• 대한한방내과학회지
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• 제32권4호
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• pp.487-496
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• 2011

Objectives : The aim of this study was to investigate the hepatoprotective effect of Soshiho-tang (SSH) in mouse primary liver cells against hydrogen peroxide ($H_2O_2$)-induced oxidative stress. We also elucidated the molecular mechanism of hepatoprotective effect by SSH. Methods : Cell viability, level of ALT, AST and LDH, intracellular ROS level, mRNA expression and activity of antioxidant enzymes were used to evaluate hepatoprotection of SSH against $H_2O_2$. Target gene expressions were analyzed by real-time PCR. Results : Pre-treatment with SSH for 1 hour prevented cytotoxicity against $H_2O_2$. $H_2O_2$-induced ROS level decreased under SSH pre-treatment. mRNA expression of GPx and SOD increased in SSH-treated cells. In addition, HSP72 and HSP40 gene expression were elevated under SSH-treatment. Conclusions : These results indicate that SSH protects mouse primary liver cells from $H_2O_2$-induced oxidative injury. This hepatoprotective activity of SSH is mediated by decreasing intracellular ROS and increasing antioxidant enzyme expression (GPx and SOD) and stress response protein (HSP72 and HSP40).

• 동의생리병리학회지
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• 제21권3호
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• pp.642-646
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• 2007

It was examined that the effect of fermented traditional wine made by using mycelium of Phellinus linteus (TWPL) on the expression of inflammation-related proteins in rat liver. Levels of aspartate aminotransferase (AST) was significantly increased in the serum of ethanol-treated rats compared to normal. However, the level of AST showed no significant changes in the TWPL-treated rat compared normal. Slight histopathological changes of liver such as cloudy swelling, inflammatory cells infiltration, Kupffer cell reaction were demonstrated in the rats challenged with ethanol compared with normal. Fewer scores of these changes were observed in TWPL-treated rat with recovered glycogen in hepatocytes of whole hepatic lobule. The RT-PCR and Western analysis showed that the expression of inflammatory proteins such as cyclooxygenase-2, inducible nitric oxide synthase, tumor necrosis factor (TNF)-${\alpha}$ were decreased in the TWPL-treated rat compared with ethanol-treated ones. Immunohistochemical analysis showed that the expression of interleukin-lf and TNF-${\alpha}$ tended to decrease in TWPL-treated rat compared with ethanol-treated ones. These results suggest that TWPL may contains some protective agent for alcohol-induced liver injury through a regulating inflammation-related proteins.

• 대한한방내과학회지
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• 제44권5호
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• pp.1011-1016
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• 2023

We have experienced a case in which herbal medicine was administered to treat drug-induced liver damage and would like to introduce it. A 49-year-old man exhibited a positive result in the interferon-gamma release assay. He had never suffered from tuberculosis in the past, and the route and time of infection could not be confirmed. He had no respiratory or systemic symptoms suggestive of active tuberculosis, and a chest X-ray examination showed no active lung lesions, so he was diagnosed with latent tuberculosis infection. He was confirmed to be within the normal range in the liver function test, renal function test, and complete blood cell count test, and started taking rifampin (600 mg qd). In the screening test performed on the 19th day of taking the drug, other test items were normal, but alanine aminotransferase (ALT) increased to 50 U/L (reference value: 4-40 U/L). In a test performed on the 29th day of taking the drug, ALT was clearly elevated to 102 U/L. Ursodeoxycholic acid and Injinho-tang were taken together with rifampin, and the patient's progress was observed. In a test performed 14 days later, ALT decreased to 26 U/L, within the normal range. It is presumed that Injinho-tang may have partially contributed to alleviating liver damage in this case.

• 생명과학회지
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• 제16권6호
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• pp.978-983
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• 2006

