Crocin Protects Malathion-induced Parkinson-like Disease by Inhibiting Apoptosis and α-synuclein Accumulation in Rats’ Striatum

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Abstract BackgroundLong-term exposure to organophosphates might result in neurodegenerative diseases, comprising Parkinson's disease. Malathion is an organophosphate pesticide with high neurotoxicity. Oxidative stress, apoptosis, and α-synuclein accumulation are important underlying mechanisms in Parkinson’s disease. According to studies, crocin, an active constituent of saffron, has anti-apoptotic, anti-inflammatory, and anti-oxidant properties. Thus, the effect of crocin on malathion-induced Parkinson-like disease in rats was investigated in this study. Materials and methods6 groups of male Wistar rats were used: 1. Control (normal saline), 2. Malathion (100 mg/kg/day, i.p), 3. Crocin (10 mg/kg/day, i.p) + malathion, 4. Levodopa (10 mg/kg/day, i.p) +malathion, 5. Crocin (40 mg/kg/day, i.p), and 6. Polyethylene glycol (PEG) (vehicle of levodopa) groups. The drugs were administered for 28 days. The amounts of Bcl-2, Bax, caspases 3, 8, 9 proteins in the striatum were measured by western blotting. Also, the amounts of protein and mRNA level of the α-synuclein in striatum tissue were measured by western blotting and RT-qPCR methods.ResultsMalathion induced apoptosis by increasing the amount of Bax/Bcl2 ratio, caspase 3 and 9 proteins in rat striatum tissue. It also increased the protein and mRNA level of α-synuclein in striatal tissue. Co-administration of crocin or levodopa with malathion inhibited the toxic effects of malathion on striatal tissue. ConclusionCrocin ameliorates the neurotoxic effect of malathion by its anti-apoptotic activity and regulating the expression of proteins involved in Parkinson's disease pathogenesis. As a result, crocin has the potential to be used as a treatment for malathion-induced neurotoxicity.

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