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Ganzhen Deng - One of the best experts on this subject based on the ideXlab platform.

  • MicroRNA-106a Provides Negative Feedback Regulation in Lipopolysaccharide-Induced Inflammation by targeting TLR4.
    International journal of biological sciences, 2019
    Co-Authors: Jing Yang, Yu Chen, Kangfeng Jiang, Yaping Yang, Gan Zhao, Shuai Guo, Ganzhen Deng
    Abstract:

    Acute lung injury (ALI) is a common clinical disease with high incidence and mortality rate, which is characterized by severe inflammatory response and tissues damage. MicroRNAs (miRNAs) have been regarded as novel regulators of Inflammation, and play an important role in various inflammatory diseases. However, it remains unknown whether the regulatory mechanisms mediated by miR-106a is involved in LPS-induced ALI. In this study, we found that expression of miR-106a was significantly decreased in lung tissues of ALI mice and LPS-stimulated macrophages. We also revealed that over-expression of miR-106a significantly decreased the production of pro-inflammatory cytokines, including IL-1β, IL-6 and TNF-α, whereas this effect was reversed by the inhibition of miR-106a. Moreover, miR-106a inhibits NF-κB activation by targeting TLR4 expression. We further demonstrated that miR-106a inhibited TLR4 expression via binding directly to the 3'-UTR of TLR4. Taken together, the results of the present study illuminated that miR-106a is a negative feedback regulator in LPS-stimulated Inflammation through TLR4/NF-κB signaling pathway.

  • Downregulation of TLR4 by miR-181a Provides Negative Feedback Regulation to Lipopolysaccharide-Induced Inflammation.
    Frontiers in pharmacology, 2018
    Co-Authors: Kangfeng Jiang, Yaping Yang, Gan Zhao, Shuai Guo, Tao Zhang, Aftab Shaukat, Ganzhen Deng
    Abstract:

    Acute lung injury (ALI) is a progressive clinical disease with a high mortality rate, and characterized by an excessive uncontrolled inflammatory response. MicroRNAs (miRNAs) play a critical role in various human inflammatory diseases, and have been recognized as important regulators of Inflammation. However, the regulatory mechanisms mediated by miRNAs involved in Lipopolysaccharide (LPS)-induced Inflammation in ALI remain hazy. In this study, we found that miR-181a expression in the lung tissues of ALI mice and LPS-stimulated RAW 264.7 macrophages is dramatically reduced. We also show that over-expression of miR-181a significantly decreased the production of inflammatory cytokines, such as IL-1β, IL-6, and TNF-α, whereas inhibition of miR-181a reversed this decrease. Moreover, miR-181a inhibits NF-κB activation and accumulation of reactive oxygen species (ROS) by targeting TLR4 expression. We further verify that miR-181a suppresses TLR4 expression by binding directly to the 3'-UTR of TLR4. Therefore, we provide the first evidence for the negative regulation of miR-181a in LPS-induced Inflammation via the suppression of ROS generation and TLR4-NF-κB pathway.

Shigeaki Ohno - One of the best experts on this subject based on the ideXlab platform.

  • Effects of fucoxanthin on Lipopolysaccharide-Induced Inflammation in vitro and in vivo.
    Experimental eye research, 2005
    Co-Authors: Kenji Shiratori, Kazuhiro Ohgami, Iliyana Ilieva, Xue-hai Jin, Yoshikazu Koyama, Kazuo Miyashita, Kazuhiko Yoshida, Satoru Kase, Shigeaki Ohno
    Abstract:

