OBJECTIVETo explore the influence of exogenous putrescine on the function of liver and apoptosis of liver cells in rats.

METHODSNinety healthy clean SD rats were divided into control group (C, n = 10, intraperitoneally injected with 2 mL normal saline), low dosage putrescine group (LP, n = 40), and high dosage putrescine group (HP, n = 40) according to the random number table. Rats in the latter two groups were intraperitoneally injected with approximately 2 mL putrescine (2.5 or 5.0 g/L) with the dosage of 25 or 50 µg/g. Ten rats from group C at post injection hour (PIH) 24 and 10 rats from each of the latter two groups at PIH 24, 48, 72, 96 were sacrificed. Heart blood was obtained for determination of serum contents of ALT and AST. Liver was harvested for gross observation and histomorphological observation with HE staining. Apoptosis was shown with in situ end labeling, and apoptosis index (AI) was calculated. Data among the three groups and those at different time points within one group were processed with one-way analysis of variance or Welch test; LSD or Dunnett's T3 test was used for paired comparison; factorial design analysis of variance of two factors was applied for data between group LP and group HP.

RESULTS(1) No obvious abnormality was observed at gross observation of liver of rats in each group. Liver tissue of rats in group C was normal. Light edema was observed occasionally in liver of rats in groups LP and HP, but necrotic cells were not seen. (2) Content of ALT at PIH 24, 48, 96 and content of AST at PIH 72 and 96 in group LP were respectively (38 ± 10), (45 ± 6), (34 ± 4), (207 ± 18), (196 ± 19) U/L, and content of ALT at PIH 72 and 96 and content of AST at PIH 24, 72, 96 in group HP were respectively (38 ± 6), (48 ± 5), (213 ± 43), (209 ± 40), (230 ± 29) U/L. They were significantly higher than those of rats in group C [(29 ± 5), (163 ± 42) U/L, with P values all below 0.01]. There were statistically significant differences between group LP and group HP in the content of ALT at PIH 48, 72, 96 and content of AST at PIH 96 (with P values all below 0.05). Compared with that at PIH 24 of each group, content of ALT of rats in group LP at PIH 48 and that of rats in group HP at PIH 96, as well as content of AST of rats in group LP at PIH 48, 72, 96 and that of rats in group HP at PIH 48 were significantly increased or decreased (with P values all below 0.05). Factorial analysis showed that the differences due to different concentration of putrescine on content of AST were statistically significant (F = 12.21, P = 0.001), but not on content of ALT (F = 0.01, P = 0.974) between group LP and group HP. (3) AI values of rats in group LP at PIH 24, 48, 72 were respectively (5.69 ± 0.38)%, (13.80 ± 1.66)%, (11.56 ± 1.74)%, and AI values of rats in group HP at PIH 72 and 96 were respectively (10.29 ± 1.43)%, (15.29 ± 1.41)%. They were all obviously higher than AI value of control group at PIH 24 [(3.50 ± 0.30)%, with P values all below 0.01]. There were statistically significant differences between group LP and group HP in AI value at PIH 24, 48, 96 (with P values all below 0.05). Compared with that at PIH 24 of each group, AI value of rats in groups LP and HP at PIH 48, 72, 96 were significantly increased or decreased (with P values all below 0.05). Factorial analysis showed that the differences in the influence of concentration of putrescine and stimulation time on AI value were statistically significant (with F values respectively 22.95 and 130.44, P values all below 0.01).

CONCLUSIONSIntraperitoneal injection of exogenous putrescine in the dosage of 25 or 50 µg/g could lead to certain degree of functional damage of liver and apoptosis of liver cells of rat. The higher the dosage and the longer the stimulation time, the more obvious the damage and apoptosis would be.

