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• W2896065754 endingPage "11346" @default.
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• W2896065754 abstract "Saponins, the primary phytochemicals contributing to the health properties of G. pentaphyllum were frequently studied. However, compounds responsible for its bioactivities were still poorly understood. The saponin-rich fraction (GPMS), 3-O-[2G-(E)-Coumaroyl-3G-O-β-d-glucosyl-3R-O-β-d-glucosylrutinoside] (KCGG), gypenoside XLVI and gypenoside L were obtained by purification of G. pentaphyllum. The compounds were examined and compared with GPMS for their inhibitory effects on LPS-induced nitric oxide (NO) production. GPMS and KCGG differed in their inhibitory capacities against pro-inflammatory cytokines secretion. GPMS exhibited strong inhibition on inducible nitric oxide synthase (iNOS) and interleukin-6 (IL-6) mRNA expression but weak inhibition on tumor necrosis factor-α (TNF-α) and interleukin-1β mRNA expression. KCGG was better at inhibiting iNOS, IL-6, TNF-α, and cyclooxygenase-2 (COX-2) mRNA expression. GPMS showed similar inhibitory potency on mitogen-activated protein kinase phosphorylation and nuclear factor-κB (NF-κB) activation, as evidenced by their regulatory effects on LPS-induced P65 phosphorylation, NF-κB nuclear translocation, IκBα phosphorylation and degradation, IκKα/β phosphorylation, c-Jun N-terminal kinase phosphorylation, P38 phosphorylation, and COX-2 expression. KCGG was more powerful in inhibiting the NF-κB pathway, suggesting that KCGG might be used in the management of inflammatory-associated diseases in which NF-κB played pivotal roles. Furthermore, KCGG might be mainly responsible for the predominant effects of GPMS." @default.
• W2896065754 created "2018-10-26" @default.
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• W2896065754 date "2018-10-09" @default.
• W2896065754 modified "2023-09-24" @default.
• W2896065754 title "Comparison of the Effects and Inhibitory Pathways of the Constituents from <i>Gynostemma pentaphyllum</i> against LPS-Induced Inflammatory Response" @default.
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• W2896065754 doi "https://doi.org/10.1021/acs.jafc.8b03903" @default.
• W2896065754 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30301351" @default.
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