Anti-inflammatory effects of a methanol extract from Pulsatilla koreana in lipopolysaccharide-exposed rats

Lee, Sang Hyun; Lee, Eun; Ko, Young Tag

doi:10.5483/bmbrep.2012.45.6.018

Cited by 19 publications

(11 citation statements)

References 33 publications

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“…Although endotoxin alone does not cause relevant liver injury, it can be used to evaluate the effect of natural products on inflammatory cytokine formation (Kang et al, 2007; Lee et al, 2012). In order to trigger liver injury, the combination of galactosamine/endotoxin (Gal/ET) is generally used in mice (Galanos et al, 1979) or rats (Hong et al, 2009).…”

Section: Non-acetaminophen Models Of Hepatotoxicitymentioning

confidence: 99%

Models of drug-induced liver injury for evaluation of phytotherapeutics and other natural products

Jaeschke

Williams

McGill

et al. 2013

Food and Chemical Toxicology

106

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Extracts from medicinal plants, many of which have been used for centuries, are increasingly tested in models of hepatotoxicity. One of the most popular models to evaluate the hepatoprotective potential of natural products is acetaminophen (APAP)-induced liver injury, although other hepatotoxicity models such as carbon tetrachloride, thioacetamide, ethanol and endotoxin are occasionally used. APAP overdose is a clinically relevant model of drug-induced liver injury. Critical mechanisms and signaling pathways, which trigger necrotic cell death and sterile inflammation, are discussed. Although there is increasing understanding of the pathophysiology of APAP-induced liver injury, the mechanism is complex and prone to misinterpretation, especially when unknown chemicals such as plant extracts are tested. This review discusses the fundamental aspects that need to be considered when using this model, such as selection of the animal species or in vitro system, timing and dose-responses of signaling events, metabolic activation and protein adduct formation, the role of lipid peroxidation and apoptotic versus necrotic cell death, and the impact of the ensuing sterile inflammatory response. The goal is to enable researchers to select the appropriate model and experimental conditions for testing of natural products that will yield clinically relevant results and allow valid interpretations of the pharmacological mechanisms.

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Section: Non-acetaminophen Models Of Hepatotoxicitymentioning

confidence: 99%

Models of drug-induced liver injury for evaluation of phytotherapeutics and other natural products

Jaeschke

Williams

McGill

et al. 2013

Food and Chemical Toxicology

106

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“…Flavonoids, a kind of polyphenol, have three phenolic subcomponents and are also commonly referred to as bioflavonoids (14). Phytochemicals in the flavonoid family have noted bioactivities to suppress the ROS, inflammation, and growth of tumors (15,16).…”

Section: Introductionmentioning

confidence: 99%

Molecular mechanisms of luteolin-7-O-glucoside-induced growth inhibition on human liver cancer cells: G2/M cell cycle arrest and caspase-independent apoptotic signaling pathways

Hwang¹,

Lee²,

Kim³

et al. 2013

BMB Reports

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Luteolin-7-O-glucoside (LUT7G), a flavone subclass of flavonoids, has been found to increase anti-oxidant and anti-inflammatory activity, as well as cytotoxic effects. However, the mechanism of how LUT7G induces apoptosis and regulates cell cycles remains poorly understood. In this study, we examined the effects of LUT7G on the growth inhibition of tumors, cell cycle arrest, induction of ROS generation, and the involved signaling pathway in human hepatocarcinoma HepG2 cells. The proliferation of HepG2 cells was decreased by LUT7G in a dose-dependent manner. The growth inhibition was due primarily to the G2/M phase arrest and ROS generation. Moreover, the phosphorylation of JNK was increased by LUT7G. These results suggest that the anti-proliferative effect of LUT7G on HepG2 is associated with G2/M phase cell cycle arrest by JNK activation. [BMB Reports 2013; 46(12): 611-616]

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“…After preincubation of RAW264.7 cells (1 × 10 6 cells/mL) for 18 h, cells were pretreated with Cp-BF (0–200 μ g/mL) for 30 min and then incubated with LPS (1 μ g/mL) for an additional 24 h. The inhibitory effect of Cp-BF on NO and TNF- α production was determined by analysing NO and TNF- α levels with Griess reagent and ELISA kits as described previously [18, 19]. …”

Section: Methodsmentioning

confidence: 99%

IKKβ‐Targeted Anti‐Inflammatory Activities of a Butanol Fraction of Artificially Cultivated Cordyceps pruinosa Fruit Bodies

Kim

Yang

Sung

et al. 2014

Evidence-Based Complementary and Alternative Medicine

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The inhibitory activities of the Cordyceps pruinosa butanol fraction (Cp-BF) were investigated by determining inflammatory responses of lipopolysaccharide (LPS)-treated RAW264.7 macrophage cells and by evaluating HCl/ethanol (EtOH)-triggered gastric ulcers in mice. The molecular mechanisms of the inhibitory effects of Cp-BF were investigated by identifying target enzymes using biochemical and molecular biological approaches. Cp-BF strongly inhibited the production of NO and TNF-α, release of reactive oxygen species (ROS), phagocytic uptake of FITC-dextran, and mRNA expression levels of interleukin (IL)-6, inducible NO synthase (iNOS), and tumour necrosis factor-alpha (TNF)-α in activated RAW264.7 cells. Cp-BF also strongly downregulated the NF-κB pathway by suppressing IKKβ according to luciferase reporter assays and immunoblot analysis. Furthermore, Cp-BF blocked both increased levels of NF-κB-mediated luciferase activities and phosphorylation of p65/p50 observed by IKKβ overexpression. Finally, orally administered Cp-BF was found to attenuate gastric ulcer and block the phosphorylation of IκBα induced by HCl/EtOH. Therefore, these results suggest that the anti-inflammatory activity of Cp-BF may be mediated by suppression of IKKα and its downstream NF-κB activation. Since our group has established the mass cultivation conditions by developing culture conditions for Cordyceps pruinosa, the information presented in this study may be useful for developing new anti-inflammatory agents.

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Anti-inflammatory effects of a methanol extract from Pulsatilla koreana in lipopolysaccharide-exposed rats

Cited by 19 publications

References 33 publications

Models of drug-induced liver injury for evaluation of phytotherapeutics and other natural products

Models of drug-induced liver injury for evaluation of phytotherapeutics and other natural products

Molecular mechanisms of luteolin-7-O-glucoside-induced growth inhibition on human liver cancer cells: G2/M cell cycle arrest and caspase-independent apoptotic signaling pathways

IKKβ‐Targeted Anti‐Inflammatory Activities of a Butanol Fraction of Artificially Cultivated Cordyceps pruinosa Fruit Bodies

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