In vivo study on splenomegaly inhibition by genistein in Plasmodium berghei-infected mice

- Malaria-induced splenomegaly was inhibited by genistein.
- Genistein does not affect the viscosity of malaria-infected RBCs.
- Genistein recovers the malaria-induced disrupted architecture of spleen and liver.
- Enzymatic activity of MMPs and expression pattern of proteins are examined.

Spleen plays an important role in removing old and damaged red blood cells and malaria-infected erythrocytes. When malaria parasites invade the spleen and induce splenomegaly, splenic function tends to be impaired. Thus, the inhibition of splenomegaly is strongly required to protect the spleen. In this study, malaria-induced splenomegaly is inhibited by injecting genistein into a Plasmodium berghei-infected ICR mouse. To explain this phenomenon, the effect of genistein in spleen and liver of malaria-infected mice was evaluated by histological examination. Malaria parasites disrupted splenic architecture. After treating genistein, the disrupted architecture in which red and white pulp regions were clearly separated in recovered to uninfected ones. Changes in biophysical properties of blood were studied by measuring the viscosity of blood collected from malaria-infected and uninfected mice using a microfluidic viscometer. Genistein also had a negligible influence on variation in blood viscosity. The enzymatic activity and expression pattern of proteins were then investigated to explain the genistein effect on malaria-induced splenomegaly. Genistein is a potential drug for splenomegaly in P. berghei-infected mouse.

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