Lipopolysaccharide-stimulated activation of murine DC2.4 cells is attenuated by n-butylidenephthalide through suppression of the NF-κB pathway

Fu, Ru Huei; Hran, Horng Jyh; Chu, Ching-Liang; Huang, Chin Mao; Liu, Shih‐Ping; Wang, Yu Chi; Lin, Ya Hsien; Shyu, Woei Cherng; Lin, Shinn Zong

doi:10.1007/s10529-011-0528-5

Cited by 31 publications

(32 citation statements)

References 23 publications

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“…The endotoxin LPS, a molecule found in the outer membrane of bacteria, can trigger stimulation of macrophages and microglial cells by activating various signal transduction pathways including NF-κB [37]. It is known that LPS specifically binds to TLR4 [38]. Accumulating evidence has proved that LPS is the specific ligand of TLR4 [39].…”

Section: Discussionmentioning

confidence: 99%

Inhibition of NF-κB by Pyrrolidine Dithiocarbamate Prevents the Inflammatory Response in a Ligature-Induced Peri-Implantitis Model: A Canine Study

Jiang²,

Wang

et al. 2018

Cell Physiol Biochem

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Background/Aims: The roles of toll-like receptor 4 (TLR4) and nuclear factor-kappa B (NF-κB) in peri-implantitis are unclear. Here, we used a canine model of peri-implantitis to explore the effects of inhibiting NF-κB with pyrrolidine dithiocarbamate (PDTC) on the inflammatory response in ligature-induced peri-implantitis. Methods: After successfully establishing the peri-implantitis model, beagles were randomly assigned to normal, model or PDTC groups. ELISA tests were used to determine the levels of interleukin (IL)-1, IL-6, IL-8 and tumor necrosis factor alpha (TNF-α). Immunohistochemistry was employed to assess the expression of NF-κB p65. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was performed to determine the mRNA levels of TLR4 and NF-κB p65, and western blot analysis was used to measure the protein levels of TLR4 in periodontal tissues from each group. Periodontal ligament fibroblasts (PDLFs) were cultured and subsequently classified into PDLF normal, PDLF model, PDLF LPS, PDLF PDTC, and PDLF LPS + PDTC groups. An immunofluorescence assay was used to measure the expression level of NF-κB p65. The CCK-8 assay and flow cytometry were performed to evaluate cell proliferation and apoptosis. Results: The in vitro results indicated that NF-κB p65 and TLR4 were upregulated in canine periodontal tissues, and PDTC could suppress the expression levels of NF-κB p65 and TLR4. Inflammation could increase TLR4 protein expression in canine periodontal tissue, and PDTC could inhibit the inflammation-induced increase in TLR4 protein expression. These results revealed that PDTC could reverse the LPS-induced increases in the levels of IL-1, IL-6, IL-8 and TNF-α. In vivo, the results demonstrated that PDTC inhibited the LPS-induced NF-κB p65 upregulation, and PDTC could reverse the inhibitory effect of the PDLF model + LPS on the proliferation of periodontal fibroblasts. The results also showed that in the PDLF model, LPS promoted PDLF apoptosis by inducing implant periodontitis in canines, but PDTC inhibited the PDLF apoptosis and relieved implant periodontitis in canines. Conclusion: Based on our results, we concluded that PDTC can inhibit the expression of NF-κB and alleviate the inflammatory response induced by LPS, thereby preventing periodontal inflammation and reducing the development of peri-implantitis.

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Section: Discussionmentioning

confidence: 99%

Inhibition of NF-κB by Pyrrolidine Dithiocarbamate Prevents the Inflammatory Response in a Ligature-Induced Peri-Implantitis Model: A Canine Study

Jiang²,

Wang

et al. 2018

Cell Physiol Biochem

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“…3-n-butylphthalide, another important component of VOAS, could inhibit arachidonic acid metabolism (Lee et al, 2010). Fu et al reported that n-butylidenephthalide derived from AS decreased the secretion of IL-6 and TNF-a (Fu et al, 2011).Our previous studies showed that the content of ligustilide in J-VOAS was significantly higher than that in other kinds of VOAS, and the content of butene ester in C-VOAS was significantly higher than that in other kinds of VOAS (Guo et al, 2010). So the processing method was an important factor, which could affect the efficacy of AS.…”

