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Protective effect of erythropoietin against 1-methyl-4-phenylpyridinium-induced neurodegenaration in PC12 cells.

ABSTRACT: The neuroprotective effect of erythropoietin (EPO) against 1-methyl-4-phenylpyridinium (MPP(+))-induced oxidative stress in cultured PC12 cells, as well as the underlying mechanism, were investigated.PC12 cells impaired by MPP(+) were used as the cell model of Parkinson's disease. Methyl thiazolyl tetrazolium (MTT) was used to assay the viability of the PC12 cells exposed to gradient concentrations of EPO, and the terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) assay was used to analyze the apoptosis ratio of PC12 cells. The expression of Bcl-2 and Bax in PC12 cells were examined by Western blot, and the reactive oxygen species (ROS), the mitochondrial transmembrane potential and the activity of caspase-3 in each group were detected by spectrofluorometer.Treatment of PC12 cells with MPP(+) caused the loss of cell viability, which may be associated with the elevation in apoptotic rate, the formation of ROS and the disruption of mitochondrial transmembrane potential. It was also shown that MPP(+) significantly induced the upregulation of Bax/Bcl-2 ratio and the activation of caspase-3. In contrast, EPO significantly reversed these responses and had the maximum protective effect at 1 U/mL.The inhibitive effect of EPO on the MPP(+)-induced cytotoxicity may be ascribed to its anti-oxidative property and anti-apoptotic activity, and EPO may provide a useful therapeutic strategy for treatment of neurodegenerative diseases such as Parkinson's disease.

SUBMITTER: Wu Y

PROVIDER: S-EPMC5550630 | biostudies-other | 2007 May

REPOSITORIES: biostudies-other

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Project description:Cerebral ischemic stroke is a major cause of adult morbidity and mortality worldwide. Several long non-coding RNAs (lncRNAs) have been reported to participate in cerebral ischemia/reperfusion injury (IRI). However, to the best of our knowledge, the role of lncRNA AK139328 in cerebral ischemic stroke remains poorly understood. The present study aimed to determine the expression and function of lncRNA AK139328 in the progression of IRI. PC12 cells were injured by oxygen glucose deprivation/reoxygenation (OGD/R) to establish an in vitro ischemic stroke model. An MTT assay was performed to determine cell viability. Reverse transcription-quantitative PCR was used to analyze the expression levels of AK139328 and Netrin-1 in blood samples from patients who had suffered a cerebral ischemic stroke and healthy individuals or OGD/R PC12 cells. ELISAs were used to determine the levels of inflammatory cytokines. In addition, oxidative stress levels and the levels of cell apoptosis were evaluated by reactive oxygen species (ROS) kits, flow cytometry and western blotting. Immunofluorescence staining was used for the detection of cell neurite outgrowth. The results of the present study revealed that AK139328 expression levels were upregulated in patients who had suffered a cerebral ischemic stroke and in PC12 cells following stimulation with OGD/R. The knockdown of AK139328 alleviated OGD/R-induced decreases in cell viability, downregulation in Netrin-1 expression and increases in inflammatory cytokines levels, including TNF-α, IL-1β and IL-6. Moreover, AK139328 silencing suppressed oxidative stress and cell apoptosis in OGD/R-treated PC12 cells. Furthermore, the expression levels of microtubule associated protein 2 and growth associated protein 43 in OGD/R-injured PC12 cells were upregulated following the knockdown of AK139328 expression. In conclusion, these findings suggested that the knockdown of AK139328 expression may protect PC12 cells against OGD/R injury by regulating inflammatory responses, oxidative stress and cell apoptosis. The data suggested a potential therapeutic target for the diagnosis and treatment of cerebral ischemic stroke.

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Protective effect of erythropoietin against 1-methyl-4-phenylpyridinium-induced neurodegenaration in PC12 cells.

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