NF-ĸB expression in endometriosis induced rat uterine tissue

In: Journal of Drug Delivery and Therapeutics · 2023 · vol. 13(4) , pp. 33–36 · doi:10.22270/jddt.v13i4.6011 · W4366550078
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AI-generated summary by claude@2026-06, 2026-06-07

Endometriosis induction in rats increased serum oxidative stress and upregulated NF-κB expression in uterine epithelial, glandular, inflammatory, and endothelial cells.

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This study examined how experimentally induced endometriosis affects rat uterine tissue by using a sham group treated with corn oil and an endometriosis (EM) group induced with estradiol benzoate for 7 days, with n=8 rats per group. Serum total antioxidant status (TAS) and total oxidant status (TOS) were measured, and uterine NF-κB (immunohistochemistry staining) was assessed histologically, with NF-κB expression compared between groups. The EM group showed decreased TAS and increased TOS, and uterine NF-κB expression increased after induction, especially in degenerated epithelial and gland cells, inflammatory cells around glands, and endothelial cells. NF-κB expression was slight/mostly negative in sham tissues, and the paper’s main limitation is that it does not provide mechanistic testing beyond observational association with NF-κB staining. This paper is centrally about endometriosis — it uses an estradiol benzoate rat model to show increased NF-κB expression and oxidative imbalance in uterine tissue after endometriosis induction.

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Abstract

Objective: Our aim in this study is to examine the effects of endometriosis on uterine tissue. Materials and methods: Two groups were formed, with eight rats in each group. Sham group was subjected only saline solution for 7 days. The endometriosis (EM) model was induced with estradiol benzoate (EB). In the EM group, EB was given to rats for 7 days. At the end of the experiment, blood was taken from the animals and serum total antioxidant status (TAS) and total oxidant status (TOS) values were studied. Uterine tissues were fixed in formalin and embedded in paraffin blocks. NF-ĸB 3 immune staining were performed on uterine sections. The results were examined under the microscope. Results: Compared to sham group, TAS values were significantly decreased and TOS values were significantly increased in serum of rats belonging to EM group. In the analysis of NF-ĸB expression in uterine tissue of sham group, the expression was slight and found only in connective tissue cells and inflammatory cells. NF-ĸB expression was mainly negative. After EM induction, NF-ĸB expression was increased in degenerated epithelial cells and gland cells, inflammatory cells around the glands and blood vessel endothelial cells and lamina propria. Conclusion: We think that NF-κB signal may be a determinant in the treatment of endometriosis. Keywords: endometriosis, immunohistochemistry, NF-κB, biochemistry, rat
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Abstract

Objective: Our aim in this study is to examine the effects of endometriosis on uterine tissue.

Materials and methods

Two groups were formed, with eight rats in each group. Sham group was subjected only administration of 1% corn oil for 7 days. The endometriosis (EM) model was induced with estradiol benzoate (EB). In the EM group, EB was given to rats for 7 days. At the end of the experiment, blood was taken from the animals and serum total antioxidant status (TAS) and total oxidant status (TOS) values were studied. Uterine tissues were fixed in formalin and embedded in paraffin blocks. NF-ĸB 3 immune staining were performed on uterine sections. The results were examined under the microscope.

Results

Compared to sham group, TAS values were significantly decreased and TOS values were significantly increased in serum of rats belonging to EM group. In the analysis of NF-ĸB expression in uterine tissue of sham group, the expression was slight and found only in connective tissue cells and inflammatory cells. NF-ĸB expression was mainly negative. After EM induction, NF-ĸB expression was increased in degenerated epithelial cells and gland cells, inflammatory cells around the glands and blood vessel endothelial cells and lamina propria.

Conclusion

We think that NF-κB signal may be a determinant in the treatment of endometriosis.

Keywords

endometriosis, immunohistochemistry, NF-κB, biochemistry, rat

Keywords

endometriosis, immunohistochemistry, NF-κB, biochemistry, ratDOI https://doi.org/10.22270/jddt.v13i4.6011References Sacco K, Portelli M, Pollacco J, Schembri-Wismayer P, Calleja-Agius J. The role of prostaglandin E2 in endometriosis. Gynecol Endocrinol. 2012; 28(2):134-8. https://doi.org/10.3109/09513590.2011.588753 Ahn SH, Monsanto SP, Miller C, Singh SS, Thomas R, Tayade C. Pathophysiology and Immune Dysfunction in Endometriosis. Biomed Res Int. 2015; 2015:795976. https://doi.org/10.1155/2015/795976 de Ziegler D, Borghese B, Chapron C. Endometriosis and infertility: pathophysiology and management. The Lancet. 2010; 376(9742):730-8. https://doi.org/10.1016/S0140-6736(10)60490-4 Stilley JA, Birt JA, Sharpe-Timms KL. Cellular and molecular basis for endometriosis-associated infertility. Cell Tissue Res. 2012; 349(3):849-62. https://doi.org/10.1007/s00441-011-1309-0 Liu J, Sudom A, Min X, Cao Z, Gao X, Ayres M, et al. 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Korean Journal of Neurotrauma. 2017; 13(2):76-84 https://doi.org/10.13004/kjnt.2017.13.2.76 Published PDF Downloads: 608 PDF Downloads: 59 How to Cite Issue Section Authors who publish with this journal agree to the following terms: - Authors retain copyright and grant the journal right of first publication with the work simultaneously licensed under a Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0). that allows others to share the work with an acknowledgment of the work's authorship and initial publication in this journal. - Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgment of its initial publication in this journal. - Authors are permitted and encouraged to post their work online (e.g., in institutional repositories or on their website) prior to and during the submission process, as it can lead to productive exchanges, as well as earlier and greater citation of published work (See The Effect of Open Access).

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endometriosis

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