Baicalein antagonizes rotenone-induced apoptosis in dopaminergic SH-SY5Y cells related to Parkinsonism

Cell viability and cytotoxicity were determined by MTT assay. The degree of nuclear apoptosis was evaluated with a fluorescent DNA-binding probe Hoechst 33258. The production of reactive oxidative species (ROS) and loss of mitochondrial membrane potential (ΔΨm) were determined by fluorescent staining with DCFH-DA and Rhodanmine 123, respectively. The expression of Bax, Bcl-2, cleaved caspase-3 and phosphorylated ERK1/2 was determined by the Western blots.Baicalein significantly increased viability and decreased rotenone-induced death of SH-SY5Y cells in a dose-dependent manner. Pre- and subsequent co-treatment with baicalein preserved the cell morphology and attenuated the nuclear apoptotic characteristics triggered by rotenone. Baicalein antagonized rotenone-induced overproduction of ROS, loss of ΔΨm, the increased expression of Bax, cleaved caspase-3 and phosphorylated ERK1/2 and the decreased expression of Bcl-2.The antioxidative effect, mitochondrial protection and modulation of anti-and pro-apoptotic proteins are related to the neuroprotective effects of baicalein against rotenone induced cell death in SH-SY5Y cells.Parkinson's disease (PD) is a neurodegenerative disease mainly characterized by loss of dopaminergic neurons in the substantia nigra pars compacta [1]. Although the pathology of PD is not understood well, the neurotoxic animal models of PD represent some key neurobehavioral or pathological features [2]. Three neurotoxins, 6-hydroxydopamine (6-OHDA), 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and rotenone, are the agents to induce parkinsonism in vitro and in vivo [3]. An extensive study of these models defined important cellular actions of cell death and offered a basis for the development of novel therapeutic strategies [4]. Rotenone, a lipophilic pesticide, can cross cell membrane easily to induce systemic inhibition of mitochondrial complex I and cause selective nigrostriatal dopaminergic degeneration [5]. Rotenone-induced apoptosis in h