Isolation of major phenolics from Launaea spinosa and their protective effect on HepG2 cells damaged with t-BHP
- Isolation of major phenolics from Launaea spinosa and their protective effect on HepG2 cells damaged with t-BHP
- Hossam Abdallah; Mohamed Farag; Samir Osman; 김다혜; 강경수; 판철호; Essam Abdel-Sattar
- Cytoprotection; diferulyl methyl tartrate ester; oxidative stress
- Issue Date
- Pharmaceutical biology
- 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.
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