Tanshinone IIA inhibits LPS-induced NF-κB activation in RAW 264.7 cells: Possible involvement of the NIK–IKK, ERK1/2, p38 and JNK pathways

Jang, Seon Il; Kim, Hyung Jin; Kim, Young‐Jun; Jeong, Seung-Il; You, Yong‐Ouk

doi:10.1016/j.ejphar.2006.04.044

Cited by 170 publications

(126 citation statements)

References 31 publications

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“…ELISA results shows that in rats treated with tanshinone IIA, a significant reduction in the levels of TNF‐α, IL‐6, IL‐8 and IL‐2 was observed. Previous studies indicated that tanshinone IIA may work by inhibiting the effects of proinflammatory mediators such as NO, TNF‐α, IL‐1β and IL‐6 28. The cells ability in producing inflammatory signalling cytokines such IL‐1, TNF‐a and IL‐6A may be the reason behind the recruit of the many numbers of macrophages as well as their functions 29.…”

Section: Discussionmentioning

confidence: 99%

Retracted: Tanshinone IIA prevents left ventricular remodelling via the TLR4/MyD88/NF‐κB signalling pathway in rats with myocardial infarction

Wang

Han

et al. 2018

J Cellular Molecular Medi

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In this study, we aim to investigate the role of tanshinone IIA in myocardial infarction (MI), especially in left ventricular remodelling (VR) and the underlying mechanism involving the TLR4/MyD88/NF‐κB signalling pathway. Sprague‐Dawley (SD) rats (n = 96) were selected, and 12 of them underwent sham surgery. The remaining 84 rats were subjected to MI modelling. HE and MT staining were carried out to estimate infract size, histopathological changes and fibrosis degree. Macrophage infiltration and cardiomyocyte apoptosis were evaluated by immunohistochemistry and TUNEL staining. Reverse transcription quantitative polymerase chain reaction (RT‐qPCR) and Western blotting were used to determine the expression levels of TLR4, MyD88 and NF‐κB. Serum levels of IL‐2, IL‐6, IL‐8, TNF‐a, procollagen I Cpropeptide (PICP), and procollagen III N‐propeptide (PIIINP) were measured using enzyme‐linked immunosorbent assay (ELISA). The heart weight/body weight, mean arterial pressure (MAP), left ventricular end‐systolic pressure (LVESP), +dP/dt and −dP/dt increased while the ventricular function and the left ventricular end‐diastole pressure (LVEDP) decreased in MI rats. Compared with the rats undergoing sham surgery, MI rats showed larger infarct size, severer fibrosis, higher expression levels of TLR4, NF‐κB‐P65, MyD88, IL‐2, IL‐6, IL‐8, TNF‐a, PICP and PIIINP as well as enhanced macrophage infiltration, cardiomyocyte apoptosis. After treatment with tanshinone IIA combined with LPS for 4 weeks, the rats showed better condition than those treated with only LPS. These results indicate that tanshinone IIA attenuates MI and prevents left VR. Importantly, inhibition of TLR4/MyD88/NF‐κB signalling pathway is a key step in this process.

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Section: Discussionmentioning

confidence: 99%

Retracted: Tanshinone IIA prevents left ventricular remodelling via the TLR4/MyD88/NF‐κB signalling pathway in rats with myocardial infarction

Wang

Han

et al. 2018

J Cellular Molecular Medi

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“…Danshen (Salviae miltiorrhizae Radix) is widely prescribed in traditional Chinese medicine for cardiovascular diseases (6,7). Tanshinone IIA (Tan-IIA; C 19 H 18 O 3 ) is extracted from Danshen (8,9), and possesses anti-inflammatory (10,11) and antioxidant properties (12,13). Our previous studies have shown that Tan-IIA inhibits growth and induces apoptosis in Colo205 human colon cancer cells (14) and MDA-MB-231 breast cancer cells in vitro (15).…”

Section: Introductionmentioning

confidence: 99%

Tanshinone IIA potentiates the efficacy of 5-FU in Colo205 colon cancer cells in vivo through downregulation of P-gp and LC3-II

