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UPREGULATION OF CYSTIC FIBROSIS TRANSMEMBRANE CONDUCTANCE REGULATOR EXPRESSION BY OESTROGEN AND BAK FOONG PILL IN MOUSE UTERI

Although cystic fibrosis transmembrane conductance regulator (CFTR) has been shown to be expressed in the female reproductive tract, its functional role in the uterus is not fully understood. The present study investigated a possible physiological role of CFTR by comparing the effects of 17β-oestrad...

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Bibliographic Details
Published in:Cell biology international 2001-10, Vol.25 (10), p.1033-1035
Main Authors: Rowlands, D.K., Tsang, L.L., Cui, Y.G., Chung, Y.W., Chan, L.N., Liu, C.Q., James, Tony, Chan, H.C.
Format: Article
Language:English
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Summary:Although cystic fibrosis transmembrane conductance regulator (CFTR) has been shown to be expressed in the female reproductive tract, its functional role in the uterus is not fully understood. The present study investigated a possible physiological role of CFTR by comparing the effects of 17β-oestradiol and Bak Foong Pill (BFP), an over-the-counter Chinese medicine used for centuries for the treatment of various gynaecological disorders, on uterus size and the expression of CFTR in the uterus of ovariectomised mice using RT-PCR. Treatment of ovariectomised mice with 17β-oestradiol (0.2mg/kg, p.o.) for 12 days caused a significnat increase in uterine wet weight compared to vehicle. However, treatment with BFP (3g/kg, p.o.) for the same period failed to increase uterine wet weight, indicating a lack of direct oestrogen-like activity of BFP. Analysis of CFTR mRNA expression in the harvested uteri using RT-PCR showed that both 17β-oestradiol and BFP induced an increase in CFTR mRNA expression in mouse uteri compared to levels observed in vehicle-treated animals. These results suggest that CFTR can be upregulated by oestrogen and BFP, however, the effect exerted by BFP does not seem to be mediated by direct oestrogen-like activity. Regulation of CFTR expression by both oestrogen and gynaecological medication BFP indicates an important role of CFTR in reproductive functions.
ISSN:1065-6995
1095-8355
DOI:10.1006/cbir.2001.0746