

Current Pharmaceutical Analysis ◽

10.2174/1573412914666180315120130 ◽

2019 ◽

Vol 15 (2) ◽

pp. 130-137

Author(s):

Hui Jiang ◽

Lianhao Fu ◽

Yu Wang ◽

Shaozhi Wang ◽

Xiaoxu Zhang ◽

...

Keyword(s):

High Performance Liquid Chromatography ◽

Liquid Chromatography ◽

High Performance ◽

Gradient Elution ◽

Tanshinone Iia ◽

Array Detector ◽

Control Analysis ◽

Active Components ◽

Quality Control Analysis

Background: Jingzhiguanxin (JZGX) tablet, a traditional Chinese prescription, is commonly used for treating coronary heart disease and angina pectoris in the clinic. There are six active components (Danshensu (DSS), Protocatechuic aldehyde (PD), Paeoniflorin (PF), Ferulic acid (FA), Salvianolic acid B (Sal B) and Tanshinone IIA (TA)) in JZGX tablet. </P><P> Objective: In this paper, a simple and reliable method was used for simultaneous determining the six active components by high-performance liquid chromatography coupled with diode array detector (HPLC-DAD). Methods: These six active components were separated on an Agilent Zorbax Eclipse XDB-C18 column (150 mmx4.6 mm, 5 µm) at 30 °C. Acetonitrile (A), methanol (B) and 0.5% H3PO4 aqueous solution (C) were used as mobile phase for gradient elution. The flow rate was 1 mL/min and the detection wavelengths were set at 280 nm for DSS, PD and Sal B, 230 nm for PF, 320 nm for FA and 270 nm for TA, respectively. Results: All of the six components showed good linearity regressions (r2≥0.9997) in the detected concentration range. The recovery rates and coefficient of variation (CV) for all analytes were 98.66%- 100.18% and 0.75%-1.89%, respectively. This method was successfully applied to simultaneously determine the six components in JZGX tablet from different batches and manufacturers. Conclusion: The validated method can be used in routine quality control analysis of JZGX tablet without any interference.

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