Effect of leonurine hydrochloride on endothelin and the endothelin receptor-mediated signal pathway in medically-induced incomplete abortion in rats

Objective

Endothelin (ET) is involved in uterine contractions. Our previous study showed that leonurine hydrochloride (LH) inhibits abnormal bleeding caused by incomplete abortion through an increase in uterine contractions in rats. The present study was conducted to show that LH treatment regulates the ET-mediated signal pathway in abortion in rats.

Study design

Early pregnancies in rats had incomplete abortions induced using mifepristone in combination with misoprostol. After the abortions, the rats were treated with LH orally for 7 days and surgery was performed. The sinistro-uterus was dissected for measurement of ET and nitric oxide (NO); the dextro-uterus was stored at −80°C for ET receptor (ET_A and ET_B) analysis. Myometrial cells from the dextro-uterus were cultured for measurement of phospholipase C (PLC) activity, intra-cellular Ca²⁺ concentration (Ca²⁺]_i), and protein kinase C (PKC) activity.

Results

In in vivo experiments, LH treatment elevated the ET level and ET/NO ratio in rats with induced abortions and up-regulated ET_A mRNA expression (P < 0.01 vs. the model group), but there was no change in ET_B mRNA. LH significantly increased the Ca²⁺]_i, PLC activity, and relative production of PKC protein in myometrial cells.

Conclusion

LH increased uterine contractions in rats with incomplete abortions by modulating the ET receptor-mediated signal pathway.