Melittin administration ameliorates motor function, prevents apoptotic cell death and protects Purkinje neurons in the rat model of cerebellar ataxia induced by 3-Acetylpyridine.

Cerebellar ataxia (CA) is a condition in which cerebellar dysfunction leads to movement disorders such as dysmetria, asynergy and dysdiadochokinesia. This study investigates the therapeutic effects of Melittin (MEL) on 3-acetylpyridine-induced (3-AP) cerebellar ataxia (CA) rat model. Initially, CA rat models were generated by 3-AP administration followed by the intraperitoneal injection of MEL. Then, motor performance and electromyography (EMG) activity were assessed. Afterwards, the pro-inflammatory cytokines were analyzed in the cerebellar tissue. Moreover, the anti-apoptotic role of MEL in CA and its relationship with the protection of Purkinje cells were explored. The findings showed that the administration of MEL in a 3-AP model of ataxia improved motor coordination (P < 0.001) and neuro-muscular activity (p < 0.05), prevented the cerebellar volume loss (P < 0.01), reduced the level of inflammatory cytokines (p < 0.05) and thwarted the degeneration of Purkinje cells against 3-AP toxicity (P < 0.001). Overall, the findings imply that the MEL attenuates the 3-AP-induced inflammatory response. As such, it could be used as a treatment option for CA due to its anti-inflammatory effects.

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