BACKGROUNDStudies showed that propentofylline enhances the action of adenosine and protects hippocampal neuronal damage against transient global cerebral ischaemia. Our study was to investigate the effect of propentofylline on hypoxic-ischaemic brain damage in neonatal rat.

METHODSSeven-day-old Wistar rats were subjected to unilateral common carotid artery ligation and hypoxia in oxygen 8 kPa for two hours at 37 degrees C. Propentofylline (10 mg/kg) was administered intraperitoneally one hour after hypoxia-ischaemia (treated group). Control group rats were received an equivalent volume of saline. The effects of propentofylline were assessed by observing the body mass gain, behavioural alteration and neurohistological changes. The rats were sacrificed at 72 hours after hypoxia-ischaemia, and the brain sections were examined after haematoxylin and eosin staining.

RESULTSThe propentofylline-treated rats had better body mass gain and better behavioural response than the paired saline-controls did. In the control group, the rats either lost body mass or had little mass gain after the insult, their average body mass gain was 97.3% at 24 h, 100.3% at 48 h, and 114.1% at 72 h of recovery. In propentofylline-treated group, there was a significant improvement of body mass gain at 24 h (100.2%, P < 0.05) and 48 h (110.3%, P < 0.01) of recovery; the percentage of rats that performed well on behavioural test was significantly higher from 48 h to 72 h of recovery (P < 0.05); the incidence of severe brain damage to the cerebral cortex and dentate gyrus was significantly reduced in propentofylline-treated rats (cortex, 93% - 70.8%, P < 0.01; dentate gyrus 95% - 66.7%, P < 0.01) as compared with control rats.

CONCLUSIONSAdministration of propentofylline 1 hour after hypoxia-ischaemia significantly attenuates brain damage in both the cerebral cortex and dentate gyrus, and also improves the body mass gain as well as behavioural disturbance in 7-day-old rats.

Animals ; Animals, Newborn ; Brain ; pathology ; Female ; Hypoxia-Ischemia, Brain ; drug therapy ; pathology ; Male ; Neuroprotective Agents ; therapeutic use ; Rats ; Rats, Wistar ; Weight Gain ; drug effects ; Xanthines ; therapeutic use

AIMTo understand the biological functions of the ectoplasmic specializations between Sertoli cells and maturing spermatids in seminiferous epithelia.

METHODSIn order to disrupt the function of the ectoplasmic specializations, nectin-2, which is expressed at the specialization, was neutralized with anti-nectin-2 antibody micro-injected into the lumen of the mouse seminiferous tubule. Anti-nectin-3 antibody was also micro-injected into the lumen in order to neutralize nectin-3, which is expressed at the specialization.

RESULTSThe actin filaments at the specialization disappeared, and exfoliation of maturing spermatids was observed by electron microscopy.

CONCLUSIONNectin-2 was neutralized by anti-nectin-2 antibody and nectin-3 was neutralized by anti-nectin-3 antibody, respectively. Inactivated nectin-2 and nectin-3 disrupted the nectin-afadin-actin system, and finally the actin filaments disappeared. As a result, the specialization lost the holding function and detachment of spermatids was observed. One of the functions of the specialization seems to be to hold maturing spermatids until spermiation.

Actins ; metabolism ; Animals ; Antibodies ; immunology ; pharmacology ; Cell Adhesion Molecules ; immunology ; metabolism ; Cell Communication ; drug effects ; physiology ; Intercellular Junctions ; drug effects ; metabolism ; Male ; Mice ; Mice, Inbred ICR ; Microfilament Proteins ; metabolism ; Microscopy, Confocal ; Nectins ; Seminiferous Epithelium ; cytology ; drug effects ; metabolism ; Sertoli Cells ; cytology ; drug effects ; metabolism ; Spermatids ; cytology ; drug effects ; metabolism