Sodium tanshinone IIA sulfonate prevents lipopolysaccharide-induced inflammation via suppressing nuclear factor-κB signaling pathway in human umbilical vein endothelial cells

Cheng, Jun; Chen, Tangting; Li, Pengyun; Wen, Jing; Pang, Ningbo; Zhang, Liping; Wang, Liqun

doi:10.1139/cjpp-2017-0023

Cited by 25 publications

(19 citation statements)

References 39 publications

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“…Tan IIA has been reported to have diverse pharmacological effects, including anti-inflammation, anti-apoptosis, and regulation of the immune response (28). Previous studies have indicated that Tan IIA may inhibit the LPS-induced expression of inflammation-associated cytokines in various cell types (19,29,30). In the present study, LPS significantly increased the expression of MCP-1, IL-6, and TNF-α in VSMCs, which is consistent with a previous study (4).…”

Section: Discussionsupporting

confidence: 92%

Tanshinone IIA inhibits lipopolysaccharide‑induced inflammatory responses through the TLR4/TAK1/NF‑κB signaling pathway in vascular smooth muscle cells

Meng

Teng

et al. 2019

Int J Mol Med

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To aim of the present study was to determine whether Tanshinone IIA (Tan IIA) inhibits lipopolysaccharide (LPS)-induced inflammation in vascular smooth muscle cells (VSMcs) from rats and elucidate the underlying molecular mechanism. VSMcs were primarily cultured and then treated with LPS (1 µg/l) and Tan IIA (25, 50 and 100 µmol/l) for 24 h. Monocyte chemoattractant protein (McP)-1, interleukin (IL)-6 and tumor necrosis factor (TNF)-α levels were detected by ELISA and reverse transcription-quantitative polymerase chain reaction. Nitric oxide (NO) production was measured using the Griess reaction. The expression of Toll-like receptor 4 (TLR4), nuclear factor (NF)-κB (p65), and inducible NO synthase (iNOS), and the phosphorylation of transforming growth factor-β-activated kinase 1 (TAK1) were detected by western blot analysis. Tan IIA inhibited the LPS-induced expression of McP-1, IL-6, and TNF-α in a concentration-dependent manner and inhibited iNOS-mediated NO production. In addition, Tan IIA suppressed the expression of TLR4, the phosphorylation of TAK1, and the nuclear translocation of NF-κB (p65). The anti-TLR4 antibody and TAK1 inhibitor 5Z-7-oxozeaenol partially attenuated the LPS-induced expression of proinflammatory cytokines. In conclusion, Tan IIA inhibits LPS-induced inflammatory responses in VSMcs in vitro through the partial suppression of the TLR4/TAK1/NF-κB signaling pathway.

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Section: Discussionsupporting

confidence: 92%

Tanshinone IIA inhibits lipopolysaccharide‑induced inflammatory responses through the TLR4/TAK1/NF‑κB signaling pathway in vascular smooth muscle cells

Meng

Teng

et al. 2019

Int J Mol Med

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“…Bi et al [48] designed and tested the endothelial protective effects of tanshinone IIa derivatives and found that several derivatives have increased efficacy against H 2 O 2 -induced injury via Nrf2 (nuclear factor (erythroid-derived 2)-like-2 factor) activation and superior water solubility. (2) Preventing inflammatory responses in endothelial cells and endothelial progenitor cells and preventing monocyte adhesion to diseased endothelium: Tanshinone IIa has potent anti-inflammatory effects by blocking the upregulation of pro-inflammatory mediators, such as tumor necrosis factor α (TNF-α), intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), monocyte chemotactic protein 1 (MCP-1), E-selectin, and interleukins (IL-8 & IL-1β), in response to proinflammatory stimuli [50][51][52][53][54][55][56] , thus reducing monocyte adhesion to endothelial cells [50,54,56] . (3) Regulation of vascular tone and vasorelaxation by increasing NO and decreasing endo- thelin-1 (ET-1): Several reports have revealed that tanshinone IIa increases the production of NO [57][58][59] under different stress conditions in endothelial cells by increasing eNOS levels [58,60,61] and eNOS phosphorylation at ser1177 [61] while blocking eNOS ser1177 dephosphorylation [61] .…”

