Sun Huijuan, Dong Ling, Wang Jiaxin, et al. Protective effects of Lycium ruthenicum Murr. on hydrogen peroxide-induced cellular oxidative stress injury in heart-derived H9c2 cells[J]. Journal of Beijing University of traditional Chinese Medicine, 2018, 41(4): 301-305.
Sun Huijuan, Dong Ling, Wang Jiaxin, et al. Protective effects of Lycium ruthenicum Murr. on hydrogen peroxide-induced cellular oxidative stress injury in heart-derived H9c2 cells[J]. Journal of Beijing University of traditional Chinese Medicine, 2018, 41(4): 301-305.DOI: 10.3969/j.issn.1006-2157.2018.04.007.
Protective effects of Lycium ruthenicum Murr. on hydrogen peroxide-induced cellular oxidative stress injury in heart-derived H9c2 cells
Objective To explore the protective effects of Lycium ruthenicum Murr.( Lrm) on hydrogen peroxide( H2 O2)-induced cellular oxidative stress injury in heart-derived H9 c2 cells. Methods In this study
H2 O2-induced injury in heart-derived H9 c2 cells was established as cellular oxidative stress injury model. The H9 c2 cells were divided into blank group
model group( H2 O2400 μmol/L) and experimental group( Lrm 1. 00 g/L + H2 O2400 μmol/L). The Lrm group was pretreated with Lrm for 2 h before treated with H2 O2 for 6 h. Cellular morphology of all groups was observed. Cell viability( MTT assay)
apoptosis rate( TUNEL assay)
Bcl-2 and Bcl-2 relating x gene protein( Bax) expression were evaluated( Western Blotting). Results Compared with the blank group
abnormal cellular morphology
decreased cell activity
and increased apoptosis were observed in the model group( P < 0. 05). Anti-apoptotic Bcl-2 gene was less expressed while pro-apoptotic Bax protein level was increased. Compared with the model group
cellular morphology and activity was greatly improved in the experimental group with reduced apoptosis rate( P < 0. 05). The increased expression of Bcl-2 and reduction of Bax were also significantly different.Conclusion Our findings suggest that Lrm tended to improve the H9 c2 myocardial cellular morphology
enhance cell activity and reduce apoptosis rate. Its mechanism of action in reducing oxidative stress injury may be related to the up-regulation of Bcl-2 as well as down-regulation of Bax protein expression.
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