Li Xican, Gao Yaoxiang, Li Fei, Liang Aifeng, Xu Zhiming, Bai Ye, Mai Wenqiong, Han Lu, Chen Dongfeng
School of Chinese Herbal Medicine, Guangzhou University of Chinese Medicine, Guangzhou 510006, China. Electronic address: http://www.researchgate.net/profile/Xican_Li.
School of Chinese Herbal Medicine, Guangzhou University of Chinese Medicine, Guangzhou 510006, China.
Chem Biol Interact. 2014 Aug 5;219:221-8. doi: 10.1016/j.cbi.2014.06.014. Epub 2014 Jun 25.
Maclurin, an exceptional member of phytophenol family, was found to effectively protect against mesenchymal stem cells (MSCs) oxidative damage induced by hydroxyl radical (OH) at 62.1-310.5 μM. Antioxidant assays indicated that maclurin could efficiently protect DNA from OH-induced damage at 114.6-382.2 μM, and scavenge OH, DPPH (1,1-diphenyl-2-picrylhydrazyl radical), ABTS(+) (2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid radical), and bind Cu(2+) (IC50 values were respectively 122.87 ± 10.14, 10.15 ± 0.85, 0.97 ± 0.07, and 133.95 ± 11.92 μM). HPLC-DAD and HPLC-ESI-MS/MS analyses of the end-product of maclurin reaction with DPPH clearly suggested that maclurin (m/z = 261.12 M-H) donated two hydrogen atoms to DPPH (m/z = 394.06 M) to form ortho-benzoquinone moiety (λmax = 364 nm; m/z = 259.06 M-H, loss of m/z = 28) and DPPH2 molecule (m/z = 395.03, 396.01), via hydrogen atom transfer (HAT) or sequential electron (e) proton transfer (SEPT), not radical adduct formation (RAF) mechanisms. Therefore, we concluded that: (i) maclurin can effectively protect against OH-induced damages to DNA and MSCs, thereby it may have a therapeutic potential in prevention of many diseases or MSCs transplantation; (ii) a possible mechanism for maclurin to protect against oxidative damages is OH radical-scavenging; (iii) maclurin scavenges OH possibly through metal-chelating, and direct radical-scavenging which is mainly via HAT or SEPT mechanisms; and (iv) the protective and antioxidant effects of maclurin can be primarily attributed to ortho-dihydroxyl groups, and ultimately to the relative stability of the ortho-benzoquinone form.
杨梅素是植物酚类家族中的杰出成员，研究发现它在62.1 - 310.5 μM浓度下能有效保护间充质干细胞（MSCs）免受羟基自由基（OH）诱导的氧化损伤。抗氧化实验表明，杨梅素在114.6 - 382.2 μM浓度下能有效保护DNA免受OH诱导的损伤，并能清除OH、DPPH（1,1 - 二苯基 - 2 - 苦基肼自由基）、ABTS(+)（2,2'- 偶氮二（3 - 乙基苯并噻唑啉 - 6 - 磺酸）自由基），还能结合Cu(2+)（IC50值分别为122.87 ± 10.14、10.15 ± 0.85、0.97 ± 0.07和133.95 ± 11.92 μM）。对杨梅素与DPPH反应终产物的HPLC - DAD和HPLC - ESI - MS/MS分析清楚地表明，杨梅素（m/z = 261.12 M - H）通过氢原子转移（HAT）或顺序电子（e）质子转移（SEPT），而非自由基加成形成（RAF）机制，向DPPH（m/z = 394.06 M）提供两个氢原子，形成邻苯醌部分（λmax = 364 nm；m/z = 259.06 M - H，损失m/z = 28）和DPPH2分子（m/z = 395.03，396.01）。因此，我们得出以下结论：（i）杨梅素能有效保护DNA和MSCs免受OH诱导的损伤，因此它在预防多种疾病或MSCs移植方面可能具有治疗潜力；（ii）杨梅素保护免受氧化损伤的可能机制是清除OH自由基；（iii）杨梅素可能通过金属螯合以及主要通过HAT或SEPT机制的直接自由基清除作用来清除OH；（iv）杨梅素的保护和抗氧化作用主要归因于邻二羟基，最终归因于邻苯醌形式的相对稳定性。
