Studies on Wound Healing and Antiulcer Activities of Extract of Aerial Parts of Phyllanthus niruri L. (Euphorbiaceae)

Abstract

Problem statement: Phyllanthus niruri is widely used in many parts of the world to manage a wide range of diseases. As part of efforts to elucidate its pharmacological activities and hence medicinal potential, we studied the wound healing and antiulcer properties of extract of the aerial parts using experimentally-created wounds and ulcers in rodents. Approach: Wound healing effect was assessed using excision and dead space wound models while antiulcer activity was evaluated using indomethacin-, ethanol acid-and cold-restraint stress-induced ulcer models. Results: The extract (5,10%) significantly (p<0.05) reduced the wound diameter producing 90.9 and 93.7% wound contraction respectively on day 18 post wounding. It also reduced epithelialization time of excised wounds and increased the rate of wound closure, with WC 50 of 8.7%. The extract (400 mg kg −1) also significantly (p<0.05) increased the weight of granuloma tissue. In antiulcer studies, the extract significantly (p<0.05) inhibited the development of ulcers induced by indomethacin and moderately inhibited ethanol acid-induced ulcer. It was, however, devoid of any such effect in coldrestraint stress-induced lesions at the doses used. Phytochemical analysis of the extract revealed the presence of alkaloids, saponins, tannins, flavonoids, reducing sugar, carbohydrates and glycosides. Conclusion: These findings indicate that constituents of aerial parts of P. niruri possess wound healing and antiulcer properties.

Antiulcer activity of the chloroform extract ofBauhinia purpurealeaf

“…a,b,c mucosal reliability and consequently cytoprotection. The ethanol induced gastric ulcer has been proven to involve a combination of direct toxic action of ethanol, decrease in the presence of gastric wall mucus and reduce in the secretion of bicarbonate (see Okoli et al, 2009). In addition, ethanol has also been reported to reduce endogenous glutathione and prostaglandin levels, to increase release of histamine, influx of Ca 2+ , stimulation of leukotriene C4 (LTC4) and oxygen free radicals synthesis, which, in turn, lead to increase lipid peroxidation.…”

“…Furthermore, based on the ability of the ethanol to stimulate LTC4, antiulcer activity of CEBP against ethanol-induced gastric ulcer could due to suppression of lipoxygenase pathway (Nwafor et al, 2000). It is also claimed that agents that improve mucosal defensive factors could be used to inhibit ethanol-induced gastric ulcer (Okoli et al, 2009). This claim is in agreement with report by Goswami et al (2011) as described above and is consistent with our finding on the ability of CEBP to increase gastric wall mucus production while reducing the total acidity of the gastric content.…”

“…Despite unclear etiology associated with the development of ulcer, the imbalances between aggressive and defensive factors have been suggested to be the contributing factor (Okoli et al, 2009). Under normal physiological conditions, local production of prostaglandins helps stimulate and maintain the mucus and bicarbonate synthesis that protect the gastric mucosa.…”

“…In addition, ethanol has also been reported to reduce endogenous glutathione and prostaglandin levels, to increase release of histamine, influx of Ca 2+ , stimulation of leukotriene C4 (LTC4) and oxygen free radicals synthesis, which, in turn, lead to increase lipid peroxidation. Increase in lipid peroxidation will cause alterations in membrane permeability of cells that contributes to cells damage (see Okoli et al, 2009). This damage is attributed to the release of reactive oxygen derived species (ROS) (e.g.…”

“…In addition, the gastric mucosal damage induced by indomethacin (and other related NSAIDs) results from the inhibition of arachidonic-acid-induced prostaglandin synthesis (Okoli et al, 2009). Prostaglandins play a protective role in the stomach by maintaining the mucosal blood flow, regulating mucosal turn over and repair, and promoting the secretion of mucus and bicarbonate within the gastric compartment Okoli et al, 2009). Suppression of prostaglandins synthesis by indomethacin enhances stomach susceptibility to mucosal injury and gastroduodenal ulceration.…”