Novel antioxidant peptide from broken rice resist H2O2-induced premature senescence in 2BS cells via PI3K/Akt and JNK/Bax signaling pathway

SGDWSDIGGR (S-10-R) is a kind of antioxidant peptide derived from broken rice. In the present study, the effects of S-10-R against H2O2-induced cell damage and premature senescence in 2BS cells were determined. The results indicated that S-10-R could improve cell viability and mitochondrial membrane...

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Veröffentlicht in:Food bioscience 2023-04, Vol.52, p.102376, Article 102376
Hauptverfasser: Ren, Li-kun, Yang, Yang, Fan, Jing, Ma, Chun-min, Bian, Xin, Wang, Dang-feng, Xu, Yue, Liu, Bao-xiang, Zhang, Na
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Sprache:eng
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Zusammenfassung:SGDWSDIGGR (S-10-R) is a kind of antioxidant peptide derived from broken rice. In the present study, the effects of S-10-R against H2O2-induced cell damage and premature senescence in 2BS cells were determined. The results indicated that S-10-R could improve cell viability and mitochondrial membrane potential at least 1.06 and 1.12 folds compared with senescence cells. Moreover, S-10-R inhibited β-galactosidase, and DNA damage alleviates the effect on 2BS senescence cells due to scavenging ROS. The apoptosis rate can be reduced by 80.58%. Furthermore, S-10-R could inhibit PI3K and Akt phosphorylation, downregulate Bax and caspases-3 expression, and inhibit premature senescence through activating PI3K/Akt related intrinsic apoptotic signaling pathways and suppressing JNK/Bcl-2 related mitochondria-dependent apoptosis. The present study confirmed the feasibility of antioxidants as anti-aging drugs, as well as provided a substantial basis for future application of S-10-R as a functional ingredient against oxidative stress-induced premature aging. [Display omitted] •S-10-R can reduce H2O2-induced oxidative damage and apoptosis in 2BS cells.•S-10-R play an anti-aging role by activating PI3K/Akt related intrinsic apoptotic signaling pathways.•The anti-premature senescence effects of S-10-R related to downregulation of JNK/Bcl-2 related mitochondria-dependent apoptosis pathway.
ISSN:2212-4292
2212-4306
DOI:10.1016/j.fbio.2023.102376