• Journal of Ginseng Research
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• v.23 no.2 s.54
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• pp.105-114
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• 1999

To investigate the effects of korean ginseng on the expression of transferrin receptor (TfR) in the liver cell membrane, we had carried out the experiments of $[^{3}H]thymidine$ uptake, $^{125}I-transferrin$ binding, and TfR mRNA expression in the liver after partial hepatectomy of normal and 3'-methyl-4-dimethylaminoa-zobenzene (3'-Me-DAB) treated rat with or without treatment of korean gingseng. $[^3H]thymidine$ uptake was not changed in the liver of 3'-Me-DAB or ginseng treated rat compared to that of control rat, but increased in that of partial hepatectomy of normal or 3'-Me-DAB treated rat. And this increased $[^{3}H]thymidine$ uptake was lowered slightly by the treatment of ginseng. Transferrin binding sites in the liver plasma membrane of ginseng treated rat with or without partial hepatectomy were similar, but increased in that of 3'-Me-DAB treated rat with or without partial hepatectomy compared to those of each control rat and these increased binding sites were reduced by ginseng treatment. Transferrin binding affinity (l/kd) was not changed by ginseng treatment, but tended to decrease in the liver of 3'-Me-DAB treated rat or in those after partial hepatectomy of all groups and reverse by ginseng treatment in 3'-Me-DAB treated rat. The expression of TfR mRNA was increased in the liver of 3'-Me-DAB treated rat with partial hepatectomy (peak at 24 hours), but lowered by ginseng treatment in this rat. From these results, it is suggested that korean ginseng has no effect on the increased expression of TfR with decreased affinity in the cell membrane of regenerated liver after partial hepatectomy of rat, but could inhibt that of 3'-Me-DAB treated rat through the regulation of DNA synthesis or TfR mRNA in partial.

• Applied Microscopy
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• v.27 no.2
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• pp.197-215
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• 1997

A morphologic study on the effect of butylated hydroxytoluene (BHT) on experimental hepatocarcinogenesis induced by 3'-methyl-4-dimethyl aminoazobenzene (3'-MeDAB) was investigated. A total of 110 Sprague-Dowley male rats weighting about 200 g each were used for the experiment, and divided into 4 groups; the 3'-MeDAB, BHT, 3'-MeDAB/BHT treated group, and the control group. Four to eight rats of each group were sacrified on the 4th, 8th, 14th and 16th experimental weeks, with continuous pelletized feeding containing 0.09% 3'-MeDAB and 0.5% BHT. The liver was examined by transmission and scanning electron microscopy. The results were as follows; Electron microscopically, the fine structure of the hepatocytes remained consistently abnormal up to 16 weeks after the 3'-MeDAB treatment. There was no significant difference in the groups observed earlier than in the ones observed later. Many subcellular changes were observed : nuclear change, decreased glycogen, mitochondrial abnormalities, disaggregated rough endoplasmic reticulum, marked proliferation of smooth endoplasmic reticulum, dilatation and distortion of bile canaliculi, increased lysosomes, apoptotic bodies, migration of bile ductule cell. In the BHT treated group, the ultrastructural changes of hepatocytes were not significant, except for the lipid droplets and proliferated smooth endoplasmic reticulum among hepatocytes depending on the experimental duration. The various subcellular changes of 3'-MeDAB/BHT treated groups were simillar to those of the 3'-MeDAB treated group, but the degree of changes in the 3'-MeDAB/ BHT treated group decreased compared with those of the 3'-MeDAB treated group. These results suggest that dietary butylated hydroxytoluene has a protective/inhibitory effect on the hepatocarcinogenesis induced by 3'-methyl-4-dimethyl -aminoazobenzene.

• The Korean Journal of Pharmacology
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• v.29 no.1
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• pp.85-96
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• 1993

To investigate the alteration of transferrin receptor (TfR) in the proliferating or transformed liver cells, $^{125}I-transferrin$ binding experiment was carried out in the isolated parenchymal cells (PC) or nonparenchymal cells (NPC) from normal regenerated rat liver after partial hepatectomy and from the liver of 3-methyl-4-dimethyl-aminoazobenzene (3-Me-DAB) treated rat. With the administration of 3-Me-DAB for 8 weeks, the liver tissue showed marked morphologic changes of oval cell proliferation, regenerations of hepatocytes, and atypical proliferations of bile ducts, but these changes were little affected by partial hepatectomy. Transferrin binding values in PC or NPC homogenate from the regenerated liver of normal rat, were increased by 3rd day and diminished to control level at 7th day after partial hepatectomy. With the treatement of 3-Me-DAB for 8 weeks, transferrin binding sites in homogenates were higher than those of normal rat liver and increased by 7th day after partial hepatectomy. Transferrin binding sites (Bmax) in the cell membrane of NPC were higher than those of PC of normal rat liver, but there was no significant difference in Kd values between both groups (5.05, 6.3 nM). In the normal resenerated rat liver, transferrin binding sites in the PC or NPC plasma membrane, were increased by 3rd day and diminished to control level at 7th day after partial hepatectomy. With 3-Me-DAB tratment, transferrin binding sites in both liver NPC and PC plasma membrane were increased about 3 folds, compared to those in each plasma membrane of normal rat liver. And after partial hepatectomy of 3-Me-DAB trated rat, transferrin binding sites were increased by the 3rd day in the NPC plasma membrane but increased by the 7th day in the PC plasma membrane. In the transferrin binding sites of the PC or NPC plasma membrane of 3-Me-DAB treated liver, two kinds of Kd values $(3.1{\sim}4.7\;nM,\;25.4{\sim}54.1\;nM)$ were detected. The present results suggest that 1) TfRs are distributed in the liver PC as well as NPC; 2) Increased TfRs in PC or NPC plasma membrane of normal regenerated liver after partial hepatectomy and 3-Me-DAB treated rat liver, may be due to increased intracellular synthesis; 3) Increased TfRs in normal regenerated liver after partial hepatectomy might be related to the expression of a single type of high affinity site $(Kd,\;3.1{\sim}7.5\;nM)$, but in 3-Me-DAB treated rat liver might be related to the expression of high and low affinity types of receptors $(Kd,\;25.4{\sim}54.1\;nm)$.