Alanine Transaminase ; blood ; Animals ; Apoptosis ; drug effects ; Hepatocytes ; cytology ; drug effects ; Liver ; cytology ; pathology ; Putrescine ; toxicity ; Rats ; Rats, Sprague-Dawley

Cell Differentiation ; drug effects ; Cells, Cultured ; Culture Media, Conditioned ; Fetal Blood ; cytology ; Hepatocytes ; cytology ; drug effects ; Humans ; Stem Cells ; cytology ; drug effects

OBJECTIVETo elucidate the effects of sodium butyrate on rat hepatic oval cell differentiation in vitro.

METHODSHepatic oval cells were isolated from rats fed with a choline-deficient diet supplemented with 0.1% (w/w) ethonine for 4 to 6 weeks. The cultured hepatic oval cells were identified by immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR). After hepatic oval cells were treated with sodium butyrate, the morphological changes were studied through Giemsa staining and the albumin expression level was tested by Western blot.

RESULTSImmunohistochemical results showed the isolated cells were positive for both mature hepatocyte marker albumin and bile duct cell marker cytokeratin-19. Furthermore, RT-PCR results showed that the cells expressed stem cell marker c-kit, but not hematopoietic stem cell marker CD34. In short, the isolated cells were rat hepatic oval cells. 0.75 mmol/L sodium butyrate induced obvious phenotype changes of hepatic oval cells, including enlargement of the oval cells, a decrease in nucleus to cytoplasm ratio, and a 50% increase in the number of binucleated cells. Western blot results showed that 0.75 mmol/L sodium butyrate markedly raised the expression of albumin.

CONCLUSIONSodium butyrate, a differentiation promoting agent, can induce rat hepatic oval cells (liver progenitor cells) to differentiate into mature hepatocytes in vitro.

Animals ; Butyrates ; pharmacology ; Cell Differentiation ; drug effects ; Cells, Cultured ; Hepatocytes ; cytology ; Liver ; cytology ; Rats ; Stem Cells ; cytology

OBJECTIVETo study the DNA damage induced by methylmercury (MeHg) in mouse hepatocytes.

METHODSThe single cell gel electrophoresis (SCGE) was used to study the DNA damage of mouse hepatocytes when treated with different doses in vivo and in vitro.

RESULTSAfter treated with high, middle and low doses of MeHg for 12 h in vivo (i.p.), the proportion of DNA damage was increased and the ratio of living cells was decreased; and both effects showed significantly dose-effect relationships. Similar effects were found when different MeHg doses were administered to hepatocytes in vitro for 1 h.

CONCLUSIONMeHg induces DNA damage in mouse hepatocytes.

Animals ; Cell Survival ; drug effects ; Cells, Cultured ; DNA Damage ; Hepatocytes ; cytology ; drug effects ; Liver ; cytology ; drug effects ; Male ; Methylmercury Compounds ; adverse effects ; Mice

OBJECTIVETo investigate the effect of ginsenoside (GSS) in regulating level of sex hormone receptors in human liver cell line HL-7702.

METHODSThe growth of HL-7702 were detected by MTT [3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assay for choosing the available concentration of GSS; and the effect of GSS on sex hormone receptors in HL-7702 cells were detected by immuno-histochemistry, Western blot and RT-PCR.

RESULTSGSS significantly enhance the protein and mRNA expressions of estrogen receptor (ER), progesterone receptor (PR), androgen receptor (AR) in HL7702 cell in a dose-dependent manner, the levels of expressions in the GSS treated group were higher than those in the solvent control group respectively (P < 0.05).

CONCLUSIONGSS can up-regulate the protein and mRNA expressions of sex hormone receptors in HL-7702.

Cell Line ; Ginsenosides ; pharmacology ; Hepatocytes ; cytology ; drug effects ; metabolism ; Humans ; Receptors, Estrogen ; metabolism

Apoptosis ; drug effects ; Carcinoma, Hepatocellular ; pathology ; Cell Line, Tumor ; Doxorubicin ; pharmacology ; Hepatocytes ; cytology ; drug effects ; Humans ; Trans-Activators ; genetics

OBJECTIVETo evaluate the effect of emodin on hepatocellular apoptosis following orthotopic liver transplantation (OLT) in rats.

