Coenzyme Q prevented breach of the blood brain barrier, inflammation and organ damage in late stage of Human African Trypanosomiasis.

During the late stage of Human African Trypanosomiasis (HAT), there is severe cytokine-driven inflammation, oxidative stress and organ damage. Controlling inflammation and oxidative damage presents unique therapeutic opportunities to improve treatment outcome. The current study sought to determine the putative impact of Coenzyme-Q10 (Co-Q), a potent antioxidant and anti-inflammatory, on adverse inflammatory and oxidative events during (T.b.r) infection. Group one constituted the control; the second group was infected with T.b.r; the third group was orally administered with 200 mg/kg Co-Q for two weeks; thereafter, Co-Q administration continued after infection with T.b.r. Co-Q improved the survival rate of infected mice and prevented full blown parasite driven splenomegaly and hepatomegaly. Co-Q prevented characteristic T.b.r-driven breach of the blood brain barrier and improved neurological integrity among T.b.r infected mice. Co-Q protected from T.b.r-induced microcytic hypochromic anaemia and thrombocytopenia. T.b.r-induced oxidative stress in the vital organs was assuaged following exposure to Co-Q. Co-Q blocked T.b.r-induced derangement of high density lipoprotein and triglyceride levels. Co-Q significantly abrogated T.b.r-driven elevation of serum TNF-α and IFN-γ levels. Moreover, T.b.r-induced kidney and liver damage was assuaged by Co-Q administration. Co-Q administration downregulated T.b.r-induced elevation of uric acid and C-reactive protein. Likewise, T.b.r infected mice receiving Co-Q exhibited normal brain architecture. In conclusion, treatment with Co-Q may be useful in protecting against T.b.r-mediated organ injury, lethal inflammation and oxidative stress commonly present in severe late stage HAT; and presents unique opportunities for an adjunct therapy for late stage HAT.