상황버섯 배양균사체 추출물 (MCPL)이 알코올성 간 손상에 미치는 영향을 살펴보았다. Sprague-Dawley계 흰 쥐에 40% 알코올 3 ml을 MCPL (5 mg 및 15 mg/Kg)과 함께 1일 1회 10일간 투여하였다. 간 기능의 표지가 되는 혈청내 AST와 ALT값이 에탄올에 의해 현저히 증가하였으나 MCPL 투여에 의해 저하되며 특히 ALT 값이 유의성 있게 낮아졌다. 병리조직학적으로 살펴보면 알코올에 의해 염증세포의 침윤, 쿠퍼세포 반응 및 국소적 염증이 유발되나 MCPL투여에 의해 그 정도가 다소 완화되었다. 간소엽내 글리코겐 분포도 알코올에 의해 감소하나 MCPL투여에 의해 중심정맥주변 부위의 분포가 일부 회복되었다. 염증관련 단백질에 대한 Western blot 및 면역조직화학적 반응을 보면 에탄올 투여에 의해 COX-2, iNOS 및 $TNF-{\alpha}$ 면역반응이 증가하나 MCPL투여에 의해 발현의 감소를 볼 수 있었다. 이상의 결과로 보아 MCPL은 알코올에 의한 간 손상에 대해 보호 기능을 가짐을 알 수 있다.

• 대한핵의학회지
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• 제19권1호
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• pp.83-93
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• 1985

The ability of $^{67}Ga$, administered carrier free as the citrate complex, to localize in human and animal tumors to an extent sufficient to permit visualization of the lesion by scanning is well established. However, neither the mechanism of $^{67}Ga$ uptake by tumors or inflammatory cells nor its relationship to cell type or to the biochemical status of the cell is yet understood. Author investigated the uptake of $^{67}Ga-citrate$ using subcellular tissue fractionation of rat livers treated with $CCl_4$ associated with the $^3H-thymidine$ incorporation rate to detect subcellular localization of $^{67}Ga$ and it's relationship in DNA synthesis. Large amounts of $^{67}Ga$ associated with the soluble portion of tissue homogenate rather than with isolated cell organelles and not related nuclei residue in the regenerating period after hepatocellular injury caused by $CCl_4$. The elevated uptake of $^{67}Ga$ in the livers of $CCl_4$ treated rats was also inhibited when protein synthesis was stopped by cyclohexamide. Thus protein and the soluble portion of issue homogenates seems to play an important role in the elevated uptake of $^{67}Ga$ in liver injury induced by $CCl_4$ treated rats.

• 대한임상검사과학회지
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• 제51권3호
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• pp.370-378
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• 2019

허혈 재관류 손상은 기관 이식, 외과적 혈관 재개통 및 출혈시에 발생하며 조직 및 기관 기능 장애를 유발한다. 최근 허혈 재관류 손상의 기전적 연구를 위해 간장 허혈 모델을 많이 이용하고 있다. 본 연구는 허혈 재관류 랫드 모델을 이용하여 항산화와 항염증 효과를 가진 것으로 알려진 Vanillin에 의한 간장 및 신장 손상에 대한 보호 효과를 알아보고 관련된 기전을 조사하기 위하여 실시하였다. 시험물질은 각각 100 mg/kg의 농도로 3일간 투여한 후, 60분동안 간을 결찰하여 허혈 재관류를 유도하여 관찰하였으며, 음성대조군, sham대조군 및 허혈재관류만 실시한 허혈 재관류대조군을 따로 두어, 약물투여군과 비교하였다. Vanillin 처치군에서는 AST, ALT 활성이 허혈 재관류대조군에 비해 유의하게 억제되었고, 조직병리학적 관찰에서도 염증 부분과 괴사부분이 현저하게 감소하였다. MDA와 SOD는 허혈 재관류군에 비해 유의적인 변화를 보였다. 이상의 결과를 종합하면 Vanillin은 간장 허혈 재관류에 의한 세포염증 및 세포괴사를 완화시켜 간세포 보호작용을 나타내었고, 신장의 사구체 및 원위세뇨관에 염증 변화를 완화 시키고 있어 세포 손상을 방어하는 것으로 생각되며, 이러한 방어효과는 항산화 기능에 의한 영향으로 사료된다.

• Journal of Ginseng Research
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• 제39권4호
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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.

