Lycorine inhibits lipopolysaccharide-induced iNOS and COX-2 up-regulation in RAW264.7 cells through suppressing P38 and STATs activation and increases the survival rate of mice after LPS challenge

Kang, Jingjing; Zhang, Yushun; Cao, Xiang; Fan, Jie; Li, Guilan; Wang, Qi; Diao, Youxiang; Zhao, Zhihui; Luo, Lan; Yin, Zhimin

doi:10.1016/j.intimp.2011.11.018

Cited by 94 publications

(78 citation statements)

References 41 publications

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“…Indeed, this finding is consistent with that of a previous study showing that LY can suppress the IL-1β-induced expression of MMP-3 and MMP-13 in articular chondrocytes [55]. The present study reveals a further function of LY in addition to its known pharmacological effects, such as anti-tumour [51], antiviral [52], and anti-inflammatory [53, 54] effects.…”

Section: Discussionsupporting

confidence: 93%

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Lycorine Suppresses Endplate-Chondrocyte Degeneration and Prevents Intervertebral Disc Degeneration by Inhibiting NF-κB Signalling Pathway

Wang

Huang

Dong

et al. 2018

Cell Physiol Biochem

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Background/Aims: Cartilaginous endplate (CEP) degeneration is an important cause for intervertebral disc (IVD) degeneration that leads to low-back pain. The identification of compounds that may prevent CEP degeneration is of interest for the prevention of IVD degeneration. Methods: Catabolic protease expression in the CEP of disc degeneration patients was first assessed. The toxicity, function and underlying mechanism of lycorine (LY) on CEP-derived chondrocytes degeneration were assessed in vitro by flow cytometry analysis and western blotting. The concentration and function of LY in rat-tail disc-degeneration models were also assessed by HPLC (High Performance Liquid Chromatography) quantification and histological analysis. Results: In CEP cells, Interleukin (IL)-1β upregulated the expression of matrix metalloproteinase (MMP)-3, MMP-13, a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS)-4 and ADAMTS-5 that is critical for the degradation of cartilage extracellular matrix. Interestingly, LY suppressed the expression of these enzymes via the inhibition of nuclear factor-κB (NFκB) signalling and thus prevented IL-1β-induced endplate cell degeneration in vitro. More importantly, LY also reduced the expression of MMP-3, MMP-13, ADAMTS-4 and ADAMTS-5 in CEP and exerted a protective effect on both CEP and nucleus pulposus (NP) degeneration. In addition to its inhibitory effect on matrix-degrading protease expression, LY treatment also reduced positive regulators of proinflammatory cytokines, such as MIF, which can be secreted by CEP cells and subsequently target NP cells. Conclusion: LY could serve as a potential drug for treating IVD disease.

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Section: Discussionsupporting

confidence: 93%

“…Lycorine (LY) is the most abundant alkaloid isolated from the Amaryllidaceae family of plants [51] and can perform diverse biological functions, including anti-tumour [51], anti-viral [52] and anti-inflammatory [53, 54] functions. In addition, LY suppresses the IL-1β-induced expression of MMP-3 and MMP-13 in articular chondrocytes [55].…”

Section: Introductionmentioning

confidence: 99%

Lycorine Suppresses Endplate-Chondrocyte Degeneration and Prevents Intervertebral Disc Degeneration by Inhibiting NF-κB Signalling Pathway

Wang

Huang

Dong

et al. 2018

Cell Physiol Biochem

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“…These data imply the possibility of phosphorylation of clock proteins by Lycoris alkaloids. Effects of Lycoris alkaloids on the protein phosphorylation has not been fully elucidated yet and it has been reported that lycorine shows the inhibition of p38 and STATs, or dephosphorylation of these proteins [34], implying that the circadian period elongation by Lycoris alkaloids may be brought by the synergic effect, enhancement of BMAL1 and other biochemical activities such as protein phosphorylation. A more precise mechanism of period elongation should be elucidated and Lycoris alkaloids will be useful tools with which to analyze the circadian mechanism.…”

