Anti-angiogenic Effects of Electroacupuncture in Endometriosis: Role of the TGF-β/Smad/VEGF Axis

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Electroacupuncture treatment of endometriosis in rats reduced pain and lesion size by downregulating TGF-β1, Smad2, Smad3, MMP2, MMP9, and VEGF-A expression.

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Abstract

Objective: To evaluate the therapeutic efficacy of electroacupuncture (EA) at the Guanyuan (CV4), Qihai (CV6), and Zigong (EX-CA1) points in a rat model of endometriosis (EMs), and to elucidate its regulatory effects on the TGF-β/Smad signalling pathway and associated angiogenic factors.Methods: An EMs model was established in 30 female Sprague-Dawley rats via autotransplanta-tion. Rats were randomly assigned to three groups (n=10 each): Model, Gestrinone, and EA. The EA group received daily treatment at CV4, CV6, and EX-CA1 (2–100 Hz, 0.3–0.6 mA, 20 min) for 14 consecutive days. Therapeutic outcomes were assessed via writhing response latency and frequency, ectopic lesion volume, and histopathological analysis. The protein expression of TGF-β1, Smad2, Smad3, MMP2, MMP9, and VEGF-A was quantified using Western blot and im-munofluorescence.Results: Compared to the model group, EA significantly prolonged writhing latency and re-duced both the writhing score and ectopic tissue volume (all P < 0.01). Histopathological analysis of the model group revealed flattened, shed, or absent epithelium with a reduced glandular count. Molecular analysis demonstrated that EA treatment significantly downregulated the ex-pression of TGF-β1, Smad2, Smad3, MMP2, MMP9, and VEGF-A compared to the model group (all P < 0.05).Conclusion: EA effectively alleviates dysmenorrhea-like symptoms and inhibits the growth of ectopic endometrial lesions in rats. This therapeutic effect is likely mediated by the inhibition of the TGF-β/Smad signalling pathway, which subsequently suppresses MMP and VEGF expression to prevent pathological angiogenesis.
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Objective

To evaluate the therapeutic efficacy of electroacupuncture (EA) at the Guanyuan (CV4), Qihai (CV6), and Zigong (EX-CA1) points in a rat model of endometriosis (EMs), and to elucidate its regulatory effects on the TGF-β/Smad signalling pathway and associated angiogenic factors.

Methods

An EMs model was established in 30 female Sprague-Dawley rats via autotransplanta-tion. Rats were randomly assigned to three groups (n=10 each): Model, Gestrinone, and EA. The EA group received daily treatment at CV4, CV6, and EX-CA1 (2–100 Hz, 0.3–0.6 mA, 20 min) for 14 consecutive days. Therapeutic outcomes were assessed via writhing response latency and frequency, ectopic lesion volume, and histopathological analysis. The protein expression of TGF-β1, Smad2, Smad3, MMP2, MMP9, and VEGF-A was quantified using Western blot and im-munofluorescence.

Results

Compared to the model group, EA significantly prolonged writhing latency and re-duced both the writhing score and ectopic tissue volume (all P < 0.01). Histopathological analysis of the model group revealed flattened, shed, or absent epithelium with a reduced glandular count. Molecular analysis demonstrated that EA treatment significantly downregulated the ex-pression of TGF-β1, Smad2, Smad3, MMP2, MMP9, and VEGF-A compared to the model group (all P < 0.05).

Conclusion

EA effectively alleviates dysmenorrhea-like symptoms and inhibits the growth of ectopic endometrial lesions in rats. This therapeutic effect is likely mediated by the inhibition of the TGF-β/Smad signalling pathway, which subsequently suppresses MMP and VEGF expression to prevent pathological angiogenesis. Files 022026.pdf Files (1.5 MB) | Name | Size | Download all | |---|---|---| | md5:46528f687caf53c07b981b990bc0a6c4 | 1.5 MB | Preview Download |

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endometriosisdysmenorrhea

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