[关键词]
[摘要]
本文为了探讨酪蛋白源七肽AVPYPQR在不同体系中的抗氧化活性及构效关系,比较研究了AVPYPQR及其相关片段PYPQ、PYPQR、VPYPQ、VPYPQR和AVPYPQ在体外化学方法和细胞模型中的抗氧化能力。结果表明,在ABTS自由基清除能力和氧自由基吸收能力(ORAC)等体外化学方法中6条肽的活性都高于标准抗氧化剂Trolox,其中Val、Ala和Arg残基的同时存在降低AVPYPQR的ABTS自由基清除能力,而Arg残基存在提升了AVPYPQR的ORAC活性。在细胞氧化损伤模型中,6条多肽对AAPH诱导血红细胞溶血都有保护作用,其中AVPYPQR保护效果最好,Ala和Arg残基存在提升其保护效果;H2O2诱导HepG2细胞氧化损伤模型中,除PYPQ,其他多肽都具有显著保护效果(p<0.05),其中Ala、Val和Arg残基都可以提升保护效果,但是没有叠加作用。综上,除PYPQ,其它5条多肽在在体外化学方法和细胞模型中都表现出较强抗氧化活性,但无显著性相关,且不同方法中Val、Ala和Arg残基对AVPYPQR活性影响不同。
[Key word]
[Abstract]
In order to investigate the antioxidant activity and structure-activity relationship of casein-derived heptapeptide AVPYPQR in different systems, the antioxidant activity of AVPYPQR and its related fragments PYPQ, PYPQR, VPYPQ, VPYPQR and AVPYPQ were compared in this study using in vitro chemical assays and cellular models. The results showed that the six peptides exhibited higher ABTS free radical scavenging activity and oxygen radical absorbance capacity (ORAC) than the standard antioxidant, Trolox. The co-occurrence of Val, Ala and Arg residues led to a reduced ABTS radical scavenging activity of AVPYPQR, while the presence of Arg residue resulted in an enhanced ORAC. In the cell oxidative damage model, all the six peptides offered protection against AAPH-induced erythrocyte hemolysis. Among which, AVPYPQR exhibited the greatest protective effect, and the presence of Ala and Arg residues improved further such an effect. In H2O2-induced HepG2 cell oxidative damage model, all the peptides showed (p < 0.05) significant protective effect except for PYPQ, and the Ala, Val and Arg residues could enhance the protection but without an addictive effect. In summary, all the peptides, except for PYPQ, had strong antioxidant activity in both in vitro chemical assays and cellular models, but no significant correlation was found among the detected activities in different assays. The influence of Val, Ala and Arg residues on the antioxidant activity of AVPYPQR varied between analysis assays.
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[基金项目]
国家重点研发计划项目(2017YFD0400200);博士后创新人才支持计划资助项目(BX201700081)