• Title/Summary/Keyword: Cirsii Japonici Herba

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Effect of Cirsii Japonici Herba on LPS-induced Inflammation in Mouse BV2 Microglial cells (대계(大薊)가 LPS로 유도된 Mouse BV2 Microglial cells의 염증반응에 미치는 영향)

  • Kim, Young-Sun;Lee, Seoung-Geun;Lee, Key-Sang
    • The Journal of Internal Korean Medicine
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    • v.29 no.4
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    • pp.1048-1060
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    • 2008
  • Cirsii Japonici Herba(CJ) is a wild perennial herb found in many areas of Korea as well as China and Japan, which has been used to treat bleeding and inflammation. Silibinin is the main flavonoid extracted from milk thistle (Cirsii Japonici Herba). It exhibits potent antioxidant activity and anti-inflammatory effect. In this study, the effect of CJ and silibinin extract on lipopolysaccharide-induced inflammation was investigated using MTS assay, RT-PCR, western blot, and nitric oxide detection on mouse BV2 microglial cell lines. In the present results, CJ and silibinin extract suppressed nitric oxide production by inhibiting the lipopolysaccharide-stimulated enhancement of COX-2 and iNOS gene expression in BV2 cells. Moreover, CJ and silibinin also repressed some lipopolysaccharide-induced signaling molecules. Importantly, catalase-induced COX-2 and iNOS expression needed activations of $NF-{\kappa}B$, PI3K/Akt, and MAPK, which were important for the transcriptional up-regulation of COX-2 and iNOS. CJ and silibinin interaction on BV2 cells down-regulated $NF-{\kappa}B$-dependent proinflammatory cytokine (IL-2,IL-6) expression. They are involved in the regulation of inflammatory responses. These data shows that CJ and silibinin exerts anti-inflammatory and analgesic effects, probably by suppression of COX-2 and iNOS synthase expression in BV2 microglial cells.

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Cirsii Japonici Herba Extract Decreases the Dimethylnitrosamine-induced Hepatic Fibrosis in Rats (DMN으로 유발된 흰쥐의 간섬유화에 미치는 대산의 효과)

  • Park Seong Kyu;Lee Eun-Ju;Khil Jae Ho;Bae Hyun Su;Hong Moo Chang;Shin Min Kyu
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.18 no.2
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    • pp.413-418
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    • 2004
  • Objectives : Cirsii Japonici Herba (CJH) is one of medicinal plants that has been frequently used for styptic purposes in Asian countries. In order to evaluate a hepatoprotective effects of CJH in the liver fibrotic diseases, the present study investigated how CJH improves a hepatic function in the dimethylnitrosamine(DMN) treated rat. Methods : CJH were orally administered to rats that has been treated with DMN. Subsequently, the amount of blood L-asparate aminotransferase (AST), L-alanine aminotransferase (ALT), and hydroxyproline were quantitated. Several histopathological markers for examining the degree of hepatic fibrosis were investigated by H-E and Masson-Trichrome staining. Results: DMN treatment caused a increase of relative liver weight to the body at 14 days after DMN induction, Administration of CJH with 100mg/kg and 1,000mg/kg dose decreased significantly the AST level elevated by DMN injection(p<0.01). But ALT level was not improved. The hydroxyproline level was reduced by a simultaneous treatment of CJH with DMN for 7 days, but not recovered completely to its normal value, CJH administration improved conspicuously the DMN-induced histopathological changes of liver such as granuloma, but cell necrosis and fibrosis were not improved with CJH 1,000mg/kg dose. Conclusion: These results indicate that CJH has protective effect on liver injury and can inhibit liver fibrosis Induced by DMN in rats.