Section: Change In Relative Content Of Biomarkers and Metabolic Pathwmentioning

confidence: 99%

Evaluation of the anti-inflammatory effects of volatile oils from processed products of Angelica sinensis radix by GC–MS-based metabolomics

Zhong

Hua

et al. 2016

Journal of Ethnopharmacology

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“…It has been available for treatments such as anemia, female irregular menstruation, cardiovascular disease, amenorrhoea, hypertension, chronic bronchitis, asthma, and rheumatism [12]. n -Butylidenephthalide (Figure 1) is the key bioactive component derived from the chloroform extract of Angelica sinensis herbs, has been confirmed to have a variety of potential pharmacological activities, such as anti-cancer [13]–[15], anti-angiogenesis [16], anti-inflammatory [17], anti-platelet [18], vasorelaxant [19]–[21], anti-anginal [22], [23], and anti-atherosclerotic [24] effects. Here, we study that n -butylidenephthalide could be examined as a prophylactic as well as an adjuvant agent for its advantageous effects on PD.…”

Section: Introductionmentioning

confidence: 99%

n-Butylidenephthalide Protects against Dopaminergic Neuron Degeneration and α-Synuclein Accumulation in Caenorhabditis elegans Models of Parkinson's Disease

Harn

Liu

et al. 2014

PLoS ONE

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BackgroundParkinson's disease (PD) is the second most common degenerative disorder of the central nervous system that impairs motor skills and cognitive function. To date, the disease has no effective therapies. The identification of new drugs that provide benefit in arresting the decline seen in PD patients is the focus of much recent study. However, the lengthy time frame for the progression of neurodegeneration in PD increases both the time and cost of examining potential therapeutic compounds in mammalian models. An alternative is to first evaluate the efficacy of compounds in Caenorhabditis elegans models, which reduces examination time from months to days. n-Butylidenephthalide is the naturally-occurring component derived from the chloroform extract of Angelica sinensis. It has been shown to have anti-tumor and anti-inflammatory properties, but no reports have yet described the effects of n-butylidenephthalide on PD. The aim of this study was to assess the potential for n-butylidenephthalide to improve PD in C. elegans models.Methodology/Principal FindingsIn the current study, we employed a pharmacological strain that expresses green fluorescent protein specifically in dopaminergic neurons (BZ555) and a transgenic strain that expresses human α-synuclein in muscle cells (OW13) to investigate the antiparkinsonian activities of n-butylidenephthalide. Our results demonstrate that in PD animal models, n-butylidenephthalide significantly attenuates dopaminergic neuron degeneration induced by 6-hydroxydopamine; reduces α-synuclein accumulation; recovers lipid content, food-sensing behavior, and dopamine levels; and prolongs life-span of 6-hydroxydopamine treatment, thus revealing its potential as a possible antiparkinsonian drug. n-Butylidenephthalide may exert its effects by blocking egl-1 expression to inhibit apoptosis pathways and by raising rpn-6 expression to enhance the activity of proteasomes.Conclusions/Significance n-Butylidenephthalide may be one of the effective neuroprotective agents for PD.

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Lipopolysaccharide-stimulated activation of murine DC2.4 cells is attenuated by n-butylidenephthalide through suppression of the NF-κB pathway

Cited by 31 publications

References 23 publications

Inhibition of NF-κB by Pyrrolidine Dithiocarbamate Prevents the Inflammatory Response in a Ligature-Induced Peri-Implantitis Model: A Canine Study

Inhibition of NF-κB by Pyrrolidine Dithiocarbamate Prevents the Inflammatory Response in a Ligature-Induced Peri-Implantitis Model: A Canine Study

Evaluation of the anti-inflammatory effects of volatile oils from processed products of Angelica sinensis radix by GC–MS-based metabolomics

n-Butylidenephthalide Protects against Dopaminergic Neuron Degeneration and α-Synuclein Accumulation in Caenorhabditis elegans Models of Parkinson's Disease

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