Effect of hydrogen sulfide-induced delayed preconditioning on glutathione S-transferase expression during myocardial ischemia-reperfusion in rats / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To investigate the effect of hydrogen sulfide-induced delayed preconditioning on glutathione S-transferase (GST) expression during myocardial ischemia-reperfusion in rats.</p><p><b>METHODS</b>Sprague-Dawley male rats were randomly divided into 4 groups (n= 10 in each): Group S (sham operation group), Group IR (ischemia/reperfusion group), Group H (IR+ NaHS 0.05 mg/kg iv, 24 h before ischemia) and Groups D receiving IR+NaHS 24 h before ischemia and 5-hydroxydecanoate (5-HD)15 min before ischemia. Animals in groups IR, H and D were subjected to ischemia by 30 min of coronary artery occlusion followed by 2 h of reperfusion. At the end of the reperfusion, myocardial infarct size (IS) was examined. Glutathione S-transferase (GST) was measured by Western blotting. The myocardial ultrastructures were observed under the electron microscopy.</p><p><b>RESULTS</b>The IS was significantly smaller in Group H than that in Group IR [(25.40 ± 3.54)% compared with (38.27 ± 5.64)%, P<0.05]. The GST expression in myocardium was significantly higher in Group H than that in Group IR. Microscopic examination showed less myocardial damage in Group H than in Group IR. The protective effects of delayed preconditioning by hydrogen sulfide was prevented by 5-HD pre-treatment.</p><p><b>CONCLUSION</b>The hydrogen sulfide-induced delayed preconditioning attenuates myocardial IR injury possibly through up-regulating glutathione S-transferase expression in rats.</p>

Effect of cadmium chloride on the expression and phosphorylation of mitogen-activated protein kinase in normal rat kidney epithelial cells / 中华预防医学杂志

<p><b>OBJECTIVE</b>To explore the effect of cadmium chloride on the expression and phosphorylation of mitogen-activated protein kinase (MAPK) in normal rat kidney epithelial (NRK) cells.</p><p><b>METHODS</b>The NRK cells were incubated with cadmium chloride either at respective dose (0, 1, 5, 10, 20, 40 µmol/L) for 24 h or at same dose (10 µmol/L) for respective time (0, 0.5, 1.0, 2.0, 4.0, 8.0 h). Western blotting was applied to test the expression of MAPK in NRK cells (ERK1/2, p38, JNK); and phosphor-specific antibody to detect the phosphorylated MAPK (p-ERK1/2, p-p38, p-JNK).</p><p><b>RESULTS</b>There was no significant difference in the MAPK expression among the groups either treated with different doses or for different time; however, the level of phosphorylated MAPK was comparatively higher than it in control group. There was an obvious expression of p-ERK1/2 at 1.00 ± 0.06 in the group incubated with 10 µmol/L CdCl(2); and the expression in the 20 µmol/L and 40 µmol/L CdCl(2) group was 2.58 ± 0.11, 2.76 ± 0.23 respectively, which was 1.58 and 1.76 times more than it in 10 µmol/L CdCl(2) group. The differences were statistically significant (F = 827.70, P < 0.01). The respective expression of p-p38MAPK in the 20 µmol/L (2.47 ± 0.20)and 40 µmol/L CdCl(2) group (3.73 ± 0.25)was 1.47 and 2.73 times more than it in control group (1.00 ± 0.02), and the differences were also statistically significant (F = 280.06, P < 0.01). There was a dose-effect relationship of the concentration of cadmium in the expression of p-ERK1/2 (r = 0.919, t = 4.69, P = 0.009) and p-p38MAPK (r = 0.945, t = 5.79, P = 0.004). Additionally, phosphorylated MAPK expressed in a time-dependent manner. The expression of p-ERK1/2 was obvious in the group incubated for 1 h (1.26 ± 0.11), and the respective expression in the 4 h group (1.51 ± 0.07) and 8 h group (3.53 ± 0.23) was 1.5 and 3.5 times of it in the control group (1.00 ± 0.02). The differences were statistically significant (F = 427.82, P < 0.001). The expression of p-p38MAPK increased significantly in 1 h group (1.31 ± 0.07); while the respective expression in 4 h group (3.53 ± 0.32) and 8 h group (4.41 ± 0.38) was 3.5 and 4.4 times of it in control group (1.00 ± 0.03). The differences were also statistically significant (F = 280.06, P < 0.001).</p><p><b>CONCLUSION</b>Cadmium chloride could significantly enhance the phosphorylation of MAPK in NRK cells; and it is probably associated with the activation of MAPK.</p>

