• Title/Summary/Keyword: JYT)

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The Effects of Jayun-tang on the Changes of Cerebral Flow (자윤탕이 뇌혈류 변화에 미치는 영향)

  • Kim Yong-Jin;Jeon Sang-Yoon;Ann Jeong-Jo;Choi Chang-Won;Hong Seok
    • The Journal of Korean Medicine
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    • v.26 no.3 s.63
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    • pp.188-203
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    • 2005
  • Objectives : This study was designed to investigate the effects of Jayun-tang extract (JYT) on the change of cerebral hemodynamics [regional cerebral blood flow (rCBF), pial arterial diameter (PAD) and mean arterial blood pressure (MABP)] in normal and cerebral ischemic rats, na to determine the mechanisms of action of JYT. Methods : We investigated whether JYT inhibits lactate dehydrogenase activity in neuronal cells and cytokines production in serum of cerebral ischemic rats. Results : 1. JYT significantly increased rCBF and PAD in a dose-dependent manner, but MABP was not changed by injecting JYT. These results suggested JYT significantly increased rCBF by dilating PAD. 2. The JYT-induced increase in rCBF was significantly inhibited from pretreatment with indomethacin (1mg/kg, i.p.), an inhibitor of cyclooxygenase and methylene blue $(10{\mu}g/kg, i.p.)$, an inhibitor of guanylate cyclase. 3. The JYT-induced dilation in PAD was significantly inhibited from pretreatment with indomethacin, but was increased by pretreatment with methylene blue. 4 The JYT-induced increase in MABP was reduced by pretreatment with indomethacin and methylene blue. 5. JYT significantly inhibited lactate dehydrogenase activity in neuronal cells. These results suggest that JYT prevented the neuronal death. 6. Both rCBF and PAD were significantly and stably increased by JYT $(10{\mu}g/kg,\;i.p.)$ during the Period or cerebral reperfusion, which contrasted with the findings of rapid and marked increase in the control group. 7. In cytokine production in the serum drawn from femoral artery 1hr after middle cerebral artery occlusion, the sample group showed significantly decreased production of $IL-1\beta$ and $TNF-\alpha$ as well as increased production of IL-10 and $TGF-\beta$ compared with rho control group. 8. In cytokine production in the serum drawn from femoral artery 1hr after reperfusion, the sample group showed significantly decreased production of $IL-1\beta$ and $TNF-\alpha$ as well as significantly increased production of IL-10 and $TGF-\beta$ compared with the control group. Conclusions : JYT mediated by cyclooxygenase had an inhibitive effect on brain damage by inhibiting lactate dehydrogenase activity, $IL-1\beta$ and $TNF-\alpha$ production, and by accelerating IL-10 and $TGF-\beta$ production. The author feels that JYT had anti-ischemic effects through the improvement of cerebral hemodynamics and inhibitive effects on brain damage.

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Effect of Jak-Yak Tang water extract on expression of cytokin and chemokine

  • Oh, You-Chang;Kang, Ok-Hwa;Kwon, Dong-Yeul
    • Journal of Evidence-Based Herbal Medicine
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    • v.1 no.1
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    • pp.1-5
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    • 2008
  • Objectives : The purpose of this study was to investigate the anti-inflammatory effects of extract from Jak-Yak Tang (JYT) on the THP-1 cell and HMC-1 cell. Method : To evaluate of anti-inflammatory of JYT, we examined cytokines production in lipopolysacchride (LPS)-induced THP-1 cell and A23187, PMA-induced HMC-1 cell. Result : Extract of JYT inhibit LPS-induced interleukin (IL)-8 production in human monocyte THP-1 cells. Extract of JYT inhibit A23187, PMA-induced IL-8, tumor necrosis factor-$\alpha$ (INF-$\alpha$) production in HMC-1 cells. Conclusion : NT down-regulated LPS-induced IL-8 production and A23187, PMA-induced IL-8, TNF-$\alpha$ production, which may be provide a clinical basis for anti-inflammatory properities of JYT.

