Objectives : This study was carried out to determine whether Juglandis Semen herbal acupuncture (JSA) exerts the protective effect against toxic agent-induced live. cell damage. Methods : The cell damage was estimated by measuring lactate dehydrogenase (LDH) release, and lipid peroxidation was estimated by measuring maiondialdehyde (MDA), a product of lipid peroxidation, in rabbit liver slices. Results : When tissues were incubated with 0.5 mM Hg for $10{\sim}120\;min$, LDH release and lipid peroxidation were increased as a function of incubation time, and these effects were significantly prevented by addition of 0.1% JSA. Hg increased LDH release and lipid peroxidation in dose-dependent manner over the range of $0.1{\sim}l\;mM$ concentrations, which were reduced by 0.1% JSA. When tissues were treated with 0.5 mM Hg in the presence of $0.05{\sim}l\;%$ JSA, LDH release and lipid peroxidation induced by Hg were prevented by JSA in a dose-dependent fashion. JSA at 0.5 and 1% prevented completely effects of 0.5 mM Hg. When tissues were treated with 0.5 mM Hg for 60 min, LDH release and lipid peroxidation were increased, which were significantly prevented by addition of 0.1 % JSA. tert-Butyl hydroperoxide (tBHP) increased LDH release and lipid peroxidation, which were significantly reduced by 0.1 % JSA. Such protective effects were similar to those of N,N'-diphenyl-p-phenylenediamine (DPPD), a potent antioxidant. When tissues were treated with 0.5 mM Hg, activities of catalase and glutathione peroxidase were inhibited, and glutathione content was also reduced. Such effects were prevented by JSA, but not by DPPD. JSA prevented Hg-induced morphological changes. Conclusions : These results indicate that JSA exerts the protective effect against liver cell injury induced by toxic agents through antioxidant action, and this effect may be attributed to an increase in activities of endogeous anitoxidant enzymes and GSH content. However, antioxidant effect of JSA is different from that of a well-known potent antioxidant DPPD.
In oriental medicine, Artemisia Iwayomogi(Compositae) has been used clinically for jaundice, hepatitis, liver cirrhosis etc. The purposes of present study were to examine pharmacological effects of Artemisia lwayomogi water extract(AIWE) on weights of body, liver, kidney, spleen and adrenal, and on biochemical parameters (activities of AST, ALT and LDH, contents of cholesterol and triacylglycerol, and levels of hepatic lipid peroxide) against hepatic injury by carbon tetrachloride($CCl_4$) in rats. The results were as follow; 1. Body weights were reduced by $CCl_4$. In AIWE pretreatment groups, reduction of body weights was inhibited at 48 hours. Increased liver weights by $CCl_4$ were reduced in proportion to numbers of treatment of AIWE in AIWE pre- and posttreatment groups. Increased kidney weights by $CCl_4$ were reduced in AIWE pretreatment groups at 72 hours. Increased weights of spleen and adrenal by $CCl_4$ were not affected by AIWE treament. 2. Increased AST activities by $CCl_4$ were significantly (p<0.05) decreased in AIWE posttreatment groups at 48 and 72 hours. Increased ALT activities by $CCl_4$ were significantly(p<0.05) decreased in AIWE posttreatment groups at 48 hours. Increased LDH activities by $CCl_4$ were very significantly (p<0.01, p<0.001) decreased in AIWE posttreatment groups at 48 and 72 hours, respectively. 3. Increased cholesterol contents by $CCl_4$ were significantly (p<0.05) decreased in AIWE posttreatment groups at 24 and 48 hours. Decreased triacylglycerol contents by $CCl_4$ were significantly (p<0.05) increased in AIWE posttreatment at 48 and 72 hours. 4. Increased hepatic lipid peroxide levels by $CCl_4$ were significantly (p<0.05, p<0.01) decreased in AIWE posttreatment groups at 48 and 72 hours, respectively. In conclusion, AIWE did not affect normal liver function and had property of antioxidant, due to reduced lipid peroxidation by $CCl_4$. AIWE seems to have hepatoprotective effects rather than direct preventive effects to $CCl_4$-induced necrotic degeneration of liver cell, cholestasis and damages in metabolism of lipid.
