In vitro antioxidant effect of curcumin on human sperm quality in leucocytospermia.

Decreased sperm quality was caused by oxidative stress in semen from patients with leucocytospermia. Curcumin is a traditional Chinese herbal monomer extracted from Zingiberaceae turmeric and zedoary turmeric and has antioxidative and anti-inflammatory effects. This study aimed to investigate the effects and specific molecular mechanisms of curcumin on sperm quality in patients diagnosed with leucocytospermia. Forty cases of semen samples were collected from patients with leucocytospermia and 35 cases from normal fertile male. Computer-assisted semen analysis (CASA) was used to detect sperm motility after curcumin incubation. ELISA was used to measure the changes in H2 O2 , sperm mitochondrial DNA (mtDNA), cytochrome B (Cyt B) and NADH dehydrogenase 5 (NADH5) contents before and after curcumin treatment. The results indicate that curcumin can significantly improve sperm motility from the patients with leucocytospermia. After curcumin treatment, the level of the H2 O2 was significantly decreased in the supernatant of curcumin-incubated spermatozoa from leucocytospermic patients. The content of mtDNA was significantly decreased, while the content of Cyt B and NADH5 in spermatozoa was significantly increased. In conclusion, curcumin can significantly improve sperm motility of leucocytospermic patients, against the oxidative damage induced by H2 O2 . Therefore, curcumin may play a role in mitigating the H2 O2 -induced injury to sperm.

CFTR suppresses tumor progression through miR-193b targeting urokinase plasminogen activator (uPA) in prostate cancer.

Cystic fibrosis (CF) transmembrane conductance regulator (CFTR) is expressed in the epithelial cells of a wide range of organs/tissues from which most cancers are derived. Although accumulating reports have indicated the association of cancer incidence with genetic variations in CFTR gene, the exact role of CFTR in cancer development and the possible underlying mechanism have not been elucidated. Here, we report that CFTR expression is significantly decreased in both prostate cancer cell lines and human prostate cancer tissue samples. Overexpression of CFTR in prostate cancer cell lines suppresses tumor progression (cell growth, adhesion and migration), whereas knockdown of CFTR leads to enhanced malignancies both in vitro and in vivo. In addition, we demonstrate that CFTR knockdown-enhanced cell proliferation, cell invasion and migration are significantly reversed by antibodies against either urokinase plasminogen activator (uPA) or uPA receptor (uPAR), which are known to be involved in various malignant traits of cancer development. More interestingly, overexpression of CFTR suppresses uPA by upregulating the recently described tumor suppressor microRNA-193b (miR-193b), and overexpression of pre-miR-193b significantly reverses CFTR knockdown-enhanced malignant phenotype and abrogates elevated uPA activity in prostate cancer cell line. Finally, we show that CFTR gene transfer results in significant tumor repression in prostate cancer xenografts in vivo. Taken together, the present study has demonstrated a previously undefined tumor-suppressing role of CFTR and its involvement in regulation of miR-193b in prostate cancer development.