Inhibition of Production of Reactive Oxygen Species and Gene Expression Profiles by Cirsii Japonici Herba Extract Treatment in HepG2 Cells

  • Rho, Sam-Woong;Chung, Hwan-Suck;Kang, Moon-Kyu;Na, Young-In;Cho, Chong-Woon;Kim, Hyung-Min;Jung, Hyuk-Sang;Park, Hi-Joon;Kim, Hong-Yeoul;Hong, Moo-Chang;Shin, Min-Kyu;Kim, Sung-Soo;Bae, Hyun-Su
    • Molecular & Cellular Toxicology
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    • v.1 no.4
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    • pp.224-229
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    • 2005
  • Cirsii Japonici Herba (CJH) extract has been used for hundreds of years in Asian countries as a treatment for pollutant, radiation, and alcohol-induced liver damage. The reducing effect of CJH on hydrogen peroxide-induced reactive oxygen species (ROS) production, the main cause of cell damage or death, was evaluated using the HepG2 cell line. Cell survival was determined using MTS assay. The viability of cells treated with CJH was not significantly different from oxidative-stressed HepG2 cells. A dose-dependent inhibitory effect by CJH on ROS production was shown in oxidative-stressed cells using the $H_{2}DCFDA$ assay. To identify candidate genes responsible for the anti-oxidative effects of CJH on HepG2 cells, an oligonucleotide microarray analysis was performed. The expressions of five genes were decreased, whereas nineteen genes were up-regulated in CJH plus hydrogen peroxide treated cells, compared to only hydrogen peroxide treated cells. Among them, the expression of 5 genes was decreased in hydrogen peroxide treatment when compared to control. These genes are known to regulate cell survival and progression. On the other hand, it was shown that its main compounds were not a sylimarin or its analogs. The list of differentially expressed genes may provide further insight on the action and mechanism behind the anti-oxidative effects of Cirsii Japonici Herba.

Inhibitory Effect of YBR on Hepatic Fibrogenesis (YBR의 간섬유화(肝纖維化)억제 효과(效果)에 관한 연구(硏究))

  • Seung, Hyun-Seok;Woo, Hong-Jung
    • The Journal of Internal Korean Medicine
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    • v.31 no.2
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    • pp.314-330
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    • 2010
  • Objective : This study was performed to investigate the anti-fibrogenic effect and changes of inflammation-related genes by YBR I and YBR II (YBR I: Arteisiae Capillaris Herba, Atractylodis Rhizoma Alba, Hoelen/ YBR II: YBR I +Sanguisorbae Radix, Biotae Cacumen, Cirsii Japonici Herba) on HSC(hepatic stellate cells)-T6 and TAA-induced rat liver tissue. Materials and Methods : HSC-T6 were treated with various concentrations of distilled-water extract YBR I and YBR II extract for 24, 48 and 72 hours. After the treatment, cell viability, proliferation, procollagen levels and IL-6 levels were measured by using MTT Assay, BrdU Assay, Procollagen Type 1 C-peptide EIA kit, and Murine IL-6 ELISA Development kit. Rat liver fibrosis was induced by intraperitoneal TAA injection of 150mg/kg 3 times a week for 6 weeks. After the treatment, body weight, liver & spleen weights, liver function test, complete blood cell count and change of portal pressure were studied. In addition, gene expressions of ASMA, IL-6, MMP-2, TIMP-1 and TIMP-2, all of which are known to be associated with liver fibrosis, were analyzed by using Real-Time PCR. After YBR I and YBR IItreatment, percentages of collagen in TAA-induced rat liver tissue were measured. Results : The viability and proliferation of the HSC-T6 decreased as the concentration increased. The production of procollagen decreased as the concentration increased. The production of IL-6 was little influenced by YBR I and YBR II. There was no difference in rat body weight between the TAA-only group and the YBR groups. Compared with rat liver weight of TAA-only group, that of the YBR groups increased. In the YBR I group, the serum level of AST elevated by TAA injection significantly decreased and in the YBR I and II group, the serum level of ALP and ALT elevated by TAA injection decreased. In the YBR I group, white blood cell count elevated by TAA injection decreased but platelets increased. In the YBR I group, the portal pressure elevated by TAA injection significantly decreased. Decreases in the gene expression of ASMA and MMP-2 were observed in the YBR I group. The gene expression of IL-6 was little influenced by YBR I and YBR II -treated groups. In the histological finding, TAA injections caused severe fibrosis, but YBR I and YBR II treatment significantly reduced the amounts of hepatic collagens. Conclusions : These results suggest that YBR I and II have inhibitory effects on the hepatic fibrogenesis.