METHODThe LEW --> BN OLT models were established. A total of 24 rats were divided randomly and equally into 4 groups. Group A was treated with normal saline at dose of 0.5 mL x d(-1) intraperitoneally from 1st day to 8 th day after operation. Group B, CsA at dose of 10.0 mg x kg(-1) x d(-1). Group C, emodin at dose of 50.0 mg x kg(-1) x d(-1). Group D, CsA at dose of 10.0 mg x kg(-1) x d(-1) and emodin at dose of 50.0 mg x kg(-1) x d(-1). Fifteen days after operation, rejection active index (RAI) and hepatocellular apoptosis index (AI) was confirmed after observing the pathologic change of transplanted liver in recipients.

RESULTRespectively, the RAI of group A, B, C, D was 7.67 +/- 0.98, 5.17 +/- 0.40, 5.83 +/- 0.75, 3.83 +/- 0.75 and the AI of group A, B, C, D was 35.83 +/- 2.320, 15.83 +/- 1.33, 16.50 +/- 2.35, 11.50 +/- 1.05. The RAI and AI of group B, C, D was significantly lower than group A (P < 0.01) and group D was significantly lower than group B, C too (P < 0.05). There was no significant distinction between group B and C in RAI and AI.

CONCLUSIONEmodin has the effect of reduce the hepatocellular apoptosis following OLT in rats and the effect can stronger by CsA.

Animals ; Apoptosis ; drug effects ; Emodin ; pharmacology ; Graft Rejection ; Hepatocytes ; cytology ; drug effects ; immunology ; Liver Transplantation ; Male ; Rats ; Rats, Inbred Lew

Cell Line ; Cytochrome P-450 CYP1A1 ; drug effects ; metabolism ; Hepatocytes ; cytology ; metabolism ; Humans ; Microsomes, Liver ; drug effects ; metabolism ; Quercetin ; pharmacology

Animals ; Bone Marrow Cells ; cytology ; Cell Differentiation ; drug effects ; Ethanol ; adverse effects ; Hepatocytes ; cytology ; Liver Regeneration ; Mesenchymal Stromal Cells ; cytology ; Rats ; Rats, Sprague-Dawley

OBJECTIVESThis study was conducted to explore effects of selenium on rat hepatocellular DNA damage induced by cadmium in vitro.

METHODSodium selenite was added at concentrations of 8.75, 17.50 and 35.00 micromol/L respectively with cadmium chloride at the concentrations of 8.75, 17.50 and 35.00 micromol/L respectively and rat hepatocellular DNA damage was measured with single cell gel electrophoresis (comet assay).

RESULTSSodium selenite at the concentration of 8.75 micromol/L inhibited DNA damage caused by cadmium chloride at the concentration of 8.75, 17.50 and 35.00 micromol/L in rat liver cells (P < 0.05). Although sodium selenite at 17.50 micromol/L inhibited DNA damage induced by cadmium chloride at 17.50 and 35.00 micromol/L, it did not inhibit DNA damage induced by cadmium chloride at 8.75 micromol/L. Sodium selenite at 35.00 micromol/L did not have antagonistic effects on DNA damage induced by cadmium chloride at 8.75, 17.50 and 35.00 micromol/L. In addition, sodium selenite at 8.75 micromol/L had the best antagonistic effect while cadmium chloride at 8.75 micromol/L, but the antagonistic effect of sodium selenite at 17.50 micromol/L was better than 8.75 micromol/L while cadmium chloride at 17.50 and 35.00 micromol/L.

CONCLUSIONThe antagonistic effect of selenium on rat hepatocellular DNA damage induced by cadmium related to the concentrations of selenium and also to the concentration ratio between selenium and cadmium.

Animals ; Cadmium ; toxicity ; Comet Assay ; DNA ; drug effects ; genetics ; DNA Damage ; drug effects ; Dose-Response Relationship, Drug ; Hepatocytes ; cytology ; drug effects ; metabolism ; Rats ; Selenium ; pharmacology