Author
Sang-Chan Lee
Bio: Sang-Chan Lee is an academic researcher from Wonkwang University. The author has contributed to research in topics: Conductivity & Metallurgy. The author has an hindex of 1, co-authored 1 publications receiving 16 citations.
Papers
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TL;DR: Two new nardosinone-type sesquiterpenoids along with seven known terpenoids were isolated from the rhizomes and roots of Nardostachys jatamansi DC and exhibited anti-neuroinflammatory effects by inhibiting the production of pro-inflammatory mediators.
24 citations
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TL;DR: The ethanol extract of Ginkgo flowers and the chloroform and ethyl acetate fractions can significantly decrease nitric oxide, interleukin‐6 (IL‐6), and prostaglandin E2 (PGE2) production at 100 μg/ml.
Abstract: Ginkgo biloba L., well known as living fossil, have various pharmacological activities. Eighteen compounds were isolated from Ginkgo male flowers including a novel matsutake alcohol glycoside, Ginkgoside A (1), and 17 known compounds-calaliukiuenoside (2), benzylalcohol O-α-l-arabinopyranosyl-(1 → 6)-β-d-glucopyranoside (3), amentoflavone (4), sciadopitysin (5), bilobetin (6), isoginkgetin (7), olivil 4-O-β-d-glucopyranoside (8), dihydrodehydrodiconiferyl alcohol-4-O-β-d-glucoside (9), (+)-cyclo-olivil-6-O-β-d-glucopyranoside (10), (-)-isolariciresinol 4-O-β-d-glucopyranoside (11), coniferin (12), trans-cinnamic acid-4-O-β-d-glucopyranoside (13), p-coumaryl alchol glucoside (14), stroside B (15), methylconiferin (16), cis-p-coumaric acid 4-O-β-d-glucopyranoside (17), and cis-coniferin (18). Thirteen of these compounds had not previously found in Ginkgo. All extractive fractions and isolated compounds were evaluated for their anti-inflammatory ability in the lipopolysaccharide-induced RAW264.7 macrophages. The ethanol extract of Ginkgo flowers and the chloroform and ethyl acetate fractions can significantly decrease nitric oxide (NO), interleukin-6 (IL-6), and prostaglandin E2 (PGE2 ) production at 100 μg/ml. The most effective compounds, bilobetin (6) and isoginkgetin (7), elevated the NO inhibition ratios to 80.19% and 82.37% at 50 μM, respectively. They also exhibited significant dose-dependent inhibitory effects on tumor necrosis factor-α, IL-6, PGE2 , inducible NO synthase mRNA, and cyclooxygenase-2 mRNA levels. So they can be promising candidates for the development of new anti-inflammatory agents.
39 citations
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TL;DR: Analysis of various studies revealed a confusion about the botanical nomenclature of the plants and their geographical distributions, and development of markers using molecular, chemical and pharmacognosy based approaches for plant authentication and, in vitro propagation of authenticated material for easy availability of genuine plant material are the possible solutions to the problems identified.
33 citations
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TL;DR: Five new and four known sesquiterpenoids were isolated from Nardostachys jatamansi, and compounds 3, 4, and 8 exhibited anti-neuroinflammatory effects in LPS-stimulated BV2 microglial cells through inhibiting of NF-κB signaling pathway.
Abstract: Nardostachys jatamansi contains various types of sesquiterpenoids that may play an important role in the potency of plant’s anti-inflammatory effects, depending on their structure In this study, five new sesquiterpenoids, namely kanshone L (1), kanshone M (2), 7-methoxydesoxo-narchinol (3), kanshone N (4), and nardosdaucanol (5), were isolated along with four known terpenoids (kanshone D (6), nardosinanone G (7), narchinol A (8), and nardoaristolone B (9)) from the rhizomes and roots of Nardostachys jatamansi Their structures were determined by analyzing 1D and 2D NMR and MS data Among the nine sesquiterpenoids, compounds 3, 4, and 8 were shown to possess dose-dependent inhibitory effects against lipopolysaccharide (LPS)-stimulated nitric oxide (NO) production in BV2 microglial cells Furthermore, compounds 3, 4, and 8 exhibited anti-neuroinflammatory effects by inhibiting the production of pro-inflammatory mediators, including prostaglandin E2 (PGE2), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) proteins, as well as pro-inflammatory cytokines, such as interleukin (IL)-1β, IL-12 and tumor necrosis factor-α (TNF-α), in LPS-stimulated BV2 microglial cells Moreover, these compounds were shown to inhibit the activation of the NF-κB signaling pathway in LPS-stimulated BV2 microglial cells by suppressing the phosphorylation of IκB-α and blocking NF-κB translocation In conclusion, five new and four known sesquiterpenoids were isolated from Nardostachys jatamansi, and compounds 3, 4, and 8 exhibited anti-neuroinflammatory effects in LPS-stimulated BV2 microglial cells through inhibiting of NF-κB signaling pathway
20 citations
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TL;DR: The findings indicated that LC53 exerted the ocular-protective effect through its inhibition on neuroinflammation, glial activation, and apoptosis in EIU, suggesting a therapeutic potential with down-regulation of the NF-κB signaling for uveitis and retinal inflammatory diseases.
