s-Ethyl cysteine and s-propyl cysteine alleviate beta-amyloid induced cytotoxicity in nerve growth factor differentiated PC12 cells.

Beta-amyloid peptide (Abeta) was used to induce cytotoxicity in nerve growth factor differentiated PC12 cells, and the effects of s-ethyl cysteine (SEC) and s-propyl cysteine (SPC) on anti-inflammatory protection, DNA fragmentation, mitochondrial membrane potential (MMP), and activity of Na(+)-K(+)-ATPase and caspases were examined. Abeta treatment significantly decreased cell viability and MMP, and increased lactate dehydrogenase (LDH) activity and DNA fragmentation (P < 0.05). The pretreatments from SEC or SPC at 2.5, 5, and 10 microM significantly enhanced cell viability and MMP, and lowered LDH activity and DNA fragmentation (P < 0.05). Abeta treatment also significantly decreased Na(+)-K(+)-ATPase activity and enhanced the activity of caspase-3 and caspase-8 (P < 0.05); however, the pretreatments from SEC or SPC significantly attenuated Abeta-induced reduction in Na(+)-K(+)-ATPase activity and elevation in caspase-3 and caspase-8 activities (P < 0.05). Abeta treatment increased the protein production and mRNA expression of interleukin (IL)-1beta, IL-6, and tumor necrosis factor-alpha (P < 0.05). The pretreatments from SEC at 10 microM or SPC at 2.5, 5, and 10 microM significantly suppressed mRNA expression and decreased the protein production of these cytokines. These results suggested that SEC and SPC were potent neuroprotective agents against Alzheimer's disease.