Crypotanshione reduces the expression of metadherin in DU145 prostate cancer cells / 中华男科学杂志

<p><b>OBJECTIVE</b>To investigate the effects of crypotanshinone (CPT) on the proliferation and apoptosis of DU145 prostate cancer cells as well as on the metadherin expression and the downstream PI3K/AKT signaling pathway in the DU145 cells.</p><p><b>METHODS</b>We treated DU145 prostate cancer cells with different concentrations of CPT for 24, 48, and 72 hours followed by evaluation of the proliferation and apoptosis of the cells by MTT assay and TUNEL, respectively. We determined the expressions of metadherin protein and mRNA in the DU145 cells by Western blot and RT-PCR respectively at different time points after CPT treatment. We also detected the expressions of the proteins metadherin, AKT, p-AKT, and Bcl-2 in the CPT-treated DU145 cells at 48 hours.</p><p><b>RESULTS</b>CPT significantly inhibited the proliferation of the DU145 cells in a dose- and time-dependent manner (P < 0.05). After treatment with 10 µmol/L CPT for 24, 48, and 72 hours, the apoptosis rates of the DU145 cells were (29.42 ± 4.51), (55.07 ± 5.67) and (70.84 ± 4.66)%, respectively, significantly higher than (3.1 ± 2.48)% in the control group (P < 0.05). The expression of metadherin was remarkably downregulated at the transcription and translation levels (P < 0.05) and the expressions of the AKT signaling pathway and the Bcl-2 protein were markedly inhibited in the DU145 cells after treated with 10 µmol/L CPT for 48 hours (P < 0.05).</p><p><b>CONCLUSION</b>CPT can inhibit the proliferation and induce the apoptosis of DU145 prostate cancer cells, which may be associated with its suppression of the downstream PI3K/AKT signaling pathway by reducing the expression of metadherin in the DU145 cells.</p>

Effects of hypothermia plus dexamethasone on eNOS expression and spermatogenic cell apoptosis after testicular torsion reduction / 中华男科学杂志

<p><b>OBJECTIVE</b>To investigate the protective effects of hypothermia combined with dexamethasone on the testis of rats after testicular torsion reduction and on the expression of eNOS and apoptosis of spermatogenic cells.</p><p><b>METHODS</b>We made unilateral testicular torsion models in 80 adolescent male Sprague-Dawley rats by 720 degrees torsion of the left testis, and then randomly divided them into four groups of equal number to be treated with normal temperature + physiological saline (group A), hypothermia + physiological saline (group B), hypothermia + dexamethasone (group C), and normal temperature + dexamethasone (group D). After 48 hours, we collected the testes, observed pathological changes of the testicular tissue by HE staining under the light microscope, determined the expression of eNOS by immunohistochemistry, and detected the apoptosis of spermatogenic cells by TUNEL.</p><p><b>RESULTS</b>HE staining showed different degrees of testicular tissue injury in all the four groups of rats, most obvious in group A, while protective effect was observed in the other three groups. Immunohistochemistry revealed significantly more positive cells and higher positive staining intensity in the torsion (left) testis in group A than in B (P < 0.05), C (P < 0.01) and D (P < 0.01). The nuclei were deep brown or brown. Lots of apoptotic spermatogenic cells were seen in the torsion testis of group A, with a significantly higher apoptosis index (31.12 +/- 4.68) than in B (16.58 +/- 6.22) (P < 0.05), C (8.60 +/- 1.15) (P < 0.01) and D (13.52 +/- 3.06) (P < 0.01).</p><p><b>CONCLUSION</b>Ischemia-reperfusion injury after testicular torsion reduction can increase the apoptosis of spermatogenic cells and decrease testicular reproductivity. Hypothermia combined with dexamethasone can protect the testis from injury as well as the reproductive function of the testis after testicular torsion reduction.</p>

Effect of IL-18BP on Fractalkine chemokine expression in the kidney tissue of rats with renal fibrosis / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To study the expression of Fractalkine (FKN) in the kidney tissue of rats with renal fibrosis and the effect of IL-18BP on FKN.</p><p><b>METHODS</b>Male Wister rats were randomly assigned to sham-operation (n=24), unilatral ureteral obstruction (UUO, n=22), and IL-18 binding protein (IL-18BP) treatment groups (n=23). The UUO model was prepared by unilateral ureteral ligation in the later two groups. The IL-18BP treatment group received an intraperitoneal injection of IL-18BP (0.1 mg/kg) every other day after UUO inducement, for 7 times, while normal saline was administered in the other two groups. Seven or eight rats of every group were sacrificed at 3, 7 or 14 days after IL-18BP or normal saline injections. FKN levels at various times were detected by immunohistochemistry and Western blot.</p><p><b>RESULTS</b>Compared with the sham-operation group, FKN levels in the kidney tissue of the untreated UUO group increased significantly at all time points (P<0.01). IL-18BP treatment decreased significantly FKN levels in the kidney tissue at all time points compared with the untreated UUO group (P<0.01).</p><p><b>CONCLUSIONS</b>IL-18BP treatment may down-regulate the increased FKN levels of the rat kidney tissue caused by UUO, possibly thus delays the occurrence and development of renal fibrosis.</p>