Abstract
Visceral leishmaniasis is a vector-borne protozoan infection that is fatal if untreated. There is no vaccination against the disease, and the current chemotherapeutic agents are ineffective due to increased resistance and severe side effects. Buparvaquone is a potential drug against the leishmaniases, but it is highly hydrophobic resulting in poor bioavailability and low therapeutic efficacy. Herein, we loaded the drug into silicon nanoparticles produced from barley husk, which is an agricultural residue and widely available. The buparvaquone-loaded nanoparticles were several times more selective to kill the intracellular parasites being non-toxic to macrophages compared to the pure buparvaquone and other conventionally used anti-leishmanial agents. Furthermore, the in vivo results revealed that the intraperitoneally injected buparvaquone-loaded nanoparticles suppressed the parasite burden close to 100%. By contrast, pure buparvaquone suppressed the burden only by 50% with corresponding doses. As the conclusion, the biogenic silicon nanoparticles are promising carriers to significantly improve the therapeutic efficacy and selectivity of buparvaquone against resistant visceral leishmaniasis opening a new avenue for low-cost treatment against this neglected tropical disease threatening especially the poor people in developing nations.
Highlights
Visceral leishmaniasis (VL) is a deadly disease with a mortality rate of over 95% if untreated [1]
It has been shown to have excellent in vitro activity against L. donovani, but its lipophilic nature hinders its use in vivo
We loaded the buparvaquone in biogenic porous silicon nanoparticles to improve its bioavailability
Summary
Visceral leishmaniasis (VL) is a deadly disease with a mortality rate of over 95% if untreated [1]. It invades the immune system and damages the liver, spleen, bone marrow, and lymph nodes [2]. In the gut of the sandfly, the parasite exists in promastigote forms, which are motile, extracellular, and flagellated. Human infection takes place when the promastigotes are ingested by the macrophages and metamorphosed into nonmotile amastigote forms [3]. The amastigotes are released into the bloodstream, and they infect all organs containing macrophages and the reticuloendothelial system, where they are hosted for their replication [3]
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