Seo, Sang-Hee;Oh, Su-Young;Lee, Ji-Seon;Cho, Won-Kyung;Kim, Tae-Soo;Ma, Jin-Yeul
The Journal of Internal Korean Medicine
/
v.32
no.4
/
pp.487-496
/
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).
Journal of Physiology & Pathology in Korean Medicine
/
v.21
no.3
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pp.642-646
/
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.
Seyeon Lee;Hansung Yoon;Kibeom Ku;Mariah Kim;Irang Nam;Minhwa Kim;Changwoo Han
The Journal of Internal Korean Medicine
/
v.44
no.5
/
pp.1011-1016
/
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.
We investigated the anti-inflammatory effects of mycelial culture extract from Phellinus linteus (MCPL) for suppression in the process of ethanol-induced inflammation in rat liver. Levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were significantly increased in the serum of ethanol-treated rats compared to normal. However, the level of ALT was arrested markedly in ethanol-treated rats with MCPL compared to ethanol alone treated control ones. Severe histopathological changes of liver such as cloudy swelling, inflammatory cells infiltration, Kupffer cell reaction and focal necrosis were demonstrated in the rats challenged with ethanol compared with normal. Fewer scores of these changes were observed in MCPL-treated rat with recovered glycogen in centrolobular region of hepatic lobule. The Western analysis showed that the expression of inflammatory proteins such as cyclooxygenase (COX)-1, COX-2, inducible nitric oxide synthase (iNOS), tumor necrosis factor $(TNF)-{\alpha}$ were increased in the ethanol-treated rat. But decline of COX-2 and iNOS expression were observed in MCPL-treated rat. Immunohistochemical analysis showed that the expression of COX-2 and $TNF-{\alpha}$ tended to increase in ethanol-treated rat, but decrease of these reactions were induced by MCPL treatment. These results suggest that MCPL may act as a protective agent for alcohol-induced liver injury through a regulating inflammation-related proteins.
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.
Ahn, Yong Ho;Seok, Pu Reum;Oh, Su Jin;Choi, Jin Woo;Shin, Jae-Ho
Korean Journal of Clinical Laboratory Science
/
v.51
no.3
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pp.370-378
/
2019
The hepatic ischemic model has recently been widely used for the epidemiological study of ischemic reperfusion injury. This study was carried out to investigate the protective effect of vanillin, which is known to have antioxidant and anti-inflammatory effects, against hepatic and renal injury using an ischemia-reperfusion rat model, and we also investigated the mechanism related to vanillins' protective effect. The test material was administered at a concentration of 100 mg/kg for 3 days, followed by ligation of the liver for 60 minutes to induce ischemia reperfusion. As control groups, there was a negative control, sham control and ischemia-reperfusion-only ischemia reperfusion control, and the controls groups were compared with the drug administration group. In the vanillin group, aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities were significantly inhibited compared with the AST and ALT activities of the ischemia-reperfusion group, and histopathological examination showed significant reduction of both inflammation and necrosis. The malondialdehyde (MDA) and superoxide dismutase (SOD) levels were significantly different from the ischemia-reperfusion group. In conclusion, vanillin showed a hepatocyte protective action by alleviating the cellular inflammation and cell necrosis caused by hepatic ischemia-reperfusion, and vanillin mitigated inflammatory changes in the kidney glomeruli and distal tubules. The protective effect is considered to be caused by vanillin's antioxidant function. Further studies such as on cell death and possibly vanillin's same effect on damaged tissue will be necessary for clinical applications such as organ transplantation.
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
/
v.39
no.4
/
pp.376-383
/
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.
Ye Lim Kim;Hyo Jeong Jin;Sang Mi Park;Sung Hui Byun;Chang Hyun Song;Sang Chan Kim
Herbal Formula Science
/
v.31
no.2
/
pp.111-124
/
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.
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