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Study on the Anti-inflammatory Effect of Jakyak-tang Water Extract (작약탕(芍藥湯) 물 추출물의 항염증작용에 관한 연구)

  • Seo, Yun-Hee;Kang, Ok-Hwa;Kwon, Dong-Yeul;Lee, Jang-Suk;Han, Jong-Hyun;Lee, Ki-Nam;Chong, Myong-Soo
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.25 no.3
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    • pp.503-509
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    • 2011
  • Jakyaktang(芍藥湯; JYT) exhibits potent anti-inflammatory activity in widely intestinal disease, but its mechanism was undisclosed. To elucidate the molecular mechanisms of JYT on pharmacological and biochemical actions in inflammation, we examined the effect of JYT on pro-inflammatory mediators in phorbol 12-myristate 13-acetate (PMA) plus A23187-induced mast cell and lipopolysaccharide (LPS)-stimulated macrophages. The investigation focused on whether JYT inhibited pro-inflammatory cytokines such as interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) in PMA plus A23187- induced HMC-1 cells and inflammatory madiators such as nitric oxide (NO), TNF-${\alpha}$, IL-6, iNOS, COX-2 in LPS-stimulated RAW 264.7 cells. We found that JYT inhibited LPS-induced NO, TNF-${\alpha}$ and IL-6 productions as well as the expressions of iNOS and COX-2. These results suggest that JYT has inhibitory effects on mast cell-mediated and macropage-mediated inflammation.

Effects of Jiyutang on DSS-induced Colitis of the Mouse (Dextran Sulfate Sodium으로 유발된 생쥐의 대장염에 미치는 지유탕(地楡湯)의 효과)

  • Lee, Seong-Hwan;Choi, Heung-Min;Lim, Seong-Woo
    • The Journal of Korean Medicine
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    • v.28 no.1 s.69
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    • pp.187-197
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    • 2007
  • Objectives : We examined the effect of Jiyutaug(JYT) on the experimental ulcerative colitis induced by dextran sulfate sodium(DSS). Methods : Experimental colitis was induced in mice by daily treatment with 3% DSS in the drinking water for 5days. Afterward, the mice were divided into two groups: the control group was administered water and the sample group was administered JYT for 7 days. Results : The sample group provided JYT for 7 days demonstrated faster recovery of body weight compared with the control group. Histologic change showed faster regeneration of crypt and surface epithelial cells, decreased edema of the submucosa, and decreased Iymphatic follicles of mucosa compared with the control group. immunohistochemical stain using COX-2 gene was decreased. Regeneration of surface epithelial cells and goblet cells in mucosa was observed by transmission electron microscope. Conclusion : These results indicate therapeutic effect of JYT on DSS-induced colitis in mice.

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The Administration of Jeungmiyijin-tang to Rats with Induced Gastro Reflux Esophagitis (증미이진탕(增味二陳湯) 투여가 역류성 식도염 유발 생쥐에 미치는 영향)

  • Lee, Seul-ki;Lim, Seong-woo
    • The Journal of Internal Korean Medicine
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    • v.37 no.6
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    • pp.1030-1041
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    • 2016
  • Objectives: This study investigated the administration of Jeungmiyijin-tang (JYT) to rats with reflux esophagitis (RE) induced by pylorus and forestomach ligation operations. Methods: Twenty laboratory rats were divided into three groups with 5~7 rats in each group. The control group consisted of rats with no inflammation (CON). The RE group had rats with gastroesophageal reflux elicited by pylorus and forestomach ligation operations. The JYT group had rats that were orally administered Jeungmiyijin-tang (1.5 ml/day/300 g) once a day for 14 days before reflux esophagitis was induced by the pylorus and forestomach ligation operations. Six hours after the operations, the rats were sacrificed, morphological changes were observed, and histological examinations were done in the stomach and esophagus lesion areas. If apoptosis was observed, the apoptotic cells in the esophagus lesion areas were counted. Results: The morphological and histochemical changes consisted of various injuries from hemorrhagic erosion in the RE group, while there were significantly fewer in the JYT group. The RE group marked increases of gastric mucosa erosion and infiltration of inflammatory cells in the submucosa, as well as cell division in the epithelial layer, the proliferation and degranulation of mast cells, and increases in the IL-$1{\beta}$, TNF-${\alpha}$, and MMP-9 expressions in the esophagus of the rats. The JYT group was inhibited above expression compared with the RE group. Apoptosis was statistically significantly decreased in the JYT group compared with the RE group. Conclusions: According to the above results, it appears that Jeungmiyijin-tang inhibits the expression of pro-inflammatory cytokines (TNF-${\alpha}$, IL-$1{\beta}$, and MMP-9) and apoptosis in the esophagus mucosa, thereby preventing esophageal mucosal damage from esophageal reflux.