Abstract
In this study, attempt is made to establish changes in serum and liver lipoprotein cholesterols accompanying Plasmodium berghei malarial infection in mice treated with aqueous extract of Ganoderma lucidum at 100, 250, and 500 mg/kg body weight in comparison with 15 mg/kg chloroquine (CQ). Significant increases in all the lipoprotein fractions were observed in infected untreated mice compared with normal control mice. Treatment with 100 and 250 mg/kg G. lucidum extract produced significant reduction in serum total cholesterol (TC) and low-density cholesterol (LDL-C) contents compared with 500 mg/kg G. lucidum and CQ. Treatment with CQ, however, produced significant reduction in hepatic TC and LDL-C compared with the extract. A dose-dependent significant increase in serum high-density lipoprotein cholesterol (HDL-C) was observed in the G. lucidum treated mice compared with normal control but significantly lower compared with CQ-treated mice. Liver HDL-C level was significantly higher in CQ-treated mice compared with normal control and significantly lower compared with G. lucidum-treated and infected untreated mice. A dose-dependent effect of the extract was observed in both serum and liver very-low density lipoprotein cholesterol (VLDL-C). The implication of these results is discussed with respect to the parasite survival and proliferation in the serum and liver.
Highlights
The malarial parasite has been observed to have a tremendous requirement for lipids during the replicative stages that take place in the mammalian host
Significant decreases (P < 0.05) were observed in serum total cholesterol (TC), low-density lipoprotein (LDL), high-density lipoprotein (HDL), and very low-density lipoprotein (VLDL) levels in infected mice treated with aqueous extract of Ganoderma lucidum compared to infected untreated mice though these values were significantly higher compared to normal control level
The extract at 100 mg/kg and 250 mg/kg body weight produced significantly lower reductions in serum TC and LDL-C compared to 500 mg/kg extract concentration
Summary
The malarial parasite has been observed to have a tremendous requirement for lipids during the replicative stages that take place in the mammalian host. Biochemical studies on blood-stage Plasmodium malarial parasites have demonstrated the parasite’s proficiency at scavenging and modifying lipids obtained from the host [1]. Plasmodium parasites have the capacity to modify fatty acids as needed by elongation or desaturation and incorporate them into phospholipids, diacylglycerols (DAGs), and triacylglycerols (TAGs) [6, 7]. Such biochemical revelations have not been possible for liver-stage parasites because of the difficulty in isolating the parasite from the host hepatocytes and the low rate of infection during this stage.
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