Therapeutic Effects of Cinnamaldehyde on Neuromuscular Function in Rat Parkinson's Model Induced by Rotenone

Parkinson's disease (PD) is a multisystem neurodegenerative disorder characterized by both motor and nonmotor symptoms. This study aimed to investigate the effects of trans-cinnamaldehyde (TCA) on central and peripheral toxicity in a rotenone-induced rat model of PD. All analyses were conducted on the seventh day after intraperitoneal (i.p.) administration of rotenone (2 mg/kg). Tyrosine hydroxylase (TH), a key enzyme in catecholamine biosynthesis, and nuclear receptor-related 1 protein (Nurr1), a transcription factor essential for the differentiation, maturation, and survival of nigral neurons, were assessed by immunohistochemistry. Electrical and mechanical activities were recorded from extensor digitorum longus (EDL) muscle preparations using electromyography (EMG) and mechanogram, respectively, to evaluate motor function. Histopathological analyses were performed to determine the percentage of normal neurons in the corpus striatum and substantia nigra (SN). Catalase and cyclic adenosine monophosphate (cAMP) levels in midbrain tissue were measured using enzyme-linked immunosorbent assay (ELISA). Seven days of rotenone exposure induced alterations in the nigrostriatal dopaminergic system and neuromuscular function, as demonstrated by behavioral, biochemical, electrophysiological, and histopathological assessments. Importantly, TCA treatment significantly ameliorated many of the deficits observed in rotenone-treated rats. These findings suggest that TCA exerts neuroprotective effects and improves impaired muscle function by reducing oxidative stress and enhancing dopamine levels.