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Background   The ethanol extract of  Artocarpus champeden  stem bark (ACEE) has been proven to exhibit antimalarial activity. Despite the antimalarial effects observed, mechanisms of immune response to explain the antimalarial activity of ACEE remain poorly characterized. Here, we show the production of pro- and anti-inflammatory cytokines T helper 1 (Th1: IFN- γ , TNF- α ) and T helper 2 (Th2: IL-10) from  Plasmodium berghei -infected mice treated with formulated ACEE in order to better characterize the mechanism behind ACEE's antimalarial activity. In addition, we have also determined the effect of formulated ACEE on parasite growth and liver function.Methods   Balb/c mice were infected with  P. berghei  strain ANKA and then administered daily doses of ACEE at a dose of 20, 50, and 100 mg/kg BW, and survival time was recorded. We determined the presence of  P. berghei  strain ANKA and then administered daily doses of ACEE at a dose of 20, 50, and 100 mg/kg BW, and survival time was recorded. We determined the presence of  P. berghei  strain ANKA and then administered daily doses of ACEE at a dose of 20, 50, and 100 mg/kg BW, and survival time was recorded. We determined the presence of  γ , TNF- α ) and T helper 2 (Th2: IL-10) fromResults   We found that formulated ACEE inhibited parasite growth and showed the highest antimalarial activity at 100 mg/kg BW. AST and ALT levels were found to be in the normal range, and there was no significant difference among control and treatment groups ( P  > 0.05). Infected mice treated with formulated ACEE showed a significant increase in the production of IFN- γ , TNF- α ) and T helper 2 (Th2: IL-10) fromConclusion   This study suggests that the administration of ACEE was effective in inhibiting  P. berghei  strain ANKA and then administered daily doses of ACEE at a dose of 20, 50, and 100 mg/kg BW, and survival time was recorded. We determined the presence of  γ , TNF- α ) and T helper 2 (Th2: IL-10) from

Effect of Formulated Artocarpus champeden Extract on Parasite Growth and Immune Response of Plasmodium berghei-Infected Mice