41712

A study on the possible pro-inflammatory effects promoted by thyroid hormone signaling on the rat ovaries

Thesis

Last updated: 06 Feb 2023

Subjects

-

Tags

Physiology

Advisors

El-Hamzawi, Magd M. , Kamal, Sahar M. , Shawqi, Heba M. , Rashed, Layla A.

Authors

Khalaf-Allah, Umneya Muhammad Abdel-Maqssoud

Accessioned

2017-07-12 06:40:37

Available

2017-07-12 06:40:37

type

M.D. Thesis

Abstract

The present study aimed at exploring the possible pro-inflammatory effects of thyroid hormones on the rat ovary. The experimental animals were assigned into eight groups, four normal groups (group 1, 2, 3, and 4) and four hyperthyroid groups (group 5, 6, 7, and 8). Hyperthyroidism was induced by daily IP injection of L-thyroxine, in a dose of 25µg/100 gram body weight, for two weeks. Group (1) was considered the normal control group whereas the rats in group (5) were assigned as the control hyperthyroid group. While the animals in groups (2, and 6) received tamoxifen, those in groups (3, and 7) were given progesterone. In addition, the animals in groups (4, and 8) were provided with combined tamoxifen and progesterone treatment. The results of the control hyperthyroid group revealed significant upregulation of ovarian COX2, ER, and TR expression, while the PR expression was significantly down-regulated. Both ER and TR are significantly correlated with COX2, whereas PR is negatively correlated with it. Both tamoxifen and progesterone in the hyperthyroid groups resulted in down-regulation of ER, TR, and COX2, as well as up-regulation of PR, in the treated groups as compared to the control hyperthyroid group. However, the effect of progesterone appeared to be more prominent. In conclusion, our results provided evidence that induced hyperthyroidism is associated with an inflammatory state in the rat ovary. The administration of tamoxifen and/or progesterone appeared to exert protective effects against this inflammation.

Issued

1 Jan 2012

DOI

http://dx.doi.org/10.21473/iknito-space/35649

Details

Type

Thesis

Created At

28 Jan 2023