International immunopharmacology · 2025
Curcumin modulates oxidative stress via NOX4 to ameliorate endometrial hyperplasia.
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Li Wu, Zheng Caijie, Sun Xiaolu, Lv Wen, Zhang Xinmei
Аннотация
BACKGROUND: Curcumin (Cur) is a kind of fat soluble polyphenol compound extracted from turmeric, which has a wide range of pharmacological effects.
PURPOSE: The aim of this research was to investigate the impact of Cur on endometrial hyperplasia (EH) and uncover its underlying mechanism.
METHODS: A mouse model of endometrial hyperplasia was created by administering continuous subcutaneous injections of Estradiol (E2) for a duration of 21 days. The mice were then treated with Curcumin (Cur), and the structure of the uterine tissue was assessed using hematoxylin-eosin (H&E) staining. Subsequently, the effect of Cur on the proliferation of endometrial epithelial cells (EEC) was evaluated using the MTT method. Additionally, network pharmacology will be employed to identify the target through which Cur exerts its action. Furthermore, oxidative stress-related markers were examined. Immunofluorescence (IF), RT-qPCR, and Western blot techniques were also utilized to investigate how Cur influences NOX4 expression levels.
RESULTS: Cur improved uterine pathology and inhibited EEC proliferation. Mechanistically, E2 activation led to increased NOX4 expression and subsequent oxidative stress; however, after administration of Cur, NOX4 expression was suppressed along with a reduction in oxidative stress levels.
CONCLUSIONS: It is suggested that Cur may regulate oxidative stress via targeting NOX4 to ameliorate endometrial hyperplasia.
PURPOSE: The aim of this research was to investigate the impact of Cur on endometrial hyperplasia (EH) and uncover its underlying mechanism.
METHODS: A mouse model of endometrial hyperplasia was created by administering continuous subcutaneous injections of Estradiol (E2) for a duration of 21 days. The mice were then treated with Curcumin (Cur), and the structure of the uterine tissue was assessed using hematoxylin-eosin (H&E) staining. Subsequently, the effect of Cur on the proliferation of endometrial epithelial cells (EEC) was evaluated using the MTT method. Additionally, network pharmacology will be employed to identify the target through which Cur exerts its action. Furthermore, oxidative stress-related markers were examined. Immunofluorescence (IF), RT-qPCR, and Western blot techniques were also utilized to investigate how Cur influences NOX4 expression levels.
RESULTS: Cur improved uterine pathology and inhibited EEC proliferation. Mechanistically, E2 activation led to increased NOX4 expression and subsequent oxidative stress; however, after administration of Cur, NOX4 expression was suppressed along with a reduction in oxidative stress levels.
CONCLUSIONS: It is suggested that Cur may regulate oxidative stress via targeting NOX4 to ameliorate endometrial hyperplasia.