Hetastarch reduces neuronal cell death caused by oxidative stress
- Authors
- Lee, Kyu-Yong; Koh, Seong-Ho; Kim, Sangjae; Park, Hyun-Hee; Lee, Young Joo
- Issue Date
- Feb-2012
- Publisher
- WILEY
- Keywords
- hetastarch; neuroprotection; oxidative stress; free radical; PC12 cells; hydrogen peroxide; ischemic stroke
- Citation
- DRUG DEVELOPMENT RESEARCH, v.73, no.1, pp.35 - 42
- Indexed
- SCIE
SCOPUS
- Journal Title
- DRUG DEVELOPMENT RESEARCH
- Volume
- 73
- Number
- 1
- Start Page
- 35
- End Page
- 42
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/166409
- DOI
- 10.1002/ddr.20447
- ISSN
- 1098-2299
- Abstract
- We investigated the effect of hetastarch, used for the treatment of acute ischemic stroke, on neuronal cell damage by oxidative stress, a main pathogenic mechanism in ischemic stroke. Neuronally differentiated PC12 cells (nPC12 cells) were treated with varying concentrations of hetastarch and hydrogen peroxide (H2O2), and their viability was measured with a 3,(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and trypan blue staining. The effect of hetastarch on free radical production by H2O2 was evaluated using the fluorescent probe 2','-dichlorodihydrofluorescein diacetate (DCFH-DA) and by quantifying the amount of 2,5- and 2,3-dihydroxybenzoic acid (DHBA). Additionally, the expression levels of BAX, Bid, Bcl-2, Bcl-xL, cytosolic cytochrome c, and cleaved caspase-3 were examined using Western blot analysis. Following exposure to 100 mu M H2O2, the viability of nPC12 cells significantly decreased; however, cell viability increased with hetastarch treatment. Free radical production related to H2O2 exposure was significantly reduced after 100 mu M hetastarch treatment. The expression levels of BAX, Bid, cytosolic cytochrome c, and activated caspase-3 were reduced, whereas Bcl-2 and Bcl-xL levels increased in H2O2-injured nPC12 cells treated with 100 mu M hetastarch, as compared with nPC12 cells that were treated with only 100 mu M H2O2. These results demonstrate that hetastarch can reduce oxidative stress-induced neuronal cell death. Drug Dev Res 73: 3542, 2012.
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