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- 저자 : Li Liangchang (검색결과 3 건)
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Effects of G-Rh2 on mast cell-mediated anaphylaxis via AKT-Nrf2/NF-κB and MAPK-Nrf2/NF-κB pathways
Chang Xu,Liangchang Li,Chongyang Wang,Jingzhi Jiang,Li Li,Lianhua Zhu,Shan Jin,Zhehu Jin,Jung Joon Lee,Guanhao Li,Guanghai Yan 고려인삼학회 2022 Journal of Ginseng Research Vol.46 No.4
Background: The effect of ginsenoside Rh2 (G-Rh2) on mast cell-mediated anaphylaxis remains unclear. Herein, we investigated the effects of G-Rh2 on OVA-induced asthmatic mice and on mast cell-mediatedanaphylaxis. Methods: Asthma model was established for evaluating airway changes and ear allergy. RPMCs and RBL-2H3 were used for in vitro experiments. Calcium uptake, histamine release and degranulation weredetected. ELISA and Western blot measured cytokine and protein levels, respectively. Results: G-Rh2 inhibited OVA-induced airway remodeling, the production of TNF-a, IL-4, IL-8, IL-1b andthe degranulation of mast cells of asthmatic mice. G-Rh2 inhibited the activation of Syk and Lyn in lungtissue of OVA-induced asthmatic mice. G-Rh2 inhibited serum IgE production in OVA induced asthmaticmice. Furthermore, G-Rh2 reduced the ear allergy in IgE-sensitized mice. G-Rh2 decreased the earthickness. In vitro experiments G-Rh2 significantly reduced calcium uptake and inhibited histaminerelease and degranulation in RPMCs. In addition, G-Rh2 reduced the production of IL-1b, TNF-a, IL-8, andIL-4 in IgE-sensitized RBL-2H3 cells. Interestingly, G-Rh2 was involved in the FcεRI pathway activation ofmast cells and the transduction of the Lyn/Syk signaling pathway. G-Rh2 inhibited PI3K activity in adose-dependent manner. By blocking the antigen-induced phosphorylation of Lyn, Syk, LAT, PLCg2, PI3KERK1/2 and Raf-1 expression, G-Rh2 inhibited the NF-kB, AKT-Nrf2, and p38MAPK-Nrf2 pathways. However, G-Rh2 up-regulated Keap-1 expression. Meanwhile, G-Rh2 reduced the levels of p-AKT,p38MAPK and Nrf2 in RBL-2H3 sensitized IgE cells and inhibited NF-kB signaling pathway activation byactivating the AKT-Nrf2 and p38MAPK-Nrf2 pathways. Conclusion: G-Rh2 inhibits mast cell-induced allergic inflammation, which might be mediated by theAKT-Nrf2/NF-kB and p38MAPK-Nrf2/NF-kB signaling pathways
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An antioxidant modulates expression of receptor activator of NF-κB in asthma
이경선,박희선,박승주,김소리,민경훈,진선미,Liangchang Li,이용철 생화학분자생물학회 2006 Experimental and molecular medicine Vol.38 No.3
Oxidative stress plays critical roles in airway inflammation that is usually accompanied by increased vascular permeability and plasma exudation. VEGF increases vascular permeability and leads to airway inflammation. In addition, VEGF has been shown to enhance receptor activator of NF-κB (RANK) expression in endothelial cells. An aim of the study was to determine the potential role of antioxidant in the regulation of RANK expression in murine model of asthma. We have used a C57BL/6 mouse model of allergic asthma to evaluate the effect of L-2-oxothiazolidine-4-carboxylic acid (OTC), a prodrug of cysteine, which acts as an antioxidant, and VEGF receptor inhibitor on RANK mRNA expression. The mice develop the following pathophysiological features of asthma in the lungs: increased expression of RANK mRNA, increased number of inflammatory cells of the airways, increased vascular permeability, and increased levels of VEGF. Administration of OTC and VEGF receptor inhibitor markedly reduced plasma extravasation and VEGF levels in allergen-induced asthmatic lungs. We also showed that the increased RANK mRNA expression at 72 h after ovalbumin inhalation were reduced by the administration of OTC or VEGF receptor inhibitor. The results indicate that OTC and VEGF receptor inhibitor which inhibit up-regulation of VEGF expression modulate RANK expression that may be in association with the regulation of vascular permeability, and suggest that VEGF may regulate the RANK expression. These findings provide a crucial molecular mechanism for the potential use of antioxidants to prevent and/or treat asthma and other airway inflammatory disorders.
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Effect of FTY-720 on Pulmonary Fibrosis in Mice via the TGF-β1 Signaling Pathway and Autophagy
Jin Yuying,Liu Weidong,Gao Ge,Song Yilan,Liu Hanye,Li Liangchang,Zhou Jiaxu,Yan Guanghai,Cui Hong 한국응용약물학회 2023 Biomolecules & Therapeutics(구 응용약물학회지) Vol.31 No.4
We investigated whether FTY-720 might have an effect on bleomycin-induced pulmonary fibrosis through inhibiting TGF-β1 pathway, and up-regulating autophagy. The pulmonary fibrosis was induced by bleomycin. FTY-720 (1 mg/kg) drug was intraperitoneally injected into mice. Histological changes and inflammatory factors were observed, and EMT and autophagy protein markers were studied by immunohistochemistry and immunofluorescence. The effects of bleomycin on MLE-12 cells were detected by MTT assay and flow cytometry, and the related molecular mechanisms were studied by Western Blot. FTY-720 considerably attenuated bleomycin-induced disorganization of alveolar tissue, extracellular collagen deposition, and α-SMA and E-cadherin levels in mice. The levels of IL-1β, TNF-α, and IL-6 cytokines were attenuated in bronchoalveolar lavage fluid, as well as protein content and leukocyte count. COL1A1 and MMP9 protein expressions in lung tissue were significantly reduced. Additionally, FTY- 720 treatment effectively inhibited the expressions of key proteins in TGF-β1/TAK1/P38MAPK pathway and regulated autophagy proteins. Similar results were additionally found in cellular assays with mouse alveolar epithelial cells. Our study provides proof for a new mechanism for FTY-720 to suppress pulmonary fibrosis. FTY-720 is also a target for treating pulmonary fibrosis.
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