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AIM: To investigate the effect of GSTP1 over-expression on the sensitivity of human hepatoma HepG2 cells to oxaliplatin (OXA).METHODS: Adenovirus carrying GSTP1 (Ad-GSTP1) was used to infect HepG2 cells for establishing the cell line over-expressing GSTP1.The cells were randomly divided into 6 groups: control, vehicle, Ad-GSTP1, OXA, OXA +vehicle and OXA +Ad-GSTP1.The cell survival rates were examined by CCK-8 assay, and the apoptotic rates were analyzed by flow cytometry.The protein levels of GSTP1, Akt, mTOR, p-Akt and p-mTOR were deter-mined by Western blot.RESULTS: OXA decreased the cell survival rate in a dose-dependent manner (P <0.05).The protein expression of GSTP1 increased after transfection with adenovirus.At basal level, up-regulation of GSTP1 signifi-cantly decreased the cell survival rate, increased the cell apoptosis, and inhibited the phosphorylation levels of Akt and mTOR (P <0.05).Moreover, GSTP1 over-expression enhanced the effect of OXA on the cell viability, cell apoptosis, and further inhibited the phosphorylation levels of Akt and mTOR ( P <0.05).CONCLUSION: Over-expression of GSTP1 augments the enhanced effect of OXA on HepG2 cell apoptosis, which may be related to the inactivation of Akt/mTOR signaling pathway.
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Objective To explore the correlation between hypoglycemia and the increased mortality of patients with acute decompensated liver cirrhosis.Methods A retrospective study was conducted on the clinical data of 120 patients with acute decompensated liver cirrhosis admitted to the Department of Hepatobiliary Surgery of the Second Hospital of Hebei Medical University from December 2011 to December 2014. The patients were divided into three groups: hypoglycemia group (glucose 10.0 mmol/L, 15 cases). The differences in hepatic carcinoma, decompensation symptoms, the incidence of known glycometabolic disorder, hospitalization situation, indicators of liver function and indexes of blood gas analysis were compared among three groups. The patients' age, hepatic carcinoma, ascites, hepatorenal syndrome, encephalopathy, bleeding, jaundice and glycometabolic disorder, etc were analyzed by the univariate analysis. The resulting risk factors with statistically significant differences were analyzed by multivariate logistic regression method in order to screen out the risk factors of increased mortality.Results The incidences of hepatorenal syndrome [42.9% (9/21) vs. 22.6% (19/84), 33.3% (5/15)] and jaundice [38.1% (7/21) vs. 20.2% (17/84), 13.3% (2/15)], rate of admission into intensive care unit (ICU) [14.3% (3/21) vs. 10.7% (9/84), 13.3% (2/15)] and in-hospital mortality [23.8% (5/21) vs. 10.7% (9/84), 20.0% (3/15)] in the hypoglycemia group were significantly higher than those in the normoglycemia group and hyperglycemia group (P 0.05). Univariate analysis showed that advanced age, hepatic carcinoma, hepatorenal syndrome, bleeding, jaundice and glycometabolic disorder hypoglycemia were the risk factors of the death in patients with acute decompensated liver cirrhosis (P < 0.05 orP < 0.01). Multivariate logistic regression analysis showed that advanced age [odds ratio (OR) = 2.101, 95% confidence interval (95%CI) = 1.297 - 3.403,P = 0.000], hepatorenal syndrome (OR = 3.032, 95%CI = 1.462 - 6.286,P = 0.000) and hypoglycemia (OR = 3.267, 95%CI = 2.135 - 4.999,P = 0.031) were the independent risk factors of the patients' death.Conclusion Hypoglycemia has certain correlation to the increase of mortality in patients with acute decompensated liver cirrhosis.
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To explore the effects of microRNA-150 deletion on the development and homeostasis of regulatory T cells (Treg),γδT cells,NK and NKT cells.Methods:microRNA-150 knockout mice were used and microRNA-150 expression was detected by Real-time PCR.The numbers of Treg ,γδT,NK and NKT cells in the thymus and spleen of normal control and microRNA-150 knockout mice were detected by Flow cytometry.Cell apoptosis was detected by Annexin V staining , and cell proliferation was detected by 5-Bromo-2-deoxyUridine ( Brdu ) incorporation.Results: microRNA-150 deletion did not affect the development and homeostasis of regulatory T cells (Treg) andγδT cells.However,microRNA-150 deletion resulted in a significant reduction of the NK and thymic NKT cell number.In addition, microRNA-150 deleted NK and NKT cells showed an arrested developmental and maturational phenotype with a reduced expression of NK 1.1 and CD122.Moreover , cell apoptosis was significantly increased in microRNA-150 deleted NK and thymic NKT cells ,while a lower cell proliferation rate was shown in the microRNA-150 deleted NK but not NKT cells.Conclusion: CD122 may play an important role in the development and homeostasis of mouse NK and NKT cells regulated by microRNA-150.