The effect of vitamin D on expression of TGF ß1 in ovary.

The transforming growth factor ß (TGF-ß) is thought to have important roles in several stages of folliculogenesis. Vitamin D is effective in cell proliferation, differentition and on estrogen biosynthesis. The aim of the present study was to determine the respective role of 1,25-dihydroxyvitamin D3 on expression of TGF-ß1 in developing rat ovaries. 24 (one-mounth-old n = 12 and adult n = 12) female Wistar rats were enrolled in this study. All animals were divided into 4 groups. Group I and II that consist of one-month-old (n = 6) and adult rats (n = 6) respectively served as control groups. Intramuscular vitamin D3 ( 0,05 µgr/kg/every other day) was injected for 8 weeks to group III and IV which consist of one-mounth-old and adult rats respectively. After last injection, ovaries of animals were removed and processed for immunohistochemistry assay. No remarkable differences in staining intensity and localization for TGF-ß1 were observed in group I and group III. TGF immunostaining was also predominantly found in oocytes. In granulosa cells, TGF-ß1 immunoreactivity was negative. TGF-ß1 immunostaining were observed both in nuclei and cytoplasm of granulosa cells in group II. But in group IV granulosa cells and oocytes were negative for TGF-ß1. We found that vitamin D administration resulted in a decrease in TGF-ß1 levels in the adult rats, but, TGF-ß1 expression did not significantly decrease in the newborn rats. However, in multiple linear regression analysis, TGF-ß1 expressions were independently associated with vitamin D administration. It is observed that Vitamin D attenuated TGF-ß1 expression. The results of this study suggest that vitamin D may play role in folliculogenesis via TGF-ß1.

Immunohistochemical localization of beta1 and beta4 integrins in mouse endometrium during implantation and early pregnancy.

Implantation presents the remarkable synchronisation between the development of embryo and differentiation of endometrium. Cell-cell adhesion is an important phenomenon taking place during blastocyst implantation in uterine membrane. We think that the investigation of existence and the level of integrins in women can be a guide for treatment of infertility. Our purpose in this study was to show expression beta1 and beta4 integrins on gestational days 4, 6, 12 by immunohistochemical methods and to investigate whether beta4 integrin is a useful marker for receptivity. beta1 and beta4 integrin were exhibited on surface epithelium on gestational day 4. On the other hand, strong beta4 immunoreactivity was detected on surface epithelium and glandular cells on gestational day 12 but no beta1 reactivity was present in the surface epithelium and glandular cells on day 12. In conclusion, both beta1 and beta4 integrins may have a role in implantation process because positive immunoreactivity was seen on apical membrane of surface epithelium on day 4 when implantation occurred. The localization to apical pole of surface epithelium suggest a role for beta1, beta4 integrins in initial embryo and endometrium interaction. It does not seem that beta1 integrin has a role supporting pregnancy since expression of beta4 on surface epithelium and glandular epithelium disappeared on day 12. beta4 integrin expression increasing on day 12 of pregnancy leads us to think a possible functional role supporting pregnancy.

Protective effect of cromakalim and diazoxide, and proulcerogenic effect of glibenclamide on indomethacin-induced gastric injury.

We investigated the influences of the K+ channel opening drugs cromakalim and diazoxide and their blocker, glibenclamide, in indomethacin-induced gastric injury in rats. Cromakalim (0.1 and 0.3 mg/kg) and diazoxide (10 and 30 mg/kg) produced dose-dependent gastroprotection at doses that were also effective on the cardiovascular system. Glibenclamide reversed their gastroprotective effects and aggravated indomethacin-induced gastric damage by its own. Cromakalim (10(-9)-10(-5) M) and diazoxide (10(-9)-10(-4) M) relaxed noradrenaline pre-contracted gastric arteries (94.59+/-1.58% and 93.86+/-2.99%, respectively). Their relaxant effects were inhibited by glibenclamide (10(-5) M) but not by indomethacin (10(-5) M) and LG-nitro-L-arginine (10(-4) M). Cromakalim (0.1 and 0.3 mg/kg) did not change gastric mucosal blood flow but increased the gastric mucosal vascular conductance in anaesthetized rats as measured by the hydrogen gas clearance technique. Indomethacin increased myeloperoxidase activity in the gastric mucosa, an effect which was reversed by cromakalim and diazoxide. Glibenclamide abolished their effects on myeloperoxidase activity and, alone, increased this parameter. Additionally, indomethacin caused infiltration of neutrophils which was reduced by cromakalim and diazoxide in a glibenclamide sensitive manner. The effects of cromakalim and diazoxide on mucosal myeloperoxidase activity, neutrophil infiltration and gastric injury correlated with each other. The effects of diazoxide (30 mg/kg) and glibenclamide (10 mg/kg) on blood glucose level were not correlated with their effects on gastric injury. Taken together, K+ channel opening drugs show misoprostol-like protective effects in indomethacin-induced gastric injury which seems to be related to modulation of neutrophil function.

Effect of vitamin E on adriamycin- induced nephrotoxicity at the ultrastructural level in guinea pigs.

It is known that Adriamycin, which is widely used in the treatment of various neoplastic conditions, exerts toxic effects in several organs. In this study, we have established that vitamin E has some beneficial effects on the kidney by protecting it from some of the toxicity induced by Adriamycin. A study was carried out which comprised one control group and two experimental groups of guinea pigs. In the experiment Adriamycin was administered either alone (group II) or together with vitamin E (group III). The results of groups II and III were compared with controls (group I). The kidneys were subsequently removed and examined by routine electron microscopic techniques. We found that vitamin E administered together with Adriamycin could reverse some of the degenerative changes caused by Adriamycin.