Full Title: In vitro lipolytic, antioxidant and anti-inflammatory activities of roasted pistachio kernel and skin constituents
Journal: Food and Function
Year of Publication: 2016
Mary Ann Lila
Publication Author(s): Mary H. Grace, Debora Esposito, Michael A. Timmers, Jia Xiong, Gad Yousef, Slavko Komarnytsky and Mary Ann Lila
A comprehensive phytochemical analysis was conducted on pistachios to identify the differential contributions of skin and kernel phytochemicals to in vitro bioactivity. Qualitative and quantitative analyses of skin and kernel non-polar extracts (SNP and KNP, respectively) indicated that the major components are fatty acids (696.36 and 879.70 mg g−1), phytosterols (16.08 and 4.28 mg g−1), and γ-tocopherol (304.17 and 397.10 μg g−1). Analysis of the skin and kernel polar extracts (SP and KP, respectively) showed that skin accumulated higher levels of phenolic compounds, especially flavan-3-ols, compared to the kernel. An (epi)catechin hexoside was the major component in SP and KP (9.8 mg g−1 and 3.3 mg g−1, respectively). Flavan-3-ols with different degrees of polymerization were detected in SP, but only the monomers were identified in the KP. Quercetin glycosides were the major flavonols present in both SP and KP. Bioassays with 3T3L1 mouse adipocytes demonstrated that all extracts decreased lipid accumulation, with SNP demonstrating the highest activity (17% inhibition). Bioassay guided fractionation of SNP indicated that the lipolytic activity was highest in the fraction consisting of linoleic acid (20%), linolenic acid (10%), and β-sitosterol (50%). Radical scavenging assays indicated that all pistachio extracts significantly inhibited ROS, while SP was the most inhibiting to NO production in LPS-stimulated RAW 264.7 macrophages. Gene expression profiles associated with inflammation (IL6, iNOS, and COX2) were characterized in the LPS-stimulated RAW264.7 macrophages after treatment with pistachio extracts. SP and KP were the most potent to inhibit the expression of COX2. The SNP had the strongest effect in decreasing non-mitochondrial oxidative burst associated with inflammatory response in macrophages.