Apoptotic effect of cisplatin and cordycepin on OC3 human oral cancer cells / 中国结合医学杂志

<p><b>OBJECTIVE</b>To evaluate apoptotic effects of cisplatin and cordycepin as single agent or in combination with cytotoxicity in oral cancer cells.</p><p><b>METHODS</b>The influences of cisplatin (2.5 μg/mL) and/or cordycepin treatment (10 or 100 μmol/L) to human OC3 oral cancer cell line were investigated by morphological observation for cell death appearance, methylthiazoletetrazolium (MTT) assay for cell viability, flow cytometry assay for cell apoptosis, and Western blotting for apoptotic protein expressions.</p><p><b>RESULTS</b>Data demonstrated that co-administration of cisplatin (2.5 μg/mL) and cordycepin (10 or 100 μmol/L) resulted in the enhancement of OC3 cell apoptosis compared to cisplatin or cordycepin alone treatment (24 h), respectively (P <0.05). In flow cytometry assay, percentage of cells arrested at subG1 phase with co-treatment of cordycepin and cisplatin (30%) was significantly higher than cisplatin (5%) or cordycepin (12%) alone group (P <0.05), confirming a synergistically apoptotic effect of cordycepin and cisplatin. In cellular mechanism study, co-treatment of cordycepin and cisplatin induced more stress-activated protein kinase/Jun terminal kinase (JNK), the expressions of caspase-7, and the cleavage of poly ADP-ribose polymerase (PARP) as compared to cisplatin or cordycepin alone treatment (P <0.05).</p><p><b>CONCLUSION</b>Cisplatin and cordycepin possess synergistically apoptotic effect through the activation of JNK/caspase-7/PARP pathway in human OC3 oral cancer cell line.</p>

Gonadotrophin-releasing hormone-I and -II stimulate steroidogenesis in prepubertal murine Leydig cells in vitro / 亚洲男科学杂志(英文版)

<p><b>AIM</b>To study the effect and mechanism of gonadotrophin-releasing hormone (GnRH) on murine Leydig cell steroidogenesis.</p><p><b>METHODS</b>Purified murine Leydig cells were treated with GnRH-I and -II agonists, and testosterone production and steroidogenic enzyme expressions were determined.</p><p><b>RESULTS</b>GnRH-I and -II agonists significantly stimulated murine Leydig cell steroidogenesis 60%-80% in a dose- and time-dependent manner (P < 0.05). The mRNA expressions of steroidogenic acute regulatory (StAR) protein, P450scc, 3beta-hydroxysteroid dehydrogenase (HSD), but not 17alpha-hydroxylase or 17beta-HSD, were significantly stimulated by both GnRH agonists with a 1.5- to 3-fold increase (P < 0.05). However, only 3beta-HSD protein expression was induced by both GnRH agonists, with a 1.6- to 2-fold increase (P < 0.05).</p><p><b>CONCLUSION</b>GnRH directly stimulated murine Leydig cell steroidogenesis by activating 3b-HSD enzyme expression.</p>