HESPERIDIN A BIOFLAVONOID MODULATES THE EXPRESSION LEVELS OF SNCA AND PARKIN IN 6-HYDROXYDOPAMINE INDUCED NEUROTOXICITY IN RATS

Priya Nagappan, Vijayalakshmi Krishnamurthy*

Parkinson disease (PD) is one of the neurodegenerative disease and oxidative stress plays a vital role in its causation. The present study was carried out to evaluate the role of hesperidin in the expression of SNCA, LRRK2, Parkin and PINK1 during 6 hydroxydopamine induced Parkinson rat model. Animals were divided into 5 groups: GroupI served as normal. GroupII was induced with 6-hydroxydopamine (8μg/2μl in 0.1% ascorbic acid-saline). Group III: 6 hydroxydopamine + 50mg/kg b.w hesperidin. GroupIV: 6-hydroxydopamine + 50mg/kg b.w hesperidin+100mg/kg b.w of L-Dopa. GroupV: 6-hydroxydopamine+100mg/kg b.w L-Dopa. The mRNA and protein expression of SNCA, LRRK2, Parkin and PINK1 was evaluated. Hesperidin 50mg/kg b.w and L-Dopa 100mg/kg b.w treated rats showed better results. It may be attributed that treatment with hesperidin and L-Dopa in combination suppress the expression level of SNCA and LRRK2, while it enhanced the expression level of parkin and PINK1. By western blot analysis, group IV treated animals showed suppressed protein levels of SNCA and LRRK2 genes while elevation in the protein level of Parkin and PINKI was noticed. The findings of these studies show that hesperidin can ameliorate 6 hydroxydopamine induced degeneration of dopaminergic neurons during Parkinson disease.