Cai et al., demonstrated that basic fibroblast growth factor (bFGF), as a neurotrophic factor, inhibited Endoplasmic reticulum (ER) stress-induced neuronal cell apoptosis and that Oxidopamine (6-hydroxydopamine 6-OHDA)-induced ER stress was involved in the progression of Parkinson's disease (PD) in rats. bFGF administration improved motor function recovery, increased tyrosine hydroxylase (TH)-positive neuron survival, and upregulated the levels of neurotransmitters in PD rats.

The 6-OHDA-induced ER stress response proteins were inhibited by bFGF treatment. Meanwhile, bFGF also increased expression of TH. The administration of bFGF activated the downstream signals PI3K/Akt and Erk1/2 in vivo and in vitro. Inhibition of the PI3K/Akt and Erk1/2 pathways by specific inhibitors partially reduced the protective effect of bFGF. This study provides new insight towards bFGF translational drug development for PD involving the regulation of ER stress ¹⁾.