Crocin Protects Malathion-Induced Striatal Biochemical Deficits by Inhibiting Apoptosis and Increasing α-Synuclein in Rats' Striatum.

Abstract

Long-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 antioxidant properties. Thus, the effect of crocin on malathion-induced striatal biochemical deficits in rats was investigated in this study. Six groups of male Wistar rats were used: 1. control (normal saline); 2. malathion (100mg/kg/day, i.p.); 3. crocin (10mg/kg/day, i.p.) + malathion; 4. levodopa (10mg/kg/day, i.p.) + malathion; 5. crocin (40mg/kg/day, i.p.); and 6. polyethylene glycol (PEG) (vehicle of levodopa) groups. The drugs were administered for 28days. The amounts of Bcl-2, Bax, and caspases 3, 8, and 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. Malathion induced apoptosis by increasing the amount of Bax/Bcl2 ratio and caspases 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. Crocin 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.