Purpose: To investigate anti-diabetic effect of the ethanol leaf extract of Newbouldia laevis (P. Beauv
Background: The leaves of Alchornea laxiflora are traditionally used in the south of Nigeria to prevent preterm births. Aim: This study was designed to investigate the activity of A. laxiflora on uterine contractility. Setting: The leaves of the plant were collected from forests in Egor, Benin City, Nigeria. Methods: The leaves were cleaned and extracted in methanol. The extract (0.005 mg/mL–3.5 mg/mL) was tested on spontaneous uterine contraction and on oxytocin-induced contraction in normal and Ca2+-free media. The plant extract (0.0035 mg/mL, 0.035 mg/mL, 0.35 mg/mL and 3.5 mg/mL) was tested on high KCl-induced uterine contractions (80 mM). The plant extract (3.5 mg/mL) was also studied in the presence of amiodarone and glibenclamide in separate experiments. Mass spectrometric analysis was additionally performed on the plant extract in order to identify significant secondary metabolites that may have contributed to the activity of the plant. Results: The plant extract inhibited spontaneous, oxytocin and high KCl-induced uterine contractions and also significantly inhibited (p < 0.01) oxytocin-induced uterine contraction in Ca2+-free medium. The plant extract significantly inhibited (p < 0.01 and p < 0.05) oxytocin’s amplitude in the presence of amiodarone and glibenclamide, respectively. Secondary metabolites belonging to classes of fatty acids, glycols, terpenes, flavonoid glycosides and porphyrins were identified. Conclusion: Alchornea laxiflora inhibited mouse uterine contractility possibly through interaction with potassium and calcium channels. Of the known metabolites identified, 3-deoxy-arabino-hept-2-ulosonic acid, 17-hydroxyingenol and phaeophorbide-a methyl inhibit uterine contractility and may contribute to the activity of A. laxiflora in utero.
Traditional herbal medicine and their preparations have been widely used for thousands of years and are still in use in developing and developed countries owing to their medicinal values and their presumed relative safety. This belief that medicinal plants are not toxic or are with less side effect due to their natural origin is debatable; hence this study was conducted to evaluate the safety and (or) toxicity of Ethanol leaf extract of Simarouba glauca (EESG) on liver, kidney and heart functions of Wistar rats. The oral acute toxicity of EESG was evaluated in line with Lorke’s method. The sub-chronic toxicity of EESG was carried out according to the OECD guidelines with modification and using a total of twenty-four (24) male Wistar rats; divided into four groups of six rats each, following a two-week acclimatization. Test rats were orally administered EESG at doses of 500, 1000 and 2000 mg/kg body weight respectively daily for thirty (30) days, while the control was given only feed and water ad libitum. At the end of the experiment, the rats were fasted overnight and sacrificed under chloroform anesthesia; relevant biochemical and histopathology analyses were carried out. The data obtained from the oral acute test indicate that the LD50 was above 5000 mg/kg and there was no death recorded. There were significant increases (P ˂ 0.05) in percentage (%) body weight of rats administered respective doses of EESG. There were significant reductions (P˂0.05) in mean liver: body weight ratio of rats administered EESG 500 and 2000 mg/kg respectively, significant reductions (P˂0.05) in mean kidney: body weight ratios of rats given EESG 1000 and 2000 mg/kg respectively; significant reductions (P˂0.05) in mean heart: body weight ratios of test rats administered EESG 2000 mg/kg; whereas others were not significantly different (P˃0.05) relative to their respective control. Plasma ALT and GGT activities of rats administered respective dose of EESG were significantly reduced (P˂0.05); plasma ALP activities were significantly elevated (P˂0.05) relative to the control after 30 days. There were no significant differences (P˃0.05) in plasma total proteins and albumin levels. Plasma total and unconjugated bilirubin of rats administered respective dose of EESG were not significantly different (P˃0.05); whereas, rats given EESG recorded significant reduction in plasma conjugated bilirubin. Plasma urea was significantly elevated (P˂0.05) in rats administered EESG 1000 and 2000 mg/kg respectively. Test rats given EESG 500 and 1000 mg/kg respectively recorded significant elevations in plasma creatinine and rats given EESG 2000 mg/kg recorded significant decrease in plasma creatinine levels; others were not significantly different relative to the control. Plasma chloride and potassium ion levels of rats administered respective doses of EESG were not significantly different (P˃0.05); significant reduction (P˂0.05) in plasma sodium ions concentration in all group compared to the control. Plasma calcium ion levels in all group were not significantly different (P˃0.05); whereas there were significant reductions (P˂0.05) in plasma bicarbonate ion levels relative to their respective controls. Although plasma ALP activity were significantly elevated, there were no elevations in specific liver function enzymes and no visible hepatocellular damage. Furthermore, the conspicuous elevations observed in plasma urea and creatinine levels do not exclusively indicate EESG-induced organ injury. Therefore, it is suggestive that EESG was not significantly toxic to the to the liver, kidney and heart respectively and may be administered at lower doses in further studies.
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