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Stanniocalcin-1 protects bovine intestinal epithelial cells from oxidative stress-induced damage

Chronic enteritis can produce an excess of reactive oxygen species resulting in cellular damage. Stanniocalcin-1(STC-1) reportedly possesses anti-oxidative activity, the aim of this study was to define more clearly the direct contribution of STC-1 to anti-oxidative stress in cattle. In this study, p...

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Detalles Bibliográficos
Autores principales: Wu, Li-ming, Guo, Rui, Hui, Lin, Ye, Yong-gang, Xiang, Jing-mei, Wan, Chun-yun, Zou, Miao, Ma, Rui, Sun, Xiao-zhuan, Yang, Shi-jin, Guo, Ding-zong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Society of Veterinary Science 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4269589/
https://www.ncbi.nlm.nih.gov/pubmed/24962416
http://dx.doi.org/10.4142/jvs.2014.15.4.475
Descripción
Sumario:Chronic enteritis can produce an excess of reactive oxygen species resulting in cellular damage. Stanniocalcin-1(STC-1) reportedly possesses anti-oxidative activity, the aim of this study was to define more clearly the direct contribution of STC-1 to anti-oxidative stress in cattle. In this study, primary intestinal epithelial cells (IECs) were exposed to hydrogen peroxide (H(2)O(2)) for different time intervals to mimic chronic enteritis-induced cellular damage. Prior to treatment with 200 µM H(2)O(2), the cells were transfected with a recombinant plasmid for 48 h to over-express STC-1. Acridine orange/ethidium bromide (AO/EB) double staining and trypan blue exclusion assays were then performed to measure cell viability and apoptosis of the cells, respectively. The expression of STC-1 and apoptosis-related proteins in the cells was monitored by real-time PCR and Western blotting. The results indicated that both STC-1 mRNA and protein expression levels positively correlated with the duration of H(2)O(2) treatment. H(2)O(2) damaged the bovine IECs in a time-dependent manner, and this effect was attenuated by STC-1 over-expression. Furthermore, over-expression of STC-1 up-regulated Bcl-2 protein expression and slightly down-regulated caspase-3 production in the damaged cells. Findings from this study suggested that STC-1 plays a protective role in intestinal cells through an antioxidant mechanism.