    The aim of the present study was to investigate the efficacy of fucoxanthin on endotoxin-induced uveitis (EIU) in rats. The effects of fucoxanthin on endotoxin-induced leucocyte and protein infiltration, nitric oxide (NO), prostaglandin (PG)-E2 and tumour necrosis factor (TNF)-alpha concentrations in rat aqueous humour, as well as on the cyclooxygenase (COX)-2 and inducible nitric oxide synthase (iNOS) protein expression in a mouse macrophage cell line (RAW 264.7 cells) were studied. EIU was induced in male Lewis rats by a footpad injection of lipopolysaccharide (LPS). Immediately after the LPS injection, either 0.1, 1 or 10mgkg(-1) of fucoxanthin was injected intravenously. The aqueous humour was collected 24hr later from both eyes, and both the number of cells infiltrating into the aqueous humour and the aqueous humour protein concentration were measured. The levels of PGE2, NO and TNF-alpha were determined by enzyme-linked immunosorbent assay. The RAW 264.7 cells were pretreated with various concentrations of fucoxanthin for 24hr and subsequently incubated with LPS for 24hr. COX-2 and iNOS protein expression was analysed by the Western blotting method. Levels of PGE2, NO and TNF-alpha production were determined. Fucoxanthin suppressed the development of EIU in a dose-dependent fashion. Treatment with fucoxanthin resulted in a reduction in PGE2, NO and TNF-alpha concentrations in the aqueous humour. The expression of COX and iNOS protein in the fucoxanthin treated RAW264.7 cells decreased significantly compared to that the LPS group. It also significantly reduced the concentration of PGE2, NO and TNF-alpha production in the medium of cells. The present result indicate fucoxanthin suppresses the Inflammation of EIU by blocking the iNOS and COX-2 protein expression and its anti-inflammatory effect on eye is comparable with the effect of predinisolone used in similar doses.

  • Effects of Astaxanthin on Lipopolysaccharide-Induced Inflammation In Vitro and In Vivo
    Investigative ophthalmology & visual science, 2003
    Co-Authors: Kazuhiro Ohgami, Kenji Shiratori, Satoshi Kotake, Tomomi Nishida, Nobuhisa Mizuki, Kazunaga Yazawa, Shigeaki Ohno
    Abstract:

    PURPOSE. Astaxanthin (AST) is a carotenoid that is found in marine animals and vegetables. Several previous studies have demonstrated that AST exhibits a wide variety of biological activities including antioxidant, antitumor, and anti-Helicobacter pylori effects. In this study, attention was focused on the antioxidant effect of AST. The object of the present study was to investigate the efficacy of AST in endotoxin-induced uveitis (EIU) in rats. In addition, the effect of AST on endotoxininduced nitric oxide (NO), prostaglandin E2 (PGE2), and tumor necrosis factor (TNF)- production in a mouse macrophage cell line (RAW 264.7) was studied in vitro. METHODS. EIU was induced in male Lewis rats by a footpad injection of lipopolysaccharide (LPS). AST or prednisolone was administered intravenously at 30 minutes before, at the same time as, or at 30 minutes after LPS treatment. The number of infiltrating cells and protein concentration in the aqueous humor collected at 24 hours after LPS treatment was determined. RAW 264.7 cells were pretreated with various concentrations of AST for 24 hours and subsequently stimulated with 10 g/mL of LPS for 24 hours. The levels of PGE2, TNF-, and NO production were determined in vivo and in vitro. RESULTS. AST suppressed the development of EIU in a dosedependent fashion. The anti-inflammatory effect of 100 mg/kg AST was as strong as that of 10 mg/kg prednisolone. AST also decreased production of NO, activity of inducible nitric oxide synthase (NOS), and production of PGE2 and TNF- in RAW264.7 cells in vitro in a dose-dependent manner. CONCLUSIONS. This study suggests that AST has a dose-dependent ocular anti-inflammatory effect, by the suppression of NO, PGE2, and TNF- production, through directly blocking NOS enzyme activity. (Invest Ophthalmol Vis Sci. 2003;44:

Daping Fan - One of the best experts on this subject based on the ideXlab platform.

  • Sparstolonin B suppresses Lipopolysaccharide-Induced Inflammation in human umbilical vein endothelial cells
    Archives of pharmacal research, 2013
    Co-Authors: Qiaoli Liang, Xiaodong Cui, Jinao Duan, Prakash S. Nagarkatti, Daping Fan
    Abstract:

