Objective To study the L-carnosine induced apoptosis of human hepatocellular carcinoma HepG2 cells and its mechanism.Methods Human hepatocellular carcinoma HepG2 cells were cultured in vitro,then the cells in logarithmic phase were divided into 5 mM,20 mM,50 mM L-carnosine group and control group,treated with 5 mM,20 mM,50 mM L-carnosine and saline respectively.The proliferation of HepG2 cells was measured by CCK-8 assay after 24 hours and 48 hours treatment.The cell apoptosis and cell cycle were detected by flow cytometry after 48 hours treatment.The protein expression of Caspase-8,PI3K and Akt were detected by Western blot in each group after 48 hours treatment.Results CCK-8 and flow cytometry assay showed that both 20 mM and 50 mM L-carnosine treated group significantly inhibited the proliferation of HepG2 cells after 24 hours and 48 hours,and the inhibition were in a time and dose-dependent manner.Western blot revealed that the expressions of PI3K and Akt were down-regulated with the increase of L-carnosine concentration,while the expression of Caspase-8 was increased.Conclusion L-carnosine exhibits an inhibitory effect of the proliferation and promote apoptosis of human liver cancer cell line HepG2.The mechanism may be associated with the inhibition of the PI3K/Akt signaling pathway and activation of Caspase-8 signaling pathway.

OBJECTIVETo investigate the changes of left ventricular structure and function in patients with liver cirrhosis and their correlation with the model for end-stage liver disease (MELD) score.

METHODSA total of 89 cirrhotic patients admitted between June, 2012 and June, 2014 and 30 healthy control subjects were enrolled in the study. According to MELD score, the cirrhotic patients were divided into 3 groups with MELD scores ≤9, between 10 and 19, and ≥20. The parameters of the left ventricle in resting state were measured using Doppler echocardiography, including left ventricular end systolic diameter (LVESD), left ventricular end diastolic diameter (LVEDD), interventricular septal thickness (IVST), left ventricular posterior wall thickness (LVPWT), left atrial diameter (LAD), ejection fraction (LVEF), cardiac output (CO), mitral flow velocity, and E wave deceleration time (DT), and evaluated their relationship with MELD score.

RESULTSCompared with the control subjects, the cirrhotic patients showed significantly increased LVESD, LVEDD, IVST, LAD, CO and DT but reduced VE/VA ratio (P<0.05 or 0.01). The values of LVESD, LVEDD, IVST, LAD and DT increased gradually with MELD scores (P<0.05 or 0.01). VE/VA ratio was higher in patients with MELD score of 10-19 than in those with MELD score ≤9, and decreased significantly in those with MELD score ≥20. Of the cirrhotic patients, 55% were found to have left atrial enlargement and 44% had a VE/VA ratio ≤1; left atrial enlargement and a VE/VA ratio below 1 were more common in patients with a MELD score ≥20 than in those with lower MELD scores. The LAD, LVEDD and DT were positively correlated with MELD scores (r=0.208, 0.319 and 0.197, respectively; P<0.05 or 0.01).

CONCLUSIONSThe patients with liver cirrhosis can have cardiac function deficiency manifested mainly by left ventricular diastolic dysfunction in positive correlation with the severity of liver disease.

Cardiac Output ; Case-Control Studies ; End Stage Liver Disease ; physiopathology ; Heart Atria ; pathology ; Heart Ventricles ; physiopathology ; Humans ; Liver Cirrhosis ; physiopathology ; Severity of Illness Index ; Ventricular Function, Left