Section: Protective Effects Of Tanshinone Iia On Endothelial Functionmentioning

confidence: 99%

Salvia miltiorrhizaBurge (Danshen): a golden herbal medicine in cardiovascular therapeutics

2018

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Salvia miltiorrhiza Burge (Danshen) is an eminent medicinal herb that possesses broad cardiovascular and cerebrovascular protective actions and has been used in Asian countries for many centuries. Accumulating evidence suggests that Danshen and its components prevent vascular diseases, in particular, atherosclerosis and cardiac diseases, including myocardial infarction, myocardial ischemia/reperfusion injury, arrhythmia, cardiac hypertrophy and cardiac fibrosis. The published literature indicates that lipophilic constituents (tanshinone I, tanshinone IIa, tanshinone IIb, cryptotanshinone, dihydrotanshinone, etc) as well as hydrophilic constituents (danshensu, salvianolic acid A and B, protocatechuic aldehyde, etc) contribute to the cardiovascular protective actions of Danshen, suggesting a potential synergism among these constituents. Herein, we provide a systematic up-to-date review on the cardiovascular actions and therapeutic potential of major pharmacologically active constituents of Danshen. These bioactive compounds will serve as excellent drug candidates in small-molecule cardiovascular drug discovery. This article also provides a scientific rationale for understanding the traditional use of Danshen in cardiovascular therapeutics.

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“…The present experimental study illustrated that the reduced apoptotic levels were detected in tumorbearing mice exposed to the IH environment. The apoptotic levels can be improved by TSA under the IH condition in which NF-kB signaling pathway may be partly involved [35,36].…”

Section: Effect Of Tsa On Nrf2 and Nf-kb Expressionmentioning

confidence: 99%

Sodium tanshinone IIA sulfonate attenuates tumor oxidative stress and enhances apoptosis in an intermittent hypoxia mouse model

Zhang

Chen

et al. 2019

Preprint

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Objective The present study was designed to determine the effect of sodium tanshinone IIA sulfonate (TSA) on tumor oxidative stress and apoptosis in a mouse model of intermittent hypoxia (IH) which was considered a novel feature of obstructive sleep apnea. Materials and methods Mice were randomly assigned to control (normoxia) group (CTL), control plus TSA (CTL+TSA) group, IH group, and IH plus TSA (IH+TSA) group. The IH exposure lasted for 5 weeks. TSA was intraperitoneally injected in the CTL+TSA and IH+TSA group. Malondialdehyde (MDA) and superoxide dismutase (SOD) were detected for tumor oxidative stress levels. Terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay and western blotting of Bax, Cleaved Caspase-3 were conducted for evaluating tumor apoptotic levels. The expression levels of nuclear factor erythroid 2-related factor 2 (Nrf2) and NF-κB were also evaluated by western blotting. Results Compared with the CTL group, mice exposed to the IH had higher MDA and lower SOD levels, and the TUNEL-positive cell rate, Bax and Cleaved Caspase-3 expressive levels were decreased in the IH group. The oxidative stress indexes were suppressed and the apoptotic levels were upregulated after treatment with TSA under the IH condition. The lower Nrf2 and higher NF-κB levels can be reversed by tretment with TSA under the IH condition. Conclusions The IH contributes to high oxidative stress and low apoptosis in tumor-bearing mice. TSA appears to improve IH-induced oxidative stress and apoptosis via Nrf2/NF-κB signaling pathway.

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Sodium tanshinone IIA sulfonate prevents lipopolysaccharide-induced inflammation via suppressing nuclear factor-κB signaling pathway in human umbilical vein endothelial cells

Cited by 25 publications

References 39 publications

Tanshinone IIA inhibits lipopolysaccharide‑induced inflammatory responses through the TLR4/TAK1/NF‑κB signaling pathway in vascular smooth muscle cells

Tanshinone IIA inhibits lipopolysaccharide‑induced inflammatory responses through the TLR4/TAK1/NF‑κB signaling pathway in vascular smooth muscle cells

Salvia miltiorrhizaBurge (Danshen): a golden herbal medicine in cardiovascular therapeutics

Sodium tanshinone IIA sulfonate attenuates tumor oxidative stress and enhances apoptosis in an intermittent hypoxia mouse model

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