化学
槲皮素
熊果酸
抗氧化剂
一氧化氮
DPPH
食品科学
生物化学
色谱法
有机化学
作者
You Jin Lim,Hye Jeong Park,Wooki Kim,Seok Hyun Eom
标识
DOI:10.1016/j.postharvbio.2023.112580
摘要
Postharvest ultraviolet (UV) treatment is a promising method for enhancing the coloration of apple skin. However, the effects of this treatment on the bioactivities of apple skin components are not fully understood. This study aimed to evaluate changes in antioxidant and proinflammatory cytokine inhibition activities as well as the components of apple skin extracts following UV-B treatment. The results showed that UV-B treatment had minimal effects on the quality parameters of the fruit, such as firmness, soluble solids content, and titratable acidity, but it stimulated the accumulation of cyanidin-3-O-galactoside (C3gal). Quercetin-3-O-galactoside (Q3gal), quercetin-3-O-glucoside (Q3glu), and ursolic acid were the major components that exhibited significantly increased content in UV-B–irradiated apple skin extracts presenting 24.9, 7.9, and 11.1-fold higher content than dark treatment, respectively, with this study the first to reveal that UV-B treatment alters ursolic acid content in apples. UV-B treatment also increased both 2,2-diphenyl-1-picrylhydrazyl (DPPH) and 2,2′-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid antioxidant activities, although excessive UV-B intensity (>4 W m−2 s−1) decreased DPPH activity. Furthermore, UV-B–treated skin showed significantly suppressed nitric oxide and tumor necrosis factor-α (TNF-α) production but not interleukin-6 (IL-6) inhibition, which was not a specific effect of UV-B treatment as it is common effect of apple skin extracts. C3gal and Q3gal significantly inhibited IL-6 but not nitric oxide and TNF-α suppression. Overall, our findings indicate that UV-B intensity positively correlates with antioxidant activity resulting from the accumulation of C3gal, Q3gal, Q3glu, and ursolic acid. However, UV-B intensity did not correlate with anti-inflammatory effects, although the extract of UV-B–treated apple skin exhibited relatively strong inhibition of inflammation.
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