Gastro-duodenal ulcers are diseases that constitute a major public health problem all over the world and particularly in Côte d'Ivoire. The aim of this study was to evaluate the acute toxicity and gastric anti-ulcer activity of an aqueous extract of the leaves of Macaranga barteri (AEMb). Acute toxicity was carried out using the Organization for Economic Co-operation and Development (OECD) Guidelines 420. The anti-ulcer activity of AEMb was evaluated using four models of gastric ulcer induction which are HCl/ethanol solution, ibuprofen solution, pylorus ligation and cold restraint stress in rats. The parameters assessed were mucus production, ulcer surface, ulcer index, pH, acid concentration and volume of gastric contents. Cimetidine, aluminium hydroxide and ranitidine were used as anti-ulcer standard drugs. The results of this preventive gastric anti-ulcer study revealed that for doses ranging from 62.5 to 500 mg/kg body weight (b.w), AEMb dose dependently prevented gastric lesion formation (p<0.001) in the four models. The inhibition values were 98.96, 94.11, 90.73 and 96.89% on ulcerations induced respectively by HCl/ethanol, ibuprofen, pylorus ligation and cold restraint stress at the dose of 500 mg/kg b.w. This cytoprotective action was accompanied by a significant increase in gastric mucus production. These results suggested that the preventive anti-ulcer activity of AEMb may be due to a cytoprotective effect. The median acute toxicity LD 50 value of AEMb was higher than 5000 mg/kg b.w. This extract was classified as nontoxic in the Globally Harmonized System of Classification and Labelling of Chemicals (GHS). Phytochemical compounds such as polyphenols, saponins, alkaloids, sterols and polyterpenes found out in AEMb could be responsible for its effects. In conclusion, the antigastric ulcer and the non-toxic effects of the aqueous extract of M. barteri could justify its use in traditional medicine for the treatment of gastro-duodenal ulcers.
Macaranga barteri is a plant used in traditional medicine to treat non-alcoholic fatty liver disease. However, its potential against hepatic steatosis has not been scientifically proven yet. This work aimed to investigate the preventive effect of the aqueous extract of Macaranga barteri leaves (AEMb) on hepatic steatosis experimentally induced with amiodarone in rats. 36 rats were divided into 6 groups of 6 rats each. Group 1, the non-intoxicated group and Group 2, used as controls were pretreated with distilled water (10 ml/kg b.w.). Group 3 received silymarin at 100 mg/kg b.w. while Groups 4, 5 and 6 were pretreated with AEMb at doses of 125, 250 and 500 mg/kg b.w. respectively. The weights of the rats were monitored during the experimentation. After 7 days of daily pretreatment with the different substances, rats of groups 2 to 6 were administered intraperitoneally amiodarone (200 mg/kg bw) three times daily for seven other consecutive days. At the end of the experiments, blood samples were collected on fasted and anesthetized rats kept in dried and EDTA tubes in order to assess some hematological and biochemical parameters and also rats livers were removed for gross observation and hepatic triglyceride assessment. The results revealed that AEMb and silymarin inhibited the weight loss induced by amiodarone and even favored weight gain. The reduction of heamatological indices (leukocytes and leukocyte indices, erythrocytes and erythrocyte indices (MCV, MCH and MCHC), hemoglobin, hematocrit and thrombocytes) by amiodarone was impeded in AEMb treated rats. AEMb significantly reduced (p <0.001) lipid profile parameters (plasma triglycerides, cholesterols (LDL, HDL and total)) augmented by amiodarone. Increased hepatic parameters (alkaline phosphatase, bilirubins (total and conjugated), transaminases (AST and ALT)) elicited by amiodarone were restored by AEMb pretreatment while decreased HDL values were normalized as well. Silymarin and AEMb also restored livers appearance and hepatic triglyceride. In conclusion, AEMb have a real preventive potential against amiodarone induced-hepatic steatosis in rats.
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