Protective effects of marrubiin improve endometriosis through suppression of the expression of RANTES

Xiao-Hong Sun, Xiaohong Sun
Molecular medicine reports · 2017 · vol. 16(3) , pp. 3339–3344 · doi:10.3892/mmr.2017.6969 · PMID:28713901 · W2735836260
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Marrubiin treatment in a mouse endometriosis model reduced lesion size and monocyte migration by suppressing RANTES, calcium, PGE2, and TXB2 expression.

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Abstract

Marrubiin can improve blood and lymph microcirculation disturbance, and has pharmacological effects in myocardial protection, anti‑inflammation and anti‑oxidation. The aim of the present study was to evaluate the protective effects of marrubiin on endometriosis through suppression of the expression of regulated on activation, normal T cell expressed and secreted (RANTES). Endometriotic cells were implanted into the peritoneal cavity of mice, and these mice were injected estradiol benzoate (30 µg/kg) once each day for 14 days. The mice with endometriosis were then treated with 12, 25 or 50 mg/kg marrubiin. Reverse transcription‑quantitative polymerase chain reaction was used to assess the mRNA expression of RANTES, and western blot analysis was used to analyze the protein expression of RANTES, TNF‑α and PGE2. Inflammation factors were measured by ELISA. Treatment with marrubiin effectively improved lesion regression and inhibited toxicity in the mouse model of endometriosis. Marrubiin significantly inhibited endometrial lesions and monocyte chemotaxis in the mice with endometriosis, and reduced U937 cell migration. Calcium mobilization, levels of tumor necrosis factor‑α and the secretion of RANTES were effectively suppressed by marrubiin treatment. The calcium levels were effectively induced, whereas the protein expression of prostaglandin E2 (PGE2) and formation of thromboxane B2 (TXB2) were effectively inhibited by marrubiin treatment. These findings indicated that the protective effect of marrubiin improved endometriosis in the mice through the suppression of inflammation and downregulation of the expression of RANTES, followed by mediation of the levels of calcium, PGE2 and TXB2.

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Condition tags

endometriosis

MeSH descriptors

Chemokine CCL5 Diterpenes Endometriosis Endometriosis Protective Agents Animals Calcium Calcium Chemokine CCL5 Chemotaxis Chemotaxis Dinoprostone Dinoprostone Diterpenes Diterpenes Endometriosis Endometriosis Female Humans Interleukin-1beta

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