• 대한한의학방제학회지
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• 제31권2호
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• pp.111-124
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• 2023

Objectives : Oxidative stress is an important cause of many diseases including liver injury. Therefore, adequate regulation of oxidative stress plays a pivotal role in maintaining liver function. Until recently, there has been no studies on the hepatoprotective effect of Samchulgeonbi-tang (SCGBT). Therefore, the hepatoprotective effect of SCGBT was investigated in HepG2 cells. In this study, oxidative stress was induced by arachidonic acid (AA) and iron. Methods : To analyze the hepatoprotective effects of SCGBT against oxidative stress induced by AA + iron, the cell viability, apoptosis-related proteins and intracellular ROS, glutathione (GSH), and mitochondrial membrane permeability (MMP) were measured. In addition, nuclear factor erythroid 2-related factor 2 (Nrf2) transcription activation and expressions of Nrf2 target gene were analyzed through immunoblot analysis. Results : SCGBT increased the cell viability from AA + iron - induced cell death and inhibited apoptosis by regulating apoptosis related proteins. SCGBT protected cells by inhibiting ROS production, GSH depletion, and MMP degradation against AA + iron induced oxidative stress. Furthermore, Nrf2 activation was increased by SCGBT, and the Nrf2 target genes were also activated by SCGBT. Conclusions : These results suggest that the SCGBT has a hepatocyte protection effect and antioxidant effect from AA + iron induced oxidative stress.

• Journal of Preventive Medicine and Public Health
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• 제24권3호
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• pp.287-304
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• 1991

Tolerance to several toxic effects of cadmium, including lethality has been shown following pretreatment with cadmium and zinc. This study was designed to determine if tolerance also develops to Cd-induced hepatotoxicityandrenaltoxicity. Three groups of rats (A, B, C), each consisting of 16 rats, were studied and each group was divided into four subgroups (1, 2, 3, 4), 4 rats for each subgroup. Rats were subcutaneously pretreated with saline (A), $CdCl_2$ (0.5 mg/kg, B), and $ZnCl_2$ (13.0 mg/kg, C) during time periods of $1{\sim}6$ weeks. At the end of the period, rats were challenged with $CdCl_2$ (3.0, 6.0 and 9.0 mg/kg, ip). After giving the challenge dose, cadmium and metallothionein (MT) concentrations were determined and also observed the histologic change in liver and kidney. The concentration of cadmium in liver and kidney increased dose-dependently to the challenge dosage. These da indicate the kidney is a major target organ of chronic cadmium poisoning, and suggest that cadmium induced hepatic injury, via release of Cd-MT, may play an important role in the nephrotoxicity observed in response to long-term exposure to cadmium. In addition, histologic examination of group $A_2,\;A_3\;and\;A_4$ revealed moderate to severe cadmium toxicity, evidenced by infiltration of inflammatory cells, cell swelling, pyknosis, enlarged sinusoids and necrosis in liver, and tubule cell necrosis and degeneration in kidney. However, MT concentrations in liver and kidney were increased by the pretreatment of $CdCl_2$ and $ZnCl_2$, and their morphological findings were not significantly changed, comparing with control group. Higher MT concentration in liver and kidney observed in the pretreated groups constitutes a plausible explanation of the protective effects of pretreatment against the cadmium toxicity after challenge dosing.

• Archives of Plastic Surgery
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• 제32권3호
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• pp.369-375
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• 2005

Apoptosis is a physiologic or programmed cell death process which is controlled by genes. It is essential for the function and the appropriate development of multicellular organism. It is also thought to be one of the main mechanisms of cell death in ischemic tissues. The effect of prostaglandin $E_1$($PGE_1$) is proven to be useful in the recovery of ischemic changes by inducing vasodilation of peripheral vessels and platelet disaggregation. $PGE_1$ is also known to suppress apoptosis in human liver sinusoidal endothelial cell from ischemia-reperfusion injury. The purpose of this study is to evaluate the effects of $PGE_1$ on the apoptosis in the ischemia reperfusion injury of rat intestine. Thirty Sprague-Dawley rats were used. In control group(N=15), superior mesenteric artery was occluded for 60 minutes and after removing the vessel clamp, it was reperfused for 60 minutes and harvested. In experimental group(N=15), a jejunal flap was also made as in the control group except for the intraarterial administration of the $PGE_1$ right after clamping the artery and removing the clamp. H&E, TUNEL and immunohistochemical stains for p53, bax, and bcl-2 were performed. There were ischemic changes in gross and microscopic findings in both groups. The apoptotic index was significantly lower in the experimental group($1.29{\pm}0.82$(p=0.003)) than in the control group ($2.33{\pm}0.95$). The rat intestinal ischemia apoptosis by ischemia-reperfusion was partly related to the modulating of bcl-2, bax, and p53 expression. Our results indicate that $PGE_1$ suppresses the apoptosis in the ischemic jejunal flap and this effect is probably the result of a increase in expression of bcl-2.