Amiodarone promoted autophagy and enhanced tissue repair, outperforming albendazole in treating the muscular phase of experimental trichinellosis spiralis.

Targeting autophagy as a therapeutic approach against infections has gained significant attention nowadays. Amiodarone (AMD), the antiarrhythmic drug with autophagy-stimulating property, was used in this study, compared to Albendazole (ALB) (the commonly used drug) against experimental trichinellosis. Our in vivo study used two assessment tools for evaluating the autophagy process: quantitative analysis of local microtubule-associated protein 1 light chain 3 (LC3) autophagy protein marker, in addition to detecting autophagic compartments by transmission electron microscopy (TEM). AMD showed the most significant upregulation of local LC3 expression (15.54 ± 1.33 vs. 13.37 ± 2.03 with ALB, P < 0.005), besides identification of a wide range of autophagosomal cellular compartments, which most likely succeeded in controlling infection and inflammation, compared to few phagosomes and numerous macrophages seen in the ALB-treated group reflecting the lesser ability of the latter to stimulate the full autophagy process and suppress inflammation. In addition, signs of cellular repair were also noticed in TEM in the AMD-treated group, such as normal nuclear chromatin distribution with relatively normal mitochondrial allocation and regular muscle fibers. Autophagy detected in the ALB-treated group, despite being characterized by significant expression of LC3, seemed dysfunctional and inefficient in regulating inflammation and recovering normal cellular features. Our results revealed, for the first time, the exceptional potential of AMD as an autophagy modulator and regenerative supporter in treating trichinellosis. Thus, further investigations for the role of autophagy inducers as therapeutic options against other parasitic infections are recommended.