    Sparstolonin B (SsnB) is an isocoumarin compound isolated from the tubers of both Sparganium stoloniferum and Scirpus yagara. We previously demonstrated that SsnB blocked the Toll-like receptor (TLR) 2- and TLR4-triggered inflammatory signaling in macrophages by inhibiting the recruitment of MyD88 to the TIR domains of TLR2 and TLR4. The present study was designed to examine the effects of SsnB on vascular inflammatory responses in human umbilical vein endothelial cells (HUVECs) challenged by lipopolysaccharide (LPS, a TLR4 ligand). We found that SsnB dose-dependently attenuated the LPS-induced expression of interleukin (IL)-1β and monocyte chemoattractant protein 1 both at the transcription and translation levels in HUVEC. LPS-induced endothelial cell adhesion molecules, intercellular adhesion molecular-1 and vascular cell adhesion molecule-1 expressions were also reduced by treatment with SsnB. In addition, co-incubation with SsnB attenuated THP-1 monocyte adhesion to LPS-activated HUVECs. Furthermore, SsnB efficiently suppressed LPS-induced phosphorylation of extracellular -signal-regulated kinase (Erk1/2) and Akt in HUVECs. These findings show that SsnB can suppress endothelial cell Inflammation, suggesting that SsnB might be suitable for development as a therapeutic agent for inflammatory cardiovascular disease.

Ming Liu - One of the best experts on this subject based on the ideXlab platform.

  • Biochanin A inhibits Lipopolysaccharide-Induced Inflammation in human umbilical vein endothelial cells.
    Life sciences, 2015
    Co-Authors: Xiaodong Ming, Mingfeng Ding, Bo Zhai, Lei Xiao, Taikui Piao, Ming Liu
    Abstract:

    Abstract Aim Biochanin A, an isoflavone isolated from red clover, cabbage or alfalfa, has been reported to have anti-inflammatory activity. However, the effects of biochanin A on vascular Inflammation have not been investigated. In this study, we investigate the anti-inflammatory effects of biochanin A on lipopolysaccharide (LPS)-induced inflammatory response in human umbilical vein endothelial cells (HUVEC cells). Main methods The HUVEC cells were treated with biochanin A for 12 h before exposure to LPS. The expression of ECAMs, including VCAM-1, ICAM-1, E-selectin, NF-κB and PPAR-γ was detected by Western blotting. The expression of cytokines TNF-α and IL-8 was detected by ELISA. Key findings The results showed that biochanin A inhibited LPS-induced TNF-α and IL-8 production. Meanwhile, biochanin A also suppressed VCAM-1, ICAM-1, and E-selectin expression induced by LPS. We also found that biochanin A inhibited NF-κB activation induced by LPS. Furthermore, biochanin A could activate PPAR-γ and the anti-inflammatory effects of biochanin A can be reversed by GW9662, a specific antagonist for PPAR-γ. Significance In conclusion, the anti-inflammatory effect of biochanin A is associated with activating PPAR-γ, thereby attenuating NF-κB activation and LPS-induced inflammatory response. These findings suggest that biochanin A may be a therapeutic agent for inflammatory cardiovascular disease.

Ryoichi Oyasu - One of the best experts on this subject based on the ideXlab platform.

  • Enhancement of Rat Urinary Bladder Tumorigenesis by Lipopolysaccharide-Induced Inflammation
    Cancer research, 1993
    Co-Authors: Koji Kawai, Masashi Yamamoto, Shuji Kameyama, Hitoshi Kawamata, Alfred W. Rademaker, Ryoichi Oyasu
    Abstract:

    Chronic Inflammation of the urinary tract is a significant risk factor for the development of urinary bladder cancer in humans. We previously demonstrated that weekly treatment with killed Escherichia coli enhanced rat urinary bladder tumorigenesis initiated by the carcinogen N-methyl-N-nitrosourea. We conducted the present study to determine whether lipopolysaccharide (LPS), a major cell wall component of E. coli, had a tumor-enhancing effect. LPS was instilled twice a week at three doses (100, 1.0, and 0.01 microgram/ml) into heterotopically transplanted rat urinary bladders which were treated with a single low dose (0.25 mg) of N-methyl-N-nitrosourea or vehicle. Rats treated with 100 micrograms/ml of LPS showed a significant increase in the incidence and number of tumors in the bladders pretreated with N-methyl-N-nitrosourea. Treatment with LPS alone did not induce tumors. The enhancing effects were associated with a marked increase in the numbers of polymorphonuclear leukocytes and an increase in the H2O2 concentration in the bladder lumen. Oxidative stress by reactive oxygen intermediates and a proliferative response of the carcinogen-exposed urothelium to the inflammatory stimulation appeared to play a significant role in tumor enhancement by LPS.