Experimental evidences and signal transduction pathways involved in the activation of NF-κB/Rel by angelan in murine macrophages

Jeon, Young Jin; Kim, Hwan Mook

doi:10.1016/s1567-5769(01)00065-0

Cited by 27 publications

(9 citation statements)

References 29 publications

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“…A possible candidate could be CR3 which is identified as the leukocyte membrane receptor for β-glucan (Thornton et al, 1996). Angelan, a polysaccharide from Angelica gigas, also stimulated macrophages and induced NF-κB in murine macrophages (Jeon and Kim, 2001). Since PDTC, a relatively specific inhibitor of the activation of NF-κB in macrophages, blocked the NOS induction, it appeared that NF-κB is involved in the induction of iNOS gene itself in corn silk-stimulated macrophages.…”

Section: Lpsmentioning

confidence: 98%

Corn silk induces nitric oxide synthase in murine macrophages

Kim

Choi²,

Choi³

2004

Exp Mol Med

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Section: Lpsmentioning

confidence: 98%

Corn silk induces nitric oxide synthase in murine macrophages

Kim

Choi²,

Choi³

2004

Exp Mol Med

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“…The dried roots of angelica sinensis contain phthalides, polysaccharides, coumarin, and ferulate. Previous studies have shown that Chinese angelica polysaccharide (CAP) is the main effective ingredient of angelica sinensis and has effective functions in enhancing immunity, antivirus, anti-tumor, reducing blood glucose, antioxidant and etc [10,12,13]. What's more, it has been reported that CAP plays an important role in regulating inflammatory and apoptosis in SCI model [14,15].…”

Section: Original Papermentioning

confidence: 99%

Chinese Angelica Polysaccharide (CAP) Alleviates LPS-Induced Inflammation and Apoptosis by Down-Regulating COX-1 in PC12 Cells

Xie

Zhang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Chinese angelica polysaccharide (CAP) is the main effective ingredient of angelica sinensis and exerts anti-inflammatory and anti-apoptotic effects on many diseases. This study aimed to explore the pharmacological potential of CAP on spinal cord injury (SCI). Methods: PC12 cells were pretreated by CAP and were subjected to LPS. Transfection was performed to alter the expression of COX-1. Cell viability and apoptotic cell rate were measured by CCK-8 and flow cytometry respectively. qRT-PCR and western blot analysis were performed to assess the expression changes of pro-inflammatory cytokines, apoptosis-related factor and core kinases in PI3K/AKT pathway. Results: LPS stimulation induced significant cell damage in PC12 cells as cell viability was repressed, apoptosis was induced and the expression levels of IL-1β, IL-6, IL-8, and TNF-α were increased. CAP pretreatment protected PC12 cells against LPS-induced cell damage. Meanwhile CAP treatment reduced the expression of COX-1 even in LPS-stimulated PC12 cells. More importantly, COX-1 overexpression abolished the protective effects of CAP on LPS-injured PC12 cells. Finally, Western blot analytical results showed that CAP activated PI3K/AKT pathway also in a COX-1-dependent manner. Conclusion: CAP exerted anti-apoptotic and anti-inflammatory effects on LPS-injured PC12 cells via down-regulation of COX-1.

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“…Nuclear extracts were prepared as previously described [22]. The oligonucleotide sequences for AP-1 and Oct were: 5V-GAT CTG CAT GAG TCA GAC ACA-3V, and 5V -GAT CTT CTA GAG GAT CAT GCA AAT GAT CA-3V , respectively.…”

Section: Electrophoretic Mobility Shift Assay (Emsa)mentioning

confidence: 99%