Effects of chronic estradiol treatment on the thyroid gland structure and function of ovariectomized rats

Estrogen therapy is widely used nowadays in women to treat many postmenopausal symptoms but it may have some undesirable effects due to multiple organs affection. The aim of this study was to determine the effects of chronic estradiol treatment oh the structure and function of the thyroid gland in ovarictomized rats as a model simulating menopause. Thirty adult female albino rats divided into three groups were used in this study, the first group was sham-operated, while the second and third groups were ovariectomized. The first and second groups were injected with olive oil while the third group was injected with estradiol diproprionate daily for three months, after that hormonal assay for T3, T4, TSH and histological specimens of the thyroid were taken and examined by light and electron microscopy. Serum levels of T3 and T4 were significantly decreased in ovariectomized animals and increased with estradiol treatment, while TSH increased in ovariectomized animals and decreased with estradiol. Histological and morphometric study in ovariectomized group revealed marked accumulation of colloid in follicular lumens with decreased epithelial height in addition to increased connective tissue amount while with estradiol treatment the follicles were smaller with small amount of colloid with increased epithelial height in addition to decreased connective tissue content. Ultrastructural study supported these results in addition to the presence of large amount of intracytoplasmic colloid vesicles after estradiol treatment. Decreased amount of estrogen may lead to thyroid hypofunction while estradiol treatment may lead to hyperactivity so it should be used very cautiously in the treatment of postmenopausal symptoms to avoid its undesirable stimulatory effect on the thyroid

Effect of honey on TNBS-induced colitis in rats: histological and immunohistochemical study

IBD is a chronic relapsing and nonspecific disorder characterized by colonic mucosal disruption and ulceration. Drugs currently used to manage IBD have potentially serious side effects that limit their use. Developing new drug treatment is, therefore, an important goal in treating IBD. Honey has known wound healing, antimicrobial and even antitumouricidal properties, hence, it could represent an alternate, safer treatment for IBD. The aim of this study was to investigate the potential therapeutic role of honey in an experimental model of inflammatory bowel disease [IBD]. After the induction of colitis with 2,4,6-trinitrobenzene sulphonic acid [TNBS] in rats, physiological saline, honey or prednisolone enemas were applied to the rats once daily for 3 days [short-term treatment groups, acute colitis model] or 14 days [long-term treatment groups, chronic colitis model]. Control groups received only ethanol [the solvent of TNBS] and saline enemas. Rats were killed on the 4[th] or 15[th] days and colonic mucosal damage was assessed histologically, histochemically [goblet cell area% in Alcian blue-stained sections] and immunohistochemically [COX-2 immunostaining]. Histological evaluation of colon specimens revealed that prednisolone was superior to honey in the short-term model. However, in the long-term model honey appeared to be more effective treatment than prednisolone as it had stronger effects on inflammation. Honey significantly attenuated the damage score, corrected the disturbances in morphology associated to TNBS-induced colitis and significantly increased the amount of mucous stained by Alcian blue, but it did not affect mucosal mast cell numbers. Immunohistochemical results showed that short-term therapy with either honey or prednisolone, did not reduce the upregulated COX-2 immunoreactivity associated to TNBS administration, however, long-term treatment with honey markedly reduced COX-2 expression in the colon mucosa compared with prednisolone. Long-term intrarectal administration of honey appeared to be as effective method of treatment as prednisolone, in an experimental model of chronic colitis simulating human IBD