Cyclovirobuxinum D suppresses lipopolysaccharide-induced inflammatory responses in murine macrophages in vitro by blocking JAK-STAT signaling pathway

Guo, Dan; Li, Jingrong; Wang, Ying; Lei, Lin-sheng; Yu, Chunhe; Chen, Nana

doi:10.1038/aps.2014.16

Cited by 49 publications

(31 citation statements)

References 38 publications

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“…Total nitric oxide assay. Total nitric oxide production in the culture medium was determined by measuring the concentration of nitrate and nitrite, a stable metabolite of NO, by the modified Griess reaction method (29,30). The procedure was performed according to the manufacturer's protocol of the Total Nitric Oxide assay kit (Beyotime Institute of Biotechnology).…”

Section: Chemicals and Reagents Rpmi-1640 (Gibco Thermo Fishermentioning

confidence: 99%

Nitric oxide functions in stromal cell‑derived factor‑1‑induced cytoskeleton changes and the migration of Jurkat cells

Luo

Wei

et al. 2018

Oncol Lett

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Stromal cell-derived factor-1 (SDF-1) regulates multiple cell signal pathways in a variety of cellular functions, including cell migration, proliferation, survival and angiogenesis. SDF-1-induced chemotaxis is an important step of lymphocyte migration. However, the molecular mechanisms that modulate SDF-1-mediated lymphocyte migration are not well identified. Nitric oxide (NO) has been found to function as a signaling molecule in a number of signaling pathways, including migration. In the present study, the potential role of NO in SDF-1-induced migration and the association between NO and the cytoskeletal changes of Jurkat cells was investigated. The present study demonstrated that Jurkat cells induced the production of NO by SDF-1 stimulation, using Griess reaction method and western blot analysis, and that NO was involved in SDF-1-induced rearrangement and polymerization of the cytoskeleton, using NOS inhibitor L-NMMA. Furthermore, NO was required for the migration of Jurkat cells. The research suggested that NO signaling pathways exerted a critical role in SDF-1-induced cytoskeleton changes and the migration of Jurkat cells. This work provides insight into the migration mechanism of acute lymphoblastic leukemia and provides an effective theoretical basis for therapy strategies for acute lymphoblastic leukemia.

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Section: Chemicals and Reagents Rpmi-1640 (Gibco Thermo Fishermentioning

confidence: 99%

Nitric oxide functions in stromal cell‑derived factor‑1‑induced cytoskeleton changes and the migration of Jurkat cells

Luo

Wei

et al. 2018

Oncol Lett

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“…The whole protein extraction and Western blot analyses were performed as previously described [28] . Briefly, cells were lysed on ice for 30 min with RIPA lysis buffer including protease and phosphatase inhibitors (Sigma, St Louis, MO, USA).…”

Section: Western Blot Analysismentioning

confidence: 99%

Resveratrol ameliorates experimental periodontitis in diabetic mice through negative regulation of TLR4 signaling

et al. 2014

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Aim: To investigate the therapeutic effects of resveratrol (RSV) on periodontitis in diabetic mice and to explore the underlying mechanisms in vitro. Methods: Experimental periodontitis was induced in db/db mice by ligature application of porphyromonas gingivalis. The mice were treated with RSV (20 mg/kg, po) daily for 4 weeks. Alveolar bone loss, proinflammatory cytokines and TLR4 expression in the gingival tissue were measured. Cultured gingival epithelial cells (GECs) were used for in vitro studies. The transcriptional activity of TLR4 downstream signaling was analyzed using Western blotting. Results: RSV administration significantly decreased the blood glucose levels, and ameliorated alveolar bone loss in db/db mice with experimental periodontitis. RSV administration also suppressed the high levels of IL-1β, IL-6, IL-8, TNF-α, and TLR4 in gingival tissue of the mice. In the GECs incubated in high glucose medium, TLR4 expression was substantially upregulated, which was partly blocked in the presence of RSV. Lipopolysaccharides markedly increased the expression and secretion of IL-1β, IL-6, IL-8, and TNF-α in the GECs cultured in high glucose medium, which was also partly blocked in the presence of RSV. Furthermore, RSV significantly suppressed the phosphorylation of TLR4 downstream factors NF-κB p65, p38MAPK, and STAT3. Conclusion: RSV exerts protective effects against experimental periodontitis in db/db mice via negative regulation of TLR4 signaling.

