Submitted on April 15, 2008
Revised on June 9, 2008
Accepted on June 23, 2008
Effects of Adlay Hull Extracts on Uterine Contraction and Ca2+ Mobilization in the Rat
Shih-Min Hsia1, Yueh-Hsiung Kuo2, Wenchang Chiang3, and Paulus S. Wang4*
1 Cardinal Tien College of Healthcare and Management, Taipei 231, Taiwan; Graduate Institute of Food Science and Technology, Center for Food and Biomolecules, College of Bioresources and Agriculture,
2 Tsuzuki Institute for Traditional Medicine, College of Pharmacy, China Medical University, Taichung, Taiwan 404
3 Graduate Institute of Food Science and Technology, Center for Food and Biomolecules, College of Bioresources and Agriculture, National Taiwan University, Taipei 106, Taiwan
4 National Yang-Ming University
* To whom correspondence should be addressed. E-mail: pswang{at}ym.edu.tw.
Dysmenorrhea is directly related to elevated PGF2
(prostaglandin F2) levels. It is treated with NSAIDs (nonsteroid antiinflammatory drugs) in Western medicine. Since NSAIDs produce many side effects, Chinese medicinal therapy is considered as a feasible alternative medicine. Adlay (Coix lachryma-jobi L. var. ma-yuen Stapf.) has been used as a traditional Chinese medicine for treating dysmenorrhea. However, the relationship between smooth muscle contraction and adlay extracts remains veiled. Therefore, we investigated this relationship in the rat uterus by measuring uterine contraction activity and recording the intrauterine pressure. We studied the in vivo and in vitro effects of the methanolic extracts of adlay hull (AHM) on uterine smooth muscle contraction. The extracts were fractionated using 4 different solvents: water, 1-butanol, ethyl acetate, and n-hexane; the 4 respective fractions were AHM-Wa, AHM-Bu, AHM-EA, and AHM-Hex. AHM-EA and its subfractions (175 µg/mL) inhibited uterine contractions induced by PGF2, Ca2+ channel activator Bay K 8644, and high K+ in a concentration-dependent manner in vitro. AHM-EA also inhibited PGF2-induced uterine contractions in vivo; furthermore, 375 µg/mL AHM-EA inhibited the Ca2+-dependent uterine contractions. Thus, 375 µg/mL AHM-EA consistently suppressed the increases in intracellular Ca2+ concentrations ([Ca2+]i) induced by PGF2 and high K+. We also demonstrated that naringenin and quercetin are the major pure chemical components of AHM-EA that inhibit PGF2-induced uterine contractions. Thus, AHM-EA probably inhibited uterine contraction by blocking external Ca2+ influx, leading to a decrease in [Ca2+]i. Thus, adlay hull may be considered as a feasible alternative therapeutic agent for dysmenorrhea.
