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BackgroundFicus deltoidea, is a perennial herb that is used to assist labor, firm the uterus post-delivery and to prevent postpartum bleeding. In view of its claimed uterotonic action, the mechanisms underlying plant’s effect on uterine contraction were investigated.MethodsAdult female SD rats were injected with 2 mg/kg 17β-oestradiol (E2) to synchronize their oestrous cycle. A day after injection, uteri were removed for in-vitro contraction studies. The dose dependent effect of Ficus deltoidea aqeous extract (FDA) on the tension produced by the isolated rat’s uteri was determined. The effects of atropine (2×10-8 M), atosiban (0.5 IU), THG113.31 (10 μM), oxodipine (0.25 mM), EDTA (1 mM), 2-amino-ethoxy-diphenylborate (2-APB) (40 mM) and thapsigargin (1 mM) on the maximum force of contraction (Emax) achieved following 2 mg/ml FDA administration were also investigated.ResultsFDA induced in-vitro contraction of the isolated rat’s uteri in a dose-dependent manner. Administration of atropine, atosiban and THG113.31 reduced the Emax with atosiban having the greatest effect. The Emax was also reduced following oxodipine and EDTA administration. There was no significant change observed following 2-APB administration. Thapsigargin, however, augmented Emax.ConclusionsFDA-induced contraction of the isolated rat’s uteri is mediated via multiple uterotonin receptors (muscarinic, oxytocin and prostaglandin F2α) and was dependent on the extracellular Ca2+. Contraction, however, was not dependent on the Ca2+ release from the internal stores. This in-vitro study provides the first scientific evidence on the claimed effect of Ficus Deltoidea on uterine contraction.

Dillapiole is one of the major compounds in Peperomia pellucida. Dillapiole exerts cytotoxicity effect on several cancer cells such as breast and colon with a minimal effect on normal cells. However, its effect on cancers in head and neck region remains ambiguous. Therefore, in the current study, the cytotoxicity effect of dillapiole on human nasal squamous cell carcinoma, RPMI 2650 and the underlying mechanism were investigated. Normal human gingival fibroblast, HGnF cells was used as comparison. Cisplatin and untreated cells were used as positive and negative controls, respectively. Cell cytotoxicity was determined using WST-1 assay; and validated by trypan blue exclusion assays. Cell death mechanism was determined using Annexin V-FITC detection kit and analyzed by flow cytometer. The cytotoxic effect of dillapiole on RPMI 2650 cells was shown significantly increased with the increasing amount of dillapiole from 25.93 ± 6.39 % to 83.87 ± 8.43 % (p<0.05, n=3) with the respective IC50 and IC75 of 46 µM and 125 µM. None of both IC50 and IC75 were obtained for HGnF cells up to 150 µM. Loss of normal shape, cytoplasm shrinkage and reduction in cell volume were detected in RPMI 2650 cells after dillapiole treatment at respective IC50 (46 µM) and IC75 (125 µM), indicating apoptosis. These findings indicate that dillapiole cytotoxicity effect is more selective towards RPMI 2650 compared to HGnF cells and the mechanism of death was through the induction of apoptosis.

A precise regulation of the uterine fluid volume and pH is essential for a successful embryo implantation. Progesterone has been reported to participate in uterine fluid volume regulation during this period, however its effect on the uterine fluid pH is unknown. As endometrial fluid absorption has been proposed to occur secondary to sodium (Na +) absorption under progesterone mediated effect, we therefore hypothesize that there may be a concomitant changes in fluid volume and pH if sodium-hydrogen exchanger (NHE), a protein responsible for both luminal Na + absorption and H + extrusion is involved. In view of these, our study aimed to investigate the possibility that progesterone affect the uterine fluid pH and endometrial NHE expression. Ovariectomised female Sprague-Dawley (SD) rats were treated with peanut oil (vehicle), oestradiol-3-benzoate and progesterone for three consecutive days. On the fourth day, in-vivo uterine perfusions were performed on anaesthetized rats. The collected perfusate were analyzed for the changes in pH. The effect of amiloride, a non-specific Na +-channel blocker on the pH was investigated. The expression of uterine NHE-1 protein was detected by Western blotting and immunohistochemistry. Our findings indicate that the fluid pH is the lowest in progesterone-treated group and amiloride administration significantly increased the pH in the same treatment group (p < 0.05). NHE-1 proteins were significantly expressed in the progesterone-treated group. In conclusion, progesterone induces a reduction of the uterine fluid pH and is amiloride-sensitive. The up-regulation of NHE-1 under a common progesterone effect may explain the role of this exchanger in regulating the uterine fluid pH.