Asiatic acid influences parasitaemia reduction and ameliorates malaria anaemia in P. berghei infected Sprague-Dawley male rats

Abstract

Background: Current malaria treatment is either "anti-parasitic", "anti-infectivity" or both without addressing the pathophysiological derangement (anti-disease aspect) associated with the disease. Asiatic acid is a natural phytochemical with oxidant, antioxidant and anti-inflammatory properties whose effect on malarial and accompanying pathophysiology are yet to be investigated. Asiatic acid influence in P. berghei-infected Sprague Dawley rats on %parasitaemia and malarial anaemia were investigated.

Methods: Plasmodium berghei-infected rats (90-120 g) were orally administered with Asiatic acid (5, 10, 20 mg/kg) and 30 mg/kg chloroquine as a positive control. Changes in %parasitaemia and haematological parameters in Asiatic acid administered rats were monitored in a 21 day study and compared to controls.

Results: All animals developed stable parasitaemia (15-20 %) by day 7. Asiatic acid doses suppressed parasitaemia, normalised haematological measurements and influenced biophysical characteristics changes. Most positive changes were associated with intragastric administration of 10 mg/kg Asiatic acid dose. Peak %parasitaemia in Asiatic acid administration occurred at days 12 with a shorter time course compared to day 9 for chloroquine (30 mg/kg) treatment with a longer time course.

Conclusions: Oral Asiatic acid administration influenced %parasitaemia suppression, ameliorated malarial anaemia and increased biophysical properties on infected animals. Asiatic acid may be a replacement alternative for chloroquine treatment with concomitant amelioration of malaria pathophysiology. Due to different action time courses, Asiatic acid and chloroquine may be possible candidates in combination therapy.

Keywords: Asiatic acid; Chloroquine; Malaria parasitaemia; Plasmodium berghei.

Fig. 1

Influence of oral AA on % parasitaemia compared to controls. IC is infected-non treated control. 30CHQ is chloroquine 30 mg/kg. Values are presented as means ± SEM, (n = 6 in each group). *, # p < 0.05 compared to IC, CHQ controls, respectively

Fig. 2

Influence of AA administration on haemoglobin changes over time. NIC is non infected treated control; IC is infected non treated control; 30CHQ is chloroquine treated with 30 mg/kg. Values are presented as means ± SEM, (n = 6 in each group). α,*, # p < 0.05 compared to NIC, IC, CHQ controls

Fig. 3

Influence of AA administration on haematocrit changes over time. NIC is non infected treated control; IC is infected non treated control; 30CHQ is chloroquine treated with 30 mg/kg. Values are presented as means ± SEM, (n = 6 in each group). α,*, #p < 0.05 compared to NIC, IC, CHQ controls

Fig. 4

Influence of AA administration on red blood cell count compared to controls. NIC is non infected treated control; IC is infected non treated control; 30CHQ is chloroquine treated with 30 mg/kg. Values are presented as means ± SEM, (n = 6 in each group). α,*, #p < 0.05 compared to NIC, IC, CHQ controls

Fig. 5

AUC_0-21Days of %parasitaemia for post-infection AA oral administration. IC is infected-non treated control. 30CHQ is chloroquine 30 mg/kg. Values are presented as means ± SEM, (n = 6 in each group). *, # p < 0.05 compared to IC, CHQ controls, respectively