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Attenuation of Oxidative Stress-Induced Cell Apoptosis in Schwann RSC96 Cells by Ocimum Gratissimum Aqueous Extract

Objectives:Cell transplantation therapy of Schwann cells (SCs) is a promising therapeutic strategy after spinal cord injury. However, challenges such as oxidative stress hinder satisfactory cell viability and intervention for enhancing SCs survival is critical throughout the transplantation procedur...

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Detalles Bibliográficos
Autores principales: Chao, Pei-Yu, Lin, James A., Ye, Je-Chiuan, Hwang, Jin-Ming, Ting, Wei-Jen, Huang, Chih-Yang, Liu, Jer-Yuh
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Ivyspring International Publisher 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5562131/
https://www.ncbi.nlm.nih.gov/pubmed/28824312
http://dx.doi.org/10.7150/ijms.19535
Descripción
Sumario:Objectives:Cell transplantation therapy of Schwann cells (SCs) is a promising therapeutic strategy after spinal cord injury. However, challenges such as oxidative stress hinder satisfactory cell viability and intervention for enhancing SCs survival is critical throughout the transplantation procedures. Ocimum gratissimum, widely used as a folk medicine in many countries, has therapeutic and anti-oxidative properties and may protect SCs survival. Methods:We examined the protective effects of aqueous O. gratissimum extract (OGE) against cell damage caused by H(2)O(2)-induced oxidative stress in RSC96 Schwann cells. Results:Our results showed that the RSC96 cells, damaged by H(2)O(2 )oxidative stress, decreased their viability up to 32% after treatment with different concentrations of up to 300 μM H(2)O(2), but OGE pretreatment (150 or 200 μg/mL) increased cell viability by approximately 62% or 66%, respectively. Cell cycle analysis indicated a high (43%) sub-G1 cell population in the H(2)O(2)-treated RSC96 cells compared with untreated cells (1%); whereas OGE pretreatment (150 and 200 μg/mL) of RSC96 cells significantly reduced the sub-G1 cells (7% and 8%, respectively). Furthermore, Western blot analysis revealed that OGE pretreatment inhibited H(2)O(2)-induced apoptotic protein caspase-3 activation and PARP cleavage, as well as it reversed Bax up-regulation and Bcl-2 down-regulation. The amelioration of OGE of cell stress and stress-induced apoptosis was proved by the HSP70 and HSP72 decrease. Conclusion: Our data suggest that OGE may minimize the cytotoxic effects of H(2)O(2)-induced SCs apoptosis by modulating the apoptotic pathway and could potentially supplement cell transplantation therapy.