Abstract: The aim of this study was to investigate the effects of a natural component, theissenolactone C (LC53), on the ocular inflammation of experimental endotoxin-induced uveitis (EIU) and its related mechanisms in microglia. Evaluation of the severity of anterior uveitis indicated that LC53 treatment significantly decreased iridal hyperemia and restored the clinical scores. Additionally, the deficient retina functions of electroretinography were improved by LC53. LC53 significantly reduced levels of tumor necrosis factor (TNF)-α, monocyte chemoattractant protein-1, protein leakage and activation of matrix metalloproteinases in the anterior section during EIU. Moreover, LC53 treatment decreased the oxidative stress as well as neuroinflammatory reactivities of GFAP and Iba-1 in the posterior section. Furthermore, LC53 decreased the phosphorylation of p65, expression of HSP90, Bax, and cleaved-caspase-3 in EIU. According to the microglia studies, LC53 significantly abrogated the productions of TNF-α, PGE2, NO and ROS, as well as inducible NO synthase and cyclooxygenase-2 expression in LPS-stimulated microglial BV2 cells. The microglial activation of IKKβ, p65 phosphorylation and nuclear phosphorylated p65 translocation were strongly attenuated by LC53. On the other hand, LC53 exhibited the inhibitory effects on JNK and ERK MAPKs activation. Our findings indicated that LC53 exerted the ocular-protective effect through its inhibition on neuroinflammation, glial activation, and apoptosis in EIU, suggesting a therapeutic potential with down-regulation of the NF-κB signaling for uveitis and retinal inflammatory diseases.
20 citations
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TL;DR: The anti-neuroinflammatory effect of desoxo-n archinol A and narchinol B was partially blocked by a selective HO-1 inhibitor, suggesting that this effect is partly mediated by HO- 1 induction.
Abstract: We previously reported that desoxo-narchinol A and narchinol B from Nardostachys jatamansi DC (Valerianaceae) inhibited the production of nitric oxide (NO) and prostaglandin E2 (PGE2), and the expression of inducible NO synthase (iNOS) and cyclooxygenase (COX)-2 protein in lipopolysaccharide (LPS)-stimulated BV2 and primary microglial cells. In this study, we aimed to elucidate the molecular mechanism underlying the anti-neuroinflammatory effects of desoxo-narchinol A and narchinol B. These two compounds inhibited the nuclear factor (NF)-κB pathway, by repressing the phosphorylation and degradation of inhibitor kappa B (IκB)-α, nuclear translocation of the p65/p50 heterodimer, and DNA-binding activity of the p65 subunit. Furthermore, both compounds induced heme oxygenase-1 (HO-1) protein expression, which was mediated by the activation of nuclear transcription factor erythroid-2-related factor 2 (Nrf2). Activation of the Nrf2/HO-1 pathway by desoxo-narchinol A was shown to be regulated by increased phosphorylation of p38 and extracellular signal-regulated kinase (ERK), whereas only p38 was involved in narchinol B-induced activation of the Nrf2/HO-1 pathway. In addition, phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling was also involved in the activation of HO-1 by desoxo-narchinol A and narchinol B. These compounds also increased the phosphorylation of glycogen synthase kinase 3 beta (GSK3β) at serine-9 residue, following phosphorylation of Akt. The anti-neuroinflammatory effect of desoxo-narchinol A and narchinol B was partially blocked by a selective HO-1 inhibitor, suggesting that this effect is partly mediated by HO-1 induction. In addition, both compounds also induced HO-1 protein expression in rat-derived primary microglial cells, which was correlated with their anti-neuroinflammatory effects in LPS-stimulated primary microglial cells. In conclusion, desoxo-narchinol A and narchinol B are potential candidates for the development of preventive agents for the regulation of neuroinflammation in neurodegenerative diseases.
14 citations