2011

Experimental and Therapeutic Medicine

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Abstract. Traditional Chinese herbal medicines are widely accepted as an option for the treatment of colorectal cancers. Danshen (Salviae miltiorrhizae Radix) is widely prescribed in traditional Chinese medicine for cardiovascular diseases. Tanshinone IIA (Tan-IIA) is extracted from Danshen. Our previous studies have shown that Tan-IIA induces apoptosis in Colo205 human colon cancer cells in vitro and in vivo. In the present study, we investigated the efficacy of Tan-IIA and 5-fluorouracil (5-FU) in a Colo205 cell xenograft model. For in vivo studies, SCID mice were engrafted with Colo205 cells and from day 10 onwards were randomly divided into 3 groups and treated with 5-FU plus Tan-IIA, 5-FU plus corn oil, and the vehicle alone. At the end of a 4-week dosing schedule, the SCID mice were sacrificed and xenograft tumors were dissected for protein western blot analysis. Our results showed that the Colo205 xenograft model co-treated with Tan-IIA plus 5-FU caused a reduction in the xenograft tumor volumes and decreased P-glycoprotein (P-gp) and microtubule-associated protein light chain 3 (LC3)-II expression compared to 5-FU alone. Based on these observations, it may be possible to develop Tan-IIA plus 5-FU as therapeutic agents for human colon cancer.

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“…TSA has been found to be an effective chemical component extracted from Danshen (Radix Salviae Miltiorrhizae) (37), which harbors anti-inflammatory and anti-oxidative activities (10)(11)(12)(13). It has also been shown to have a cardioprotective effect by reducing apoptosis (38)(39)(40).…”

Section: Discussionmentioning

confidence: 99%

“…Danshen, also known as Radix Salviae miltiorrhiza, is widely prescribed in traditional Chinese medicine for the treatment of cardiovascular diseases (6,7). Tanshinone IIA (TSA; C 19 H 18 O 3 ) is extracted from Danshen (8,9) and presents anti-inflammatory (10,11) and antioxidant properties (12,13). Recently, TSA has been proven to also harbor antitumor activities in various human malignant neoplasms (14-17).…”

Section: Introductionmentioning

confidence: 99%

Tanshinone IIA enhances chemosensitivity of colon cancer cells by suppressing nuclear factor-κB

Bai

Zhang

Fang

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. The aim of the present study was to investigate the effect and molecular mechanism of tanshinone IIA (TSA) on colon cancer cells. Cell viability was determined using Cell Counting kit-8 assay and the results demonstrated that TSA treatment significantly decreased the cell viability of HCT1116 and COLO205 cells in a dose-dependent manner. TSA treatment also sensitized HCT1116 and COLO205 cells to fluorouracil therapy in a concentration-dependent manner. Western blotting was performed in order to investigate the molecular mechanisms of TSA action and determine the level of phosporylated p65 and nuclear factor-κB (NF-κB)-regulated genes, including vascular endothelial growth factor (VEGF), c-Myc, cyclooxygenase-2 (COX-2) and B-cell lymphoma-2 (Bcl-2). The results revealed that TSA treatment greatly decreased the level of phosphorylated p65 in the nucleus, which indicated the inhibition of NF-κB activation by TSA treatment. TSA also decreased the expression levels of VEGF, c-Myc, COX-2 and Bcl-2. Furthermore, the inhibition of NF-κB activation with the specific inhibitor, pyrrolidine dithiocarbamate, increased the induction of cell death and chemosensitization effect of TSA in colon cancer cells. In conclusion, these results suggest that TSA induces cell death and chemosensitizes colon cancer cells through the suppression of NF-κB signaling.

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Tanshinone IIA inhibits LPS-induced NF-κB activation in RAW 264.7 cells: Possible involvement of the NIK–IKK, ERK1/2, p38 and JNK pathways

Cited by 170 publications

References 31 publications

Retracted: Tanshinone IIA prevents left ventricular remodelling via the TLR4/MyD88/NF‐κB signalling pathway in rats with myocardial infarction

Retracted: Tanshinone IIA prevents left ventricular remodelling via the TLR4/MyD88/NF‐κB signalling pathway in rats with myocardial infarction

Tanshinone IIA potentiates the efficacy of 5-FU in Colo205 colon cancer cells in vivo through downregulation of P-gp and LC3-II

Tanshinone IIA enhances chemosensitivity of colon cancer cells by suppressing nuclear factor-κB

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