Cryptotanshinone Suppressed Inflammatory Cytokines Secretion in RAW264.7 Macrophages through Inhibition of the NF-κB and MAPK Signaling Pathways

Tang, Shu; Shen, Xizhong; Huang, Heqing; Xu, Suowen; Yu, Yang; Zhou, Changhua; Kang, Le; Wang, Yuhua; Liu, Pei-Qing

doi:10.1007/s10753-010-9214-3

Cited by 112 publications

(81 citation statements)

References 24 publications

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“…5B). These results indicated that CTN eventually inhibited NF-κB P65 to translocate to the nucleus and block the expression of its target genes, such as iNOS and COX-2, and our results corroborated that of Tang et al [13] (Fig. 7).…”

Section: Discussionsupporting

confidence: 92%

“…Proinflammatory cytokines upregulate both of COX-2 and iNOS expression via the NF-κB pathway [29]. It has been proven that CTN significantly inhibited the production of proinflammatory cytokines in RAW 264.7 cells after stimulating with LPS [13]. The induction of COX-2 was dramatically suppressed by CTN pretreatment in a dosedependent manner (Fig.…”

Section: Discussionmentioning

confidence: 88%

“…1A) was reported to have multiple pharmacological activities, such as anti-inflammatory [9], antitumor [10], antioxidative [11] and antiplatelet aggregation activities [12]. Previously, Tang et al [13] reported that CTN markedly inhibited the phosphorylation of MAPK International Immunopharmacology 11 (2011) 1871-1876…”

Section: Introductionmentioning

confidence: 99%

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Cryptotanshinone inhibits LPS-induced proinflammatory mediators via TLR4 and TAK1 signaling pathway

Lian

Bai

et al. 2011

International Immunopharmacology

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 88%

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Cryptotanshinone inhibits LPS-induced proinflammatory mediators via TLR4 and TAK1 signaling pathway

Lian

Bai

et al. 2011

International Immunopharmacology

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“…[5][6][7] Cryptotanshinone (CPT), an active ingredient isolated from traditional Chinese herb Salvia miltiorrhiza Bunge, demonstrates anti-tumor, anti-inflammation, and antiAlzheimer's disease effects. [8][9][10] A previous study reported that CPT decreases ox-LDL-induced secretion of soluble ICAM-1 (sICAM-1) and soluble VCAM-1 (sVCAM-1) in human umbilical vein endothelial cells (HUVECs), 11 but the underlying mechanisms remain unclear. In this study, the potential mechanisms of CPT inhibiting ox-LDL-induced adhesion molecule expression were investigated.…”

Section: Introductionmentioning

confidence: 99%

Cryptotanshinone inhibits oxidized LDL-induced adhesion molecule expression via ROS dependent NF-κB pathways

Zhao

Chen

2016

Cell Adhesion & Migration

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Adhesion molecules, such as intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin, play important roles in the initial stage of atherosclerosis. Cryptotanshinone (CPT), a natural compound isolated from Salvia miltiorrhiza Bunge, exhibits antiatherosclerotic activity although the underlying mechanisms remain elusive. In this study, the protective effect of CPT against oxidized low-density lipoprotein (ox-LDL)-induced adhesion molecule expression was investigated in human umbilical vein endothelial cells. Ox-LDL significantly induced ICAM-1, VCAM-1, and E-selectin expression at the mRNA and protein levels but reduced eNOS phosphorylation and NO generation, which were reversed by CPT pretreatment. Sodium nitroprusside, a NO donor, N-acetyl-L-cysteine (NAC), a reactive oxygen species (ROS) scavenger, and BAY117082, a NF-kB inhibitor, inhibited ox-LDL-induced ICAM-1, VCAM-1, and Eselectin expression. Ox-LDL-induced ROS production was significantly inhibited by CPT and NAC. Furthermore, ox-LDL activated the NF-kB signaling pathway by inducing phosphorylation of IKKb and IkBa, promoting the interaction of IKKb and IkBa, and increasing p65 nuclear translocation, which were significantly inhibited by CPT. In addition, CPT, NAC, and BAY117082 inhibited ox-LDLinduced membrane expression of ICAM-1, VCAM-1, E-selectin, and endothelial-monocyte adhesion and restored eNOS phosphorylation and NO generation. Results suggested that CPT inhibited ox-LDL-induced adhesion molecule expression by decreasing ROS and inhibiting the NF-kB pathways, which provides new insight into the anti-atherosclerotic mechanism of CPT.

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“…Activation of MAPKs signaling pathways leads to the synthesis and release of pro-inflammatory mediators by activated macrophages during the inflammatory response [6].…”

Section: Introductionmentioning

confidence: 99%

Salidroside Regulates Inflammatory Response in Raw 264.7 Macrophages via TLR4/TAK1 and Ameliorates Inflammation in Alcohol Binge Drinking Induced Liver Injury

Sun¹,

Shen²,

Jiang³

et al. 2016

Preprint

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Abstract:The current study was designed to investigate the anti-inflammatory effect of salidroside (SDS) and the underlying mechanism by using lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages in vitro and a mouse model of binge drinking induced liver injury in vivo. SDS downregulated protein expression of toll-like receptor 4 (TLR4) and CD14. SDS inhibited LPStriggered phosphorylation of LPS-activated kinase 1 (TAK1), p38, c-Jun terminal kinase (JNK), and extracellular signal-regulated kinase (ERK). Degradation of IκB-α and nuclear translocation of nuclear factor (NF)-κB were effectively blocked by SDS. SDS concentration-dependently suppressed LPS mediated inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) protein levels, as well as their downstream products, NO. SDS significantly inhibited protein secretion of interleukin (IL)-1β. Additionally C57BL/6 mice were orally administrated SDS for continuous 5 days, followed by three gavages of ethanol every 30 min. Alcohol binge drinking caused the increasing of hepatic lipid accumulation and serum transaminases levels. SDS pretreatment significantly alleviated liver inflammatory changes and serum transaminases levels. Further investigation indicated that SDS markedly decreased protein level of IL-1β in serum. Taken together, these data implied that SDS inhibits liver inflammation both in vitro and in vivo, and may be a promising candidate for the treatment of inflammatory liver injury.

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Cryptotanshinone Suppressed Inflammatory Cytokines Secretion in RAW264.7 Macrophages through Inhibition of the NF-κB and MAPK Signaling Pathways

Cited by 112 publications

References 24 publications

Cryptotanshinone inhibits LPS-induced proinflammatory mediators via TLR4 and TAK1 signaling pathway

Cryptotanshinone inhibits LPS-induced proinflammatory mediators via TLR4 and TAK1 signaling pathway

Cryptotanshinone inhibits oxidized LDL-induced adhesion molecule expression via ROS dependent NF-κB pathways

Salidroside Regulates Inflammatory Response in Raw 264.7 Macrophages via TLR4/TAK1 and Ameliorates Inflammation in Alcohol Binge Drinking Induced Liver Injury

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