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Effect of Kang Fu Yan capsule on phenol mucilage-induced intrauterine adhesion injury in female rats


Qinghong Fan
Wei Xiao
Xiaomeng Chai
Zhe Zhang
Tao Zhu
Dan Tang
Kaihe Ye
Tianjun Luo
Qing Liu
Gang Huang
Yulan Yang
Hong Nie

Abstract

Purpose: To investigate the effect of Kang fu yan capsule (KFYC) on phenol mucilage-induced intrauterine adhesion (IUA) in a rat model, and the underlying mechanisms.


Methods: An IUA model was established by injecting 0.06 mL of 25 % phenol mucilage into the uterus of female Sprague-Dawley rats. The IUA model rats (n=59) were randomly divided into 5 groups: IUA group, fuke qianjin tablet group (FKQJT, 0.22 mg/kg), and 3 KFYC groups given different doses of the drug i.e. 0.13, 0.39and 1.17 mg/kg. A group of 10 healthy female rats served as control. After 19 days treatment, blood samples were collected for determination of IL-2 and IL-10 by ELISA, while uterine tissues were subjected to histological examination using hematoxylin and eosin staining (H&E) and Masson staining. Expressions of Notch1, recombination signal binding protein-JK (RBP-JK), a disintegrin and metalloprotease (ADAM)-12, ADAM-15, matrix metalloprotein-9 (MMP-9), and inhibitor of NF-κB (IĸB) in uterine tissues were determined using RT-qPCR and western blot analysis.


Results: Compared to IUA group, histological results showed reduced inflammatory cell infiltration in rat uterine tissue of KFYC group. Moreover, KFYC significantly reversed uterine fibrosis (p < 0.05). Serum concentrations of IL-2 significantly decreased in KFYC groups (p < 0.05 or p < 0.01), and there was significant increases the serum concentrations of IL-10 in KFYC groups (p < 0.05 or < 0.01), when compared to IUA group. The mRNA and protein expressions of Notch1, RBP-JK, ADAM-12, ADAM-15, MMP-9 were also significantly down-regulated (p < 0.05), while protein expression of IĸB was upregulated in KFYC group, when compared to IUA group.


Conclusion: KFYC exerts an anti-IUA effect via amelioration of uterine inflammation and fibrosis, probably via a mechanism involving regulation of Notch1/ADAM pathway.


Journal Identifiers


eISSN: 1596-9827
print ISSN: 1596-5996