Research Article

Effects and mechanism of lipoic acid on beta-amyloid-intoxicated C6 glioma cells

Published: October 30, 2015
Genet. Mol. Res. 14 (4) : 13880-13888 DOI: 10.4238/2015.October.29.8

Abstract

β-amyloid peptides (Aβs) can exert neurotoxic effects through induction of oxidative damage, whereas lipoic acid (LA), a powerful antioxidant, can alleviate oxidative damage. In this study, we explored the effect and mechanism of action of LA on beta-amyloid-intoxicated C6 glioma cells. Cells were randomly divided into three groups: control (vehicle), Aβ, and LA + Aβ. The LA + Aβ group was treated with LA for 2 h, then both the Aβ-only and the LA + Aβ groups were incubated with 25 μM Aβ for 24 h. Cell viability was measured by the MTT method. Mitochondrial reduced glutathione (GSH) and oxidized glutathione (GSSG) levels were detected by enzyme-linked immunosorbent assay (ELISA), and the GSH to GSSG ratio calculated. Real-time polymerase chain reaction and western blot analyses were used to detect MnSOD mRNA and protein, respectively. Aβ significantly inhibited C6 cell proliferation compared with the control group (P MnSOD expression compared to controls (P MnSOD expression compared with the Aβ-only group (P

β-amyloid peptides (Aβs) can exert neurotoxic effects through induction of oxidative damage, whereas lipoic acid (LA), a powerful antioxidant, can alleviate oxidative damage. In this study, we explored the effect and mechanism of action of LA on beta-amyloid-intoxicated C6 glioma cells. Cells were randomly divided into three groups: control (vehicle), Aβ, and LA + Aβ. The LA + Aβ group was treated with LA for 2 h, then both the Aβ-only and the LA + Aβ groups were incubated with 25 μM Aβ for 24 h. Cell viability was measured by the MTT method. Mitochondrial reduced glutathione (GSH) and oxidized glutathione (GSSG) levels were detected by enzyme-linked immunosorbent assay (ELISA), and the GSH to GSSG ratio calculated. Real-time polymerase chain reaction and western blot analyses were used to detect MnSOD mRNA and protein, respectively. Aβ significantly inhibited C6 cell proliferation compared with the control group (P < 0.05). LA markedly increased cell viability compared with the Aβ group (P < 0.05). The increased GSSH and decreased GSH mitochondrial accumulation induced by Aβ was profoundly reversed by treatment with LA (P < 0.05). Aβ significantly reduced MnSOD expression compared to controls (P < 0.05), whereas LA pretreatment increased MnSOD expression compared with the Aβ-only group (P < 0.05); MnSOD protein levels showed similar patterns. These results suggest that LA might protect Aβ-intoxicated C6 glioma cells by alleviating oxidative damage, providing a new treatment strategy for neurodegenerative diseases.