Northwest A & F University, Yangling, Shaanxi, China.
Chem Biol Interact. 2010 Apr 29;185(2):101-9. doi: 10.1016/j.cbi.2010.03.003. Epub 2010 Mar 6.
Oxidative and carbonyl stress are detrimental in the pathogenesis of diabetic complications, as well as in other chronic diseases. However, this process may be decreased by dietary bioactive compounds. Almond skin is an abundant source of bioactive compounds and antioxidants, including polyphenolic flavonoids, which may contribute to the decrease in oxidative and carbonyl stress. In this study, four Almond Skin Extracts (ASEI, ASEII, ASEIII, and ASEIV) were prepared by different methods and evaluated for their antioxidant activity. The order of the polyphenol content (total muM gallic acid equivalents) of the four extracts was found to be, in decreasing order of effectiveness: ASEI>ASEIII>ASEIV>ASEII. The order of Ferric-reducing antioxidant power (FRAP, microM FeSO(4)/g) value, in decreasing order was ASEI (216)>ASEIII (176)>ASEIV (89)>ASEII (85). The order of ASE effectiveness for decreasing protein carbonyation induced by the copper Fenton reaction was ASEI>ASEIV>ASEII>ASEIII. The order of antioxidant effectiveness for inhibiting tertiary-butyl hydroperoxide (TBH) induced microsomal lipid peroxidation was ASEI>ASEIV>ASEII, ASEIII. Also, the order of ASE effectiveness for inhibiting TBH induced hepatocyte cell death was: ASEIII, ASEIV>ASEI, ASEII. Catechin also protected hepatocytes from TBH induced hepatocyte, lipid peroxidation and cytotoxicity. In a cell free model, equimolar concentrations of catechin or epicatechin rescued serum albumin from protein carbonylation induced by methylglyoxal (MGO). Catechin, epicatechin and ASEI all decreased gloxal induced hepatocyte cell death and reactive oxygen species (ROS) formation in GSH-depleted hepatocytes. Catechin and epicatechin protected against GO or MGO induced hepatocyte cell death, protein carbonylation and ROS formation. Catechin was more effective than epicatechin. Our results suggest that (a) bioactive almond skin constituents in the non-lipophilic polyphenol extract were the most effective at protecting hepatocytes against hydroperoxide induced hepatocyte oxidative stress and in protecting against dicarbonyl induced cytotoxicity; (b) catechins, the major polyphenol in the extract, were also effective at preventing GO or MGO cytotoxicity likely by trapping GO and MGO and/or rescuing hepatocytes from protein carbonylation.
氧化应激和羰基应激在糖尿病并发症的发病机制中以及其他慢性疾病中都是有害的。然而，这种过程可以通过饮食中的生物活性化合物来减少。杏仁皮是生物活性化合物和抗氧化剂的丰富来源，包括多酚类黄酮，这可能有助于减少氧化应激和羰基应激。在这项研究中，通过不同的方法制备了四种杏仁皮提取物（ASEI、ASEII、ASEIII 和 ASEIV），并评估了它们的抗氧化活性。四种提取物中多酚含量（总 µM 没食子酸当量）的顺序为，按效力降低的顺序为：ASEI>ASEIII>ASEIV>ASEII。铁还原抗氧化能力（FRAP，µM FeSO4/g）值的顺序为，按效力降低的顺序为 ASEI（216）>ASEIII（176）>ASEIV（89）>ASEII（85）。ASE 对铜芬顿反应诱导的蛋白质羰基化的抑制效果的顺序为 ASEI>ASEIV>ASEII>ASEIII。ASE 对抑制叔丁基过氧化物（TBH）诱导的微粒体脂质过氧化的抗氧化效果的顺序为 ASEI>ASEIV>ASEII。同样，ASE 对抑制 TBH 诱导的肝细胞死亡的效果顺序为：ASEIII、ASEIV>ASEI、ASEII。儿茶素也能保护肝细胞免受 TBH 诱导的肝细胞、脂质过氧化和细胞毒性。在细胞外模型中，等摩尔浓度的儿茶素或表儿茶素可从甲基乙二醛（MGO）诱导的血清白蛋白中回收蛋白质羰基化。儿茶素、表儿茶素和 ASEI 均可减少 GSH 耗尽的肝细胞中 gloxal 诱导的肝细胞死亡和活性氧（ROS）形成。儿茶素和表儿茶素可防止 GO 或 MGO 诱导的肝细胞死亡、蛋白质羰基化和 ROS 形成。儿茶素比表儿茶素更有效。我们的结果表明：（a）非脂溶性多酚提取物中的生物活性杏仁皮成分在保护肝细胞免受过氧化物诱导的肝细胞氧化应激和防止二羰基诱导的细胞毒性方面最为有效；（b）提取物中的主要多酚儿茶素也能有效防止 GO 或 MGO 的细胞毒性，可能是通过捕获 GO 和 MGO 并/或使肝细胞免受蛋白质羰基化。
