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

Li, Xin; Lian, Li-Hua; Bai, Ting; Wu, Yan-Ling; Wan, Ying; Xie, Wen-Xue; Jin, Xuejun; Nan, Ji‐Xing

doi:10.1016/j.intimp.2011.07.018

Cited by 48 publications

(39 citation statements)

References 36 publications

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“…LPS is a major activator of inflammation and a ligand for TLR4 (39). Upon LPS stimulation, inflammation is generated by TLR4 through the activation of downstream proteins, such as MyD88, TRAF6, NF-κB, MAPKs and AP-1, resulting in the production of a wide range of pro-inflammatory cytokines and chemokines (40,41).…”

Section: Discussionmentioning

confidence: 99%

Protective effect of naringin against the LPS-induced apoptosis of PC12 cells: Implications for the treatment of neurodegenerative disorders

Wang¹,

Wang

et al. 2017

International Journal of Molecular Medicine

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Several studies have demonstrated that increased apoptosis plays an essential role in neurodegenerative disorders. It has been demonstrated that lipopolysaccharide (LPS) induces apoptosis largely through the production of intracellular reactive oxygen species (ROS) and inflammatory mediators. In this study, we investigated the potential protective mechanisms of naringin (Nar), a pummelo peel extract, on LPS-induced PC12 cell apoptosis. Nar pre-conditioning prior to stimulation with LPS for 18 h was a prerequisite for evaluating PC12 cell viability and the protective mechanisms of Nar. Nar significantly improved cell survival in a time- and concentration-dependent manner. On the one hand, Nar downregulated cytochrome P450 2E1 (CYP2E1), inhibited the release of ROS, mitigated the stimulation of oxidative stress, and rectified the antioxidant protein contents of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), superoxide dismutase (SOD)2 and glutathione synthetase (GSS). On the other hand, Nar down-regulated inflammatory gene and protein expression, including interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, HMGB1, high mobility group box 1 protein (HMGB1), cyclo-oxygenase-2 (COX-2), the Toll-like receptor 4 (TLR4)-myeloid differentiation factor 88 (MyD88)-TNF receptor-associated factor 6 (TRAF6) path way and downstream mitogen activated protein kinase (MAPK) phosphorylation, activator protein transcription factor-1 (AP-1) and nuclear factor (NF)-κB. Moroever, Nar markedly attenuated the cytochrome c shift from the mitochondria to the cytosol and regulated caspase-3-related protein expression. To the best of our knowledge, this is the first study to report the antioxidant, anti-inflammatory and anti-apoptotic effects of Nar in neuronal-like PC12 cells. These results suggest that Nar can be utilized as a potential drug for the treatment of neurodegenerative disorders.

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Section: Discussionmentioning

confidence: 99%

Protective effect of naringin against the LPS-induced apoptosis of PC12 cells: Implications for the treatment of neurodegenerative disorders

Wang¹,

Wang

et al. 2017

International Journal of Molecular Medicine

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“…The interaction of LPS with LPS-binding protein (LBP) and its transfer to cellular CD14 activate macrophages [27]. Binding of LPS to Myeloid differentiation 2 (MD-2) triggers the recruitment of the adaptors myeloid differentiation factor 88 (MyD88) and Toll-interleukin-1R domain-containing adapter inducing interferon-β (Trif) [28].…”

Section: Discussionmentioning

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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“…One of its members, TLR4, a pattern-recognizing receptor, recognizes exogenous ligands like LPS of bacterial cell wall components and activates inflammatory and innate immune responses, and then initiates intracellular signaling cascade. The TLR4 signaling can lead to activation of MAPKs, which, in turn, activates nuclear translocation of NF-B and finally initiates proinflammatory responses (Ji et al, 2009;Li et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Anti-inflammatory effects of dichloromethane fraction from Orostachys japonicus in RAW 264.7 cells: Suppression of NF-κB activation and MAPK signaling

Lee

Ryu

Lee

et al. 2012

Journal of Ethnopharmacology

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

Cited by 48 publications

References 36 publications

Protective effect of naringin against the LPS-induced apoptosis of PC12 cells: Implications for the treatment of neurodegenerative disorders

Protective effect of naringin against the LPS-induced apoptosis of PC12 cells: Implications for the treatment of neurodegenerative disorders

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

Anti-inflammatory effects of dichloromethane fraction from Orostachys japonicus in RAW 264.7 cells: Suppression of NF-κB activation and MAPK signaling

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