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卵巢缺血再灌注后阴道中 E-钙黏蛋白和 NF-κB 的表达。

E-cadherin and NF-κB expression in the vagina after ovarian ischemia and reperfusion.

机构信息

İstanbul Bahcelievler Memorial Hospital - Department of Obstetrics and Gynecology - İstanbul, Turkey.

Diyarlife Hospital - Department of Obstetrics and Gynecology - Diyarbakır, Turkey.

出版信息

Acta Cir Bras. 2024 Apr 15;39:e391724. doi: 10.1590/acb391724. eCollection 2024.

DOI:10.1590/acb391724
PMID:38629650
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11020660/
Abstract

PURPOSE

To investigate inflammation and cell adhesion molecules in the vagina after ovarian ischemia-reperfusion (IR) injury.

METHODS

20 Wistar albino female rats were divided into two groups: control, and IR groups. In IR group, blood flow was restricted for 2 hours for ovarian ischemia. Then, tissues were re-blood 2 hours for reperfusion. Vagina tissues were excised and processed for histopathological analysis. Histopathological and biochemical follow-ups were performed.

RESULTS

Both malondialdehyde and myeloperoxidase values were increased in IR group compared to control group. Glutathione content was decreased in IR group compared to control group. Epithelial degeneration, inflammation, dilatation, and nuclear factor-κB (NF-κB) expression were increased in IR group compared to control group. E-cadherin expression was significantly decreased in IR group. In the IR group, E-cadherin showed a positive reaction in adenomas, gland-like cryptic structures, cellular junctions with clustered inflammatory cells. In the IR group, NF-κB expression was increased in basement membrane, inflammatory cells, in blood vessels.

CONCLUSIONS

Ovarian ischemia caused degeneration of epithelial cells in the vaginal region and disruptions in the cell junction complex, which leads to activation of E-cadherin and NF-κB signaling pathway and alterations in reproductive and embryonal development in the vaginal region.

摘要

目的

研究卵巢缺血再灌注(IR)损伤后阴道中的炎症和细胞黏附分子。

方法

将 20 只 Wistar 白化雌性大鼠分为两组:对照组和 IR 组。在 IR 组中,血流受限 2 小时以引起卵巢缺血。然后,再灌注 2 小时以恢复血流。切除阴道组织并进行组织病理学分析。进行组织病理学和生化随访。

结果

与对照组相比,IR 组的丙二醛和髓过氧化物酶值均升高。IR 组的谷胱甘肽含量低于对照组。与对照组相比,IR 组的上皮变性、炎症、扩张和核因子-κB(NF-κB)表达增加。IR 组的 E-钙黏蛋白表达明显降低。在 IR 组中,E-钙黏蛋白在腺瘤、腺体样隐窝结构、聚集有炎症细胞的细胞连接中呈阳性反应。在 IR 组中,NF-κB 表达在基底膜、炎症细胞、血管中增加。

结论

卵巢缺血导致阴道区域的上皮细胞变性和细胞连接复合物破坏,导致 E-钙黏蛋白和 NF-κB 信号通路激活,并改变阴道区域的生殖和胚胎发育。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ba6/11020660/0c5342a08dda/1678-2674-acb-39-e391724-gf02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ba6/11020660/95852a4a9d01/1678-2674-acb-39-e391724-gf01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ba6/11020660/0c5342a08dda/1678-2674-acb-39-e391724-gf02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ba6/11020660/95852a4a9d01/1678-2674-acb-39-e391724-gf01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ba6/11020660/0c5342a08dda/1678-2674-acb-39-e391724-gf02.jpg

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本文引用的文献

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Momordica charantia reduced ovarian ischemia - reperfusion injury by suppressing APAF-1 expression.苦瓜通过抑制凋亡蛋白酶激活因子-1(APAF-1)的表达减轻卵巢缺血-再灌注损伤。
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The protective effects of trimetazidine against ovary ischemia-reperfusion injury via the TLR4/Nf-kB signal pathway.
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The effects of vitamin B12 on the TLR-4/NF-κB signaling pathway in ovarian ischemia-reperfusion injury-related inflammation.维生素 B12 对卵巢缺血再灌注损伤相关炎症中 TLR-4/NF-κB 信号通路的影响。
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