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“…AG490, a selective inhibitor of JAK2 [53][54][55][56] , provided a suppressing effect on Ang II-induced fibronectin up-regulation through STAT3 dephosphorylation on Tyr705, but not Ser727. Similarly, AG490 did not affect STAT3 Lys685 acetylation.…”

Section: Acta Pharmacologica Sinica Npgmentioning

confidence: 99%

“…The inhibition of STAT3 Tyr705 phosphorylation opposed STAT3-dependent pro-fibrotic responses regulated by Ang II in tubular epithelial cells AG490, a tyrosine kinase tyrphostin that inhibits the activity of JAK2 [53][54][55][56] , suppressed Ang II-induced STAT3 phosphorylation on Tyr705 ( Figure 10A). The pretreatment of cells with AG490 also abolished downstream fibronectin expression ( Figure 10B).…”

Section: Ang II Induced Pro-fibrotic Responses and Stat3 Phosphorylatmentioning

confidence: 99%

P300-dependent STAT3 acetylation is necessary for angiotensin II-induced pro-fibrotic responses in renal tubular epithelial cells

Shen

Wang

et al. 2014

Acta Pharmacol Sin

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Aim: To explore the role of signal transducer and activator of transcription 3 (STAT3) signaling pathway, especially STAT3 acetylation, in angiotensin II (Ang II)-induced pro-fibrotic responses in renal tubular epithelial cells. Methods: Rat renal tubular epithelial cell line (NRK-52E) was used. STAT3 acetylation, phosphorylation and Janus kinase 2 (Jak2) phosphorylation, as well as the expression of fibronectin, collagen IV, transforming growth factor-β1 (TGF-β1) and p300 were examined using Western blotting. The level and localization of STAT3 phosphorylation on Tyr705 were detected with fluorescence immunocytochemistry. The cells were transfected with a plasmid vector carrying p300 gene or siRNA targeting p300 to regulate p300 expression. Results: Overexpression of p300 significantly increased STAT3 acetylation on Lys685, STAT3 phosphorylation on Tyr705, and the expression of TGF-β1, collagen IV and fibronectin in the cells. Treatment of the cells with Ang II (1 μmol/L) significantly increased STAT3 phosphorylation on Tyr705 through JAK2 activation, and dose-dependently increased the expression of fibronectin, collagen IV and TGF-β1. Pretreatment with curcumin, an inhibitor of JAK2 and p300, blocked Ang II-induced effects. Knockdown of p300 significantly decreased STAT3 acetylation on Lys685, and abolished Ang II-stimulated STAT3 phosphorylation on Tyr705, whereas pretreatment of the cells with C646, a selective inhibitor of p300, inhibited Ang II-induced STAT3 nuclear translocation and the expression of TGF-β1, collagen IV and fibronectin. Pretreatment of the cells with AG490, a JAK2 inhibitor, markedly inhibited Ang II-induced STAT3 phosphorylation on Tyr705 and fibronectin expression. Conclusion: P300-dependent STAT3 acetylation is necessary for Ang II-induced STAT3 phosphorylation and the consequent pro-fibrotic responses in renal tubular epithelial cells in vitro.

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Cyclovirobuxinum D suppresses lipopolysaccharide-induced inflammatory responses in murine macrophages in vitro by blocking JAK-STAT signaling pathway

Abstract: CVB-D exerts anti-inflammatory effects in LPS-stimulated murine macrophages in vitro at least in part by blocking the JAK-STAT signaling pathway. The anti-inflammatory actions of CVB-D may contribute to its cardioprotection.

Cited by 49 publications

References 38 publications

Nitric oxide functions in stromal cell‑derived factor‑1‑induced cytoskeleton changes and the migration of Jurkat cells

Nitric oxide functions in stromal cell‑derived factor‑1‑induced cytoskeleton changes and the migration of Jurkat cells

Resveratrol ameliorates experimental periodontitis in diabetic mice through negative regulation of TLR4 signaling

P300-dependent STAT3 acetylation is necessary for angiotensin II-induced pro-fibrotic responses in renal tubular epithelial cells

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