Isolation of major phenolics from Launaea spinosa and their protective effect on HepG2 cells damaged with t-BHP

Title
Isolation of major phenolics from Launaea spinosa and their protective effect on HepG2 cells damaged with t-BHP
Authors
Hossam AbdallahMohamed FaragSamir Osman김다혜강경수판철호Essam Abdel-Sattar
Keywords
Cytoprotection; diferulyl methyl tartrate ester; oxidative stress
Issue Date
2016-03
Publisher
Pharmaceutical biology
Abstract
Context: Some Launaea species (Asteraceae) are used traditionally to treat liver oxidative stress. Objective: The present study investigates the protective effects of isolated compounds from Launaea spinosa Sch. Bip. (Asteraceae) against oxidative stress on t-BHP-induced HepG2 cells. Materials and methods: Major phenolic content from flowering aerial parts of L. spinosa was isolated and identified. The protective effects of isolated compounds (10 and 20 lM) against oxidative stress induced by tert-butyl hydroperoxide (t-BHP) in HepG2 cells were investigated through the measurement of aspartate aminotransferase (AST), alanine transaminase (ALT), and superoxide dismutase (SOD) levels. Results: A new phenolic compound identified as 2,3-diferulyl R,R-(+) methyl tartrate (6), in addition to five known metabolites, esculetin (1), esculetin-7-O-D-glucoside (cichoriin) (2), fertaric acid (3), acacetin-7-O-D-glucoside (4), and acacetin-7-O-D-glucuronic acid (5), were isolated. Oxidant-induced damage by 200 lM t-BHP in HepG2 cells was inhibited by compounds 1, 4, and 5 (10 and 20 lM), or quercetin (10 lM; positive control). The protective effects of compounds 1, 4, and 5 were associated with decreasing in AST, ALT, and SOD levels. Compound 4 (20 lM) decreased the AST level from 128.5 ± 13.9 to 7.9 ±1.8 U/mL. Meanwhile, compound 1 (20 lM) decreased ALT activity from 20.3 ± 7.0 to 7.6 ± 2.4 U/mL, while compound 5 decreased SOD levels from 41.6 ± 9.0 to 28.3 ± 3.4 mU/mg. Conclusion: The major phenolic compounds isolated from L. spinosa displayed a significant cytoprotective effect against oxidative stress, leading to maintenance of the normal redox status of the cell.
URI
http://pubs.kist.re.kr/handle/201004/58518
ISSN
13880209
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KIST Publication > Article
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