A growing number of studies have shown that excessive iron is closely associated with the pathogenesis of Parkinson's disease.
Previous studies from Chunyan Guo and co-workers from Capital Medical University in China have shown that baicalin prevented iron accumulation after substantia nigra injury, reduced divalent metal transporter 1 expression, and increased ferroportin 1 expression in the substantia nigra of rotenone-induced Parkinson's disease rats. However, the relationship between iron concentration and transferrin expression is still unclear. Based on the previous findings, these scholars further explored the mechanisms of the inhibitory effect of baicalin on iron accumulation observed in Parkinson's disease rats.
Their findings published in the Neural Regeneration Research indicate that baicalin down-regulated iron concentration, which positively regulated divalent metal transporter 1 expression and negatively regulated ferroportin 1 expression, and decreased iron accumulation in the substantia nigra.
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