Abstract

The lipid is a vital metabolic and structural component of the malaria parasite. Malaria parasite-induced liver lipid deposits undergo peroxidation, which ultimately causes tissue damage and histopathological changes, which further lead to many complications. Therefore, it is essential to focus on the factors responsible for this stimulated lipid accumulation during malaria infection. In the present study, we have correlated the significant increase in serum TNF-α and liver triglyceride during Plasmodium yoelii MDR infection in mice. In order to explore the role of TNF-α in inducing lipid accumulation in the liver during malaria infection, we have used a competitive TNF-α inhibitor Etanercept, for the treatment of Plasmodium yoelii MDR (Py MDR) infected mice and found that Etanercept displayed up to a three-fold inhibition of the liver triglyceride level in Py MDR infected mice. These results were also confirmed by triglyceride specific oil red O staining of liver sections. In addition, all the treatment groups also showed inhibition in the level of serum TNF-α and the liver malondialdehyde (MDA), a byproduct of lipid peroxidation. Our study thus concludes that Etanercept significantly reduces Plasmodium-induced liver triglyceride and further saves the host liver from malaria-induced lipid infiltration and liver damage. Therefore, treatment with Etanercept, along with a standard antimalarial, may prove a better therapy for the disease.

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