Section: Circadian Regulation Of Bmal1 Transcriptionmentioning

confidence: 99%

Lycorine, a Candidate for the Control of Period Length in Mammalian Cells

Onishi

Kawano²,

Yamazaki³

2012

Cell Physiol Biochem

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Plants of the Amaryllidaceae family have been used as therapeutic agents against CNS related maladies such as Alzheimer′s disease. The known primary alkaloid constituents have significant biological activity. We identified the Lycoris alkaloids lycorine and lycoricidinol from Amaryllidaceae using a real-time reporter gene assay system based on NIH3T3 cells. These alkaloids have a wide spectrum of pharmacological actions and dose-dependently lengthen the circadian period. When cells that had been incubated with lycorine or lycoricidinol were washed and then incubated without these alkaloids, period length reverted to that of control cells, suggesting that elongation of the circadian period induced by lycorine and lycoricidinol is reversible. Although one of its major activities is the inhibition of protein synthesis, lycorine induced dose-dependent period elongation regardless of the presence of cycloheximide and moreover, cycloheximide, itself did not affect period length, suggesting that lycorine dose-dependently extends the circadian period by a mechanism other than translational inhibition. Real-time RT-PCR showed that lycorine enhanced RORα and Bmal1 transcription, and exogenous expression and knockdown of Bmal1 also caused long and short periods, respectively, thus confirming the phenotype indicated by lycorine. These data indicate that lycorine and lycoricidinol modulate Bmal1 transcription and the circadian period, and also suggest that Lycoris alkaloids are novel contributors to the control of period length in mammalian cells.

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“…It has recently been shown that selective inhibitors of iNOS, that reduce the release of nitric oxide in vivo, inhibited the progression of tumorigenesis in several cancers models [40,[53][54][55][56][57]. Moreover, the inhibition of lipopolysaccharide (LPS) induced NF-kB activation inhibits iNOS expression and NO production, and inhibits inflammation-mediated tumorigenesis in mouse models [58][59][60][61][62][63][64][65].…”

Section: Introductionmentioning

confidence: 99%

“…In chronic inflammation models and inflammation-related tumorigenesis, iNOS may be persistently stimulated by cytokines and NF-kB activation in the tumor microenvironment. iNOS/NO signaling can also induce cyclo-oxygenase-2 (COX-2), which is another link between inflammation and cancer [59,70]. In view of the diverse effects of iNOS-produced NO, it is important to determine how cells regulate their iNOS/NO system.…”

Section: Introductionmentioning

confidence: 99%

Contribution of Inducible Nitric Oxide Synthase to the Transformation of HTLV-1 Infected CD4+ T-Cells

Baydoun¹,

Ratner²

2015

J Leuk

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The Human T-cell Leukemia Virus type 1 (HTLV-1), is the first retrovirus associated with a human cancer. HTLV-1 is the causative agent of an aggressive and fatal malignancy of CD4+ T lymphocytes known as Adult T-cell Leukemia lymphoma (ATLL). Since the discovery of the virus in 1980, intensive investigations have been undertaken to determine how HTLV-1 drives the transformation process in infected cells. This is because the oncogenic features of HTLV-1 make it an excellent tool to dissect the molecular pathways involved in cancer development. More important, HTLV-1 induced leukemia is a typical inflammation-mediated malignancy with constitutive activation of the NF-kB pathway, which is also a critical determinant in many other cancers. How NF-kB contributes to the leukemogenic process is not completely defined. We recently demonstrated that the NF-kB pathway induces the expression of inducible nitric oxide synthase (iNOS) in HTLV-1 induced leukemia. iNOS enzymatically generates nitric oxide, which is an oxidative and nitrosative agent of DNA and proteins. Nitric oxide was found to be associated with a large number of DNA Double Strand Breaks (DSBs) in HTLV-1 transformed cells. Here, we will review the major effects of nitric oxide on HTLV-1 induced leukemia.

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Lycorine inhibits lipopolysaccharide-induced iNOS and COX-2 up-regulation in RAW264.7 cells through suppressing P38 and STATs activation and increases the survival rate of mice after LPS challenge

Cited by 94 publications

References 41 publications

Lycorine Suppresses Endplate-Chondrocyte Degeneration and Prevents Intervertebral Disc Degeneration by Inhibiting NF-κB Signalling Pathway

Lycorine Suppresses Endplate-Chondrocyte Degeneration and Prevents Intervertebral Disc Degeneration by Inhibiting NF-κB Signalling Pathway

Lycorine, a Candidate for the Control of Period Length in Mammalian Cells

Contribution of Inducible Nitric Oxide Synthase to the Transformation of HTLV-1 Infected CD4+ T-Cells

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