Efficacy of Thonningia Sanguinea Vahl. (Balanophoraceae) Root Extract Against Plasmodium Berghei, Plasmodium Chabaudi, Inflammation and Nociception in Mice.

The effects of Thonningea sanguinea Vahl. root extracts were tested against Plasmodium berghei and Plasmodium chabaudi, acetic acid induced abdominal constriction and egg albumin induced paw oedema in rodents. Eighteen mice assigned to 3 groups of 6 animals each were infected with P. berghei (NK 65 chloroquine sensitive strain). Group I was treated with 300 mg/kg bw T. sanguinea, group II with 5mg/kg bw chloroquine phosphate (standard) and group III with 20ml/kg bw normal saline (control). Another set of eighteen mice were also inoculated with P. chabaudi and treated similarly. P. berghei was significantly suppressed by the extract over the time course of the study with mice survival periods of 36, 20 and 16 days for chloroquine, plant extract and normal saline treatments respectively. T. sanguinea produced some initial suppression of parasites but subsequently resurgence in parasitaemia was observed in the case of P. chabaudi infected animals. Mice survival periods with the later were 24 days (CQ), 22 days (extract) and 10 days (normal saline). Whole body weights significantly decreased in P. chabaudi but not P. berghei infected mice. Packed Cell Volume significantly (p<0.05) decreased with both models irrespective of the treatments. The extract had a minimal (10.89%) analgesic effect and had no anti-inflammatory activity. T. sanguinea though effective only in the P. berghei model could still be further investigated.

Antimalarial drugs disrupt ion homeostasis in malarial parasites

Plasmodium chabaudi malaria parasite organelles are major elements for ion homeostasis and cellular signaling and also target for antimalarial drugs. By using confocal imaging of intraerythrocytic parasites we demonstrated that the dye acridine orange (AO) is accumulated into P. chabaudi subcellular compartments. The AO could be released from the parasite organelles by collapsing the pH gradient with the K+/H+ ionophore nigericin (20 µM), or by inhibiting the H+-pump with bafilomycin (4 µM). Similarly, in isolated parasites loaded with calcium indicator Fluo 3-AM, bafilomycin caused calcium mobilization of the acidic calcium pool that could also be release with nigericin. Interestingly after complete release of the acidic compartments, addition of thapsigargin at 10 µM was still effective in releasing parasite intracellular calcium stores in parasites at trophozoite stage. The addition of antimalarial drugs chloroquine and artemisinin resulted in AO release from acidic compartments and also affected maintenance of calcium in ER store by using different drug concentrations.