Protective Effect of Minocycline on Bax and Bcl-2 Gene Expression, Histological Damages and Oxidative Stress Induced by Ovarian Torsion in Adult Rats.

BACKGROUND: Minocycline is a widely used bacteriostatic antibiotic with various functions. The aim of this study was to investigate impact of apoptotic genes in ovary of the torsion/detorsion treated rat model by minocycline. MATERIALS AND METHODS: This experimental study was performed in 32 female Wistar rats classified in four groups, including: i. sham, ii. TD: torsion/detorsion group received normal saline, iii. TDM: torsion/detorsion group treated with 40 mg/kg Minocycline, and iv. MC: healthy group received 40 mg/kg Minocycline. After treatment period (7 days), histoplogical parameters, oxidative stress markers and hormone profile of serum as well as the expression of Bax and Bcl-2 genes were measured in the ovary of rats. RESULTS: Levels of superoxide dismutase (SOD), glutathione peroxidase (GPX) and estrogen were decreased in the TD group and significantly increased in the treated groups (P=0.001). Levels of malondialdehyde (MDA) and testosterone were increased in the TD group and decreased in the treated groups (P=0.001). Expression level of Bax was elevated in the TD group, while it was attenuated in the treated groups (P=0.001). Expression level of Bcl-2 was significantly increased in treated groups (P=0.001). CONCLUSION: Minocycline can repair oxidative damage in ovarian tissue and regulate apoptotic-related gene expressions.

Effects of hypothermia and pentoxifylline on the adnexal torsion/detorsion injuries in a rat testis model.

This study was designed to investigate the effects of separate and combined administration of hypothermia and pentoxifylline to preserve the effects on the testicles in an experimental model of testicular torsion/ detorsion injuries in rats. Forty male adult Wistar rats were randomly divided into five groups, control, torsion/detorsion (TD), torsion/detorsion/hypothermia (TD+ICE), torsion/detorsion received of pentoxifylline (40mg/kg, ip) (TD+PTX) and torsion/detorsion/hypothermia/PTX (TD+ICE+PTX). Left testicular torsion (TT) was performed for 4 and half hours, and ice fragments have been used at the beginning of torsion. After the reperfusion period (a week), oxidative maker's serum levels, testosterone hormone, sperm parameters, and histopathological and gene expression evaluations have been performed. Significant adverse changes were observed in the TD group for histological variables, sperm count, oxidative marker, testosterone hormone, Bax, BCL2 and caspase-3 expression. The parameters studied in the group receiving PTX improved in comparison with the TD group, while macroscopical parameters of both the hypothermia and PTX+ICE groups were not different compared with the TD group. The results revealed that PTX, as an antioxidant component, was protective against testicular torsion, while hypothermia and hypothermia plus PTX did not exhibit this property, which may have been due to the duration of hypothermia (4 hr) or reperfusion period.

The Effects of WW2/WW3 Domains of Smurf2 Molecule on CD4+CD25+/CD4+ Proportion in Spleen of 4T1 Tumor Bearing BALB/c Mice.

Background: TGF-ß has long been considered as the main inducer of Tregs in tumor microenvironment and is the reason for the aberrant number of Tregs in tumor-bearing individuals. Recently, it has been suggested that the enzyme arginase I is able to mediate the induction of Tregs in a TGF-ß-independent fashion. The recombinant WW2/WW3 domains from smad ubiquitination regulatory factor 2 molecule was demonstrated to increase TGF-ß signaling while reducing arginase I gene expression. In this study, we aimed to examine the effects of this recombinant protein on CD4+CD25+/CD4+ proportion in the spleen of 4T1 mammary carcinoma-bearing BALB/c mice. Methods: Flow cytometry was used to evaluate CD4+CD25+ spleen cell populations of the tumor-bearing mice that received WW2/WW3 protein treatment and those of the control group. Results: The results indicated a significant rise in CD4+CD25+/CD4+ ratio, along with an average increase in tumor mass of the subjects that underwent protein treatment. Conclusion: It can be inferred that the heightened CD4+CD25+/CD4+ proportion in the spleen of protein-treated tumor-bearing mice can be the result of the increased TGF-ß signaling despite the reduced arginase I expression.

Comparing sprint and endurance training on anxiety, depression and its relation with brain-derived neurotrophic factor in rats.

Although the response of brain-derived neurotrophic factor (BDNF) has been shown to low intensity exercise training, but the effect of intensive exercise training is not clear. Also, there is insufficient information about relationship between BDNF and depression and anxiety following intensive exercise. This study aimed to investigate the effects of 6 weeks of intensive endurance training (ET) and sprint interval training (SIT) on brain BDNF and its relationship with anxiety and depression in Albino Wistar rats. Anxiety and depression of rats were measured by elevated plus maze (EPM) and tail suspension test (TST), respectively. All data were analyzed using one-way ANOVA and Pearson's correlation coefficient at P<0.05 level. Both SIT and ET regimens increased BDNF content in the brain, and the alterations made were greater following SIT than ET. Also, both SIT and ET regimens increased number of entries and the time spent in the open arm significantly in EPM, with a higher elevation following SIT than ET. In addition, both SIT and ET regimens decreased number and duration of immobility significantly in TST, with a higher reduction following SIT than ET. Furthermore, BDNF content correlated positively with number of entries and the time spent in the open arm in EPM and negatively with number and duration of immobility in TST. Collectively, sprint interval training regimen, rather than intensive endurance training regimen, is highly potential to improve anxiety and depression through a greater increase in BDNF contents in brain.