Pathological analysis and mRNA expression of apoptosis genes in rat kidney tissue after subacute melamine treatment / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>to investigate pathological changes and mRNA expression of apoptosis genes bcl-2, bax and Caspase-3 in rat kidney tissue after rats are administrated with melamine for 28 days.</p><p><b>METHODS</b>10 male SD rats and 10 female SD rats in each group were administrated with three doses of melamine (low dose, middle dose, high dose) by gavage for 28 days. The animals were divided into three experimental groups and one control group. The doses for male rats were 200, 400, 800 mg/kg, but for female rats they were 150, 300, 600 mg/kg. After melamine treatment the animals were sacrificed and the kidneys were taken out for pathological analysis and for detecting mRNA expression of bcl-2, bax and Caspase-3 with fluorescent quantitative PCR assay.</p><p><b>RESULTS</b>the tubular cylinders were observed in three experimental groups. The positive rates of tubular cylinders in three groups (from low dose to high dose) were 11/20, 13/20, 16/20, respectively. Additionally, melamine induced a significant decrease in mRNA expression of bcl-2 at low dose, middle dose or high dose, bcl-2 expression decreased by 20.58% - 49.51% in three groups treated with melamine. Furthermore, bax mRNA levels increased by 44.66% - 300.96% in groups treated with three doses of melamine, and Caspase-3 mRNA levels increased by 64.76% - 360.75% in groups treated with three doses of melamine.</p><p><b>CONCLUSIONS</b>melamine could induce pathological changes of rat kidneys, and it also induces a significant alteration of apoptosis Bcl-2, Bax and Caspase-3 mRNA expression in rat kidney tissue.</p>

Rule of lymph node metastasis in colorectal cancer and its affecting factors / 中华胃肠外科杂志

<p><b>OBJECTIVE</b>To investigate the rule of lymph node metastasis in colorectal cancer and its affecting factors, and to provide clues for clinical diagnosis and treatment of colorectal cancer patients.</p><p><b>METHODS</b>The clinical data of 1166 cases of colorectal cancer receiving surgical resection were analyzed retrospectively.The relationships between clinicopathologic variables and lymph node metastases were evaluated by crosstabs and logistic regression in SPSS 10.0 for windows.</p><p><b>RESULTS</b>The rate of lymph node metastasis in colorectal cancer was 49.7%. After entering crosstabs estimation, gender and tumor site were not significantly correlated with lymph node metastasis in colorectal cancer(chi2=1.46, r=0.035, P>0.05 and chi2=3.86, r=0.012, P>0.05). Age, tumor size, the massive type of the tumor, the differentiating degree of the tumor, histology type and the depth of tumor invasion were proved to be independent factors influencing the lymph node metastasis in colorectal cancer (chi2 =13.1, r=0.064, P<0.05 and chi2=77.161, r=0.245, P<0.01 and chi2=144.831, r=0.341, P<0.01 and chi2=128.310, r=0.318, P<0.01 and chi2=120.418, r=0.319, P<0.01 and chi2=227.287, r=0.434, P<0.01). After entering logistic regression estimation, the correlativity of risk factor of lymph node metastasis in colorectal cancer: the depth of tumor invasion > the massive type of the tumor>the differentiating degree of the tumor > tumor size. Preoperative blood serum CEA level was significantly correlated with lymph node metastasis (chi2=509.599, r=0.661, P<0.01).</p><p><b>CONCLUSION</b>The depth of tumor invasion is the most risk factor of lymph node metastasis in colorectal cancer. Preoperative high level of blood serum CEA indicates the occurrence of lymph node metastasis.</p>