Neuroprotective Effects of Estradiol plus Lithium Chloride via Anti-Apoptosis and Neurogenesis Pathway in In Vitro and In Vivo Parkinson’s Disease Models

Figure 8

Schematic diagram of lithium chloride (LiCl) plus estradiol (E2) in 6-OHDA-induced neuronal death. 6-OHDA could induce cell apoptosis through increasing of p-Akt and p-ERK expression, decreasing p-P38, and further modulating the downstream apoptotic proteins, such as Bcl-2 and caspase-3. Our studies demonstrated that the co-treatment of LiCl and E2 could enhance neurogenesis via increasing Rho A, GAP-43, and TGase-2b protein expression. Besides, co-treatment of LiCl and E2 attenuated cell apoptosis through reversing 6-OHDA-induced downregulation of p-Akt, p-ERK and attenuating 6-OHDA-induced upregulation of p-P38 protein expression. The downstream cascade was also modulated, such as Bcl-2 and caspase-3. The 6-OHDA-induced upregulating Bcl-2 expression was reversed by the co-treatment of LiCl plus E2 and 6-OHDA-induced upregulating of caspase-3 expression was also attenuated. The neuroprotective effect of LiCl plus E2 significantly protected dopamine neurons against damage.