• Title/Summary/Keyword: $\small{D}$-galactosamine

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Protective effect of wild ginseng cambial meristematic cells on ᴅ-galactosamine-induced hepatotoxicity in rats

  • Kim, Seok-Joo;Choi, Hyo-Sun;Cho, Hong-Ik;Jin, Young-Woo;Lee, Eun-Kyong;Ahn, Jeung Youb;Lee, Sun-Mee
    • Journal of Ginseng Research
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    • v.39 no.4
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    • pp.376-383
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    • 2015
  • Background: Panax ginseng has a wide range of biological activities including anti-inflammatory, antioxidant, and immunomodulatory functions. Wild ginseng cambial meristematic cells (CMCs) were obtained from P. ginseng cambium. This study examined the protective mechanism of wild ginseng CMCs against $\small{D}$-galactosamine (GalN)-induced liver injury. GalN, a well-known hepatotoxicant, causes severe hepatocellular inflammatory damage and clinical features similar to those of human viral hepatitis in experimental animals. Methods: Hepatotoxicity was induced in rats using GalN (700 mg/kg, i.p.). Wild ginseng CMCs was administered orally once a day for 2 wks, and then 2 h prior to and 6 h after GalN injection. Results: Wild ginseng CMCs attenuated the increase in serum aminotransferase activity that occurs 24 h after GalN injection. Wild ginseng CMCs also attenuated the GalN-induced increase in serum tumor necrosis factor-${\alpha}$, interleukin-6 level, and hepatic cyclooxygenase-2 protein and mRNA expression. Wild ginseng CMCs augmented the increase in serum interleukin -10 and hepatic heme oxygenase-1 protein and mRNA expression that was induced by GalN, inhibited the increase in the nuclear level of nuclear factor-kappa B, and enhanced the increase in NF-E2-related factor 2. Conclusion: Our findings suggest that wild ginseng CMCs protects liver against GalN-induced inflammation by suppressing proinflammatory mediators and enhancing production of anti-inflammatory mediators.

랫드에서 D-galactosamine을 이용한 중기 발암성 검색법에서 natural killer 세포활성 및 c-myc 종양 단백질 발현에 관한 연구

  • 이영순;강경선;조재진;남기환
    • Proceedings of the Korean Society of Applied Pharmacology
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    • 1994.04a
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    • pp.191-191
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    • 1994
  • 본 연구는 D-galactosamine을 이용한 중기발암성 모델에서 세포성면역중의 하나인 natural killer (NK) 세포활성과 c-myc 종양단백의 발현을 알아보기 위하여 실시하였다. 수컷 6주령의 SPF SD랫드 50마리를 3개군으로 각 군당 20마리씩 나누어 배치하였다. 실험 0일에 제 1,2 군에서 DEN을 복강내로 체중 kg당 200mg 1회 투여하여 발암유발을 하였으며 대조군인 제 3군에는 saline을 투여하였다. 제 2주에 제 1군에는 강력한 발암촉진물질인 2-acetylaminofluorene (AAF)을 사료에 0.01% 투여하였으며, 제 2군은 미약한 발암촉진물질인 phenobarbital (PB)을 0.05%로 음수에 6주간 투여하였다 제 8, 15, 36주에 경시적으로 부검하였다. 제 8주에 부검시 GST-P$^{+}$ 병변이 잘 유도되어 전암병변의 유도가 잘 되었음을 확인하였다. 제 15주에 부검시 AAF를 투여한 군에서 glutathione S-transferase placental form (GST-p)에 대한 면역조직화학적 염색에서 AAF와 PB를 투여한 제 1군 및 제 2군의 간장에서는 주위조직과 한계가 명료한 GST-P$^{+}$ 증식성 결절과 병소를 관찰할 수 있었으나 기초 사료만을 투여한 제 3군은 어떠한 GST-P$^{+}$ 증식성 결절 및 병소를 관찰할 수 없었다. 랫드에서 natural killer세포는 사람이나 마우스에서 주로 자연살생능 (natural killing activity)을 보이는 LGL(lure granular lymphocyte)의 형태를 띄고 있었으며 LGL 이라고 부르는 것처럼 특징적으로 세포질 대 핵의 비율이 높고 azurophilic 과립을 세포질내에 함유하고 있으며 일반적으로 신장 형태의 핵을 가지고 있었다. 또한 세포의 크기는 small lymphocyte와 대식세포 (macrophage)의 중간 크기였다. 15주와 시험종료시 정상대조군인 제 3군의 랫드로 부터 분리한 NK 세포활성도 (% cytotoxicity)에 비하여 발암물질 투여군의 NK 활성도는 PB 투여군들의 NK활성도 보다 약간 낮았다. 랫드에서 c-myc 종양단백은 65KD 와 671KD 에서 band가 형성된 것이 관찰되었다. 시험 개시후 15주에 부검한 랫드의 간에서 c-myc 종양단백의 발현은 모든 처리군들이 대조군에 비하여 높게 발현되는. 것이 관찰되었으나 시험개시후 26주에 부검한 랫드의 간에서 c-myc 종양단백의 발현은 대조군에 비하여 차이가 거의 없었다. 따라서 랫드에서 화학적으로 유도한 간암발생 과정에서 NK 세포활성이 현저하게 억제되는 것으로 생각되며, c-myc 종양단백의 발현은 시험개시후 15주에 그 발현이 확실한 것으로 사료되어 진다.

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Effects of Low Level Laser Treatment at LR2 and LR8 acupoint on the liver damage induced in D-GalN in rats (간경(肝經)의 형화혈(滎火穴)과 합수혈(合水穴)에 시술한 레이저침이 D-GalN 간손상 유발 흰쥐에 미치는 영향)

  • Kim, Wang-In;Youn, Dae-Hwan;Choi, Chan-Hun;Na, Chang-Su
    • Korean Journal of Acupuncture
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    • v.29 no.1
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    • pp.131-141
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    • 2012
  • Objectives : This study was performed to investigate the effect of invasive laser acupuncture treatment at Liver Brook (LR2) acupoint and Liver Sea (LR8) acupoint on liver damage induced by D-galactosamine (D-GalN) in rats Methods : Liver damage was induced by D-GalN. The experimental rats were divided into two groups (control group, Low Level Laser Treatment (LLLT) group). Control groups were classified into small groups. Intact group had no liver damage and no treatment. D-GalN group was induced liver damage induced by D-GalN and not treated. LLLT group were induced liver damage induced by D-GalN and then treated at the LR2 or LR8 acupoint with 532, 658, 904 nm invasive laser acupuncture. The treatment was carried out three days at a time for 15days at both acupoints. To examine mechanism of the effect of invasive laser acupuncture, we measured the contents of ASP, ALT, ALP, TBIL in serum, CBC in blood and SOD in liver tissue. Results : The change of body weight increased in all groups. That change was AST and ALP, the AST activity decreased significantly compared with the control groups and decreased by 532 nm and 904 nm both LLLT groups. But ALP increased at LR8 acupoint by 658 nm. TBIL level significantly decreased in all LLLT groups. The SOD of LLLT groups increased in the liver tissue of rats compared to the control groups. SOD activity indicated that LLLT can help cellular defense mechanism by preventing scavenging hydrogen peroxide. In the change of WBC, it was increased in D-GalN Control group compared to intact group and LLLT groups. Conclusions : These results suggested that invasive laser acupuncture treatment at LR2 or LR8 acupoint reduced activation of hepatic enzyme and damage of liver tissue. Thus, the effect of invasive laser acupuncture was nearly identical to the way of the traditional acupuncture for the treatment of hepatocytotoxicity.