RESUMO
<p><b>OBJECTIVE</b>To investigate the relationship between serum albumin and renal function in patients with acute leukemia (AL) and its clinical significance.</p><p><b>METHODS</b>The clinical data and related test results of 267 newly diagnosed patients with acute leukemia from April 2015 to April 2017 were collected for retrospective cross-sectional analysis. Multivariate regression model was used for statistical analysis.</p><p><b>RESULTS</b>The creatinine level in serum of newly diagnosed acute leukemia patients decreased with the increase of albumin level (the first quartile-the fourth quartile had an average creatinine level of 72.0 µmol/L, 65.2 µmol/L, 62.8 µmol/L, 58.6 µmol/L); Multiple regression model results showed that each elevated albumin 1 g/L, the serum creatinine level decreased 0.89 µmol/L. The serum albumin was grouped into the model by quartile, and the first quartile was used as the reference group. With the increase of albunin, the β value decreased steply (the second and fourth quartile β values were -12.7, -14.81, -15.98), the trend line test p value was <0.05.</p><p><b>CONCLUSION</b>Serum albumin negatively correlats with creatinine level in newly diagnosed acute leukemia patients, and its elevation shows protective effect on renal function.</p>
RESUMO
<p><b>OBJECTIVE</b>To investigate the effect of Statins on proliferation and apoptosis in human acute T lymphocytic leukemia (T-ALL) cells and its possible mechanism.</p><p><b>METHODS</b>Jurkat and CCRF-CEM cells were cultured in different concentrations of Fluvastatin and Simvastatin for 24 h respectively. Then, the cell growth inhibition level was defected by CCK-8; the DNA replication was analyzed by EdU; the cell apoptosis was analyzed by Annexin V/7-AAD double labeling; the cell cycle changes were analyzed by flow cytometry; the expressions of Cyclin D1, p21, p27, BAX, BCL-2 and p-Akt were determined by Western blot.</p><p><b>RESULTS</b>Fluvastatin and Simvastatin both significantly inhibited the growth of Jurkat and CCRF-CEM cells in a dose-dependent manner. The inhibitory rate of Jurkat and CCRF-CEM cells at 0.2 mmol/L Fluvastatin was 41.14% and 57.08% respectively, while the 0.2 mmol/L Simvastatin could supress 68.42% of Jurkat and 77.10% of CCRF-CEM cells. Half or more than half of cell inhibition were observed in Statins-treated groups with significantly statistical differences, compared with the control groups (P<0.05). After the Jurkat and CCRF-CEM cells were treated with Fluvastation and Simvastation of different concentrations for 24 hours, the proportion of early and later apoptotic cells both increased; moreover, the total apoptotic rate increased significantly(P<0.05) at 0.2 mmol/L and 0.3 mmol/L concentration of Fluvastatin and Simvastatin. The detection of cell cycle showed that both of Jurkat and CCRF-CEM cells were arrested in G phase. Western blot revealed that, in comparison with the control group, the expressions of BAX, p21 and p27 in cells treated with Statins were up-regulated, while Cyclin D1, BCL-2 and p-Akt expressions were down-regulated.</p><p><b>CONCLUSION</b>Statins can suppress T-ALL cell proliferation and induce cell apoptosis through the inhibition of Akt pathway.</p>