|
|
Research on the protective effect of ferulic acid on the apoptosis of A375 cells induced by hydrogen peroxide |
LI Wei ZHENG Kun QU Yan CHEN Lijuan WANG Jiazhi |
Jiamusi College of Heilongjiang University of Chinese Medicine, Heilongjiang Province, Jiamusi 154007, China |
|
|
Abstract Objective To observe the effect of ferulic acid on the apoptosis of melanocyte induced by oxidative stress. Methods According to random number table, A375 cells were divided into five groups: control group, model group, and high, middle, low concentrations of ferulic acid groups. Cells in the control group were cultured normally, while peroxide hydrogen was added into the cultured A375 cells of model group and high, middle, low concentrations of ferulic acid groups at the final concentration of 0.1 mmol/L, duration for 4 hours. The cells were stained with fluorescent dye DAPI. The apoptosis of each group was observed by fluorescence microscope. Caspase active kit was used to measure the activity of Caspase in each group. Results Compared with the control group, the activities of Caspase-3, 8 and 9 in the model group were significantly increased, with statistically significant differences (P < 0.01). In the model group, dense and concentrated particles and the loose light colored crescent or annular fluorescence could be seen in the nucleus and cytoplasm, which implied that hydrogen peroxide can induce apoptosis of A375 cells. Compared with the model group, the expression of Caspase-3 and Caspase-8 were significantly reduced in the high does concentration of ferulic acid group, with statistically significant differences (P < 0.05 or P < 0.01), but the effect on Caspase-9 was not obvious. The nucleus of cells in the high does concentration of ferulic acid group were even bright blue, without the phenomenon of dense condensation. There were chromatin agglutination and marginalization of most cell nucleus in the low and medium does concentrations of ferulic acid groups. Conclusion Ferulic acid can protect the apoptosis of melanocyte through lower the activity of Caspase induced by hydrogen peroxide.
|
|
|
|
|
[1] Li QL,Wu YH,Niu M,et al. Protective effects of tacalcitol against oxidative damage in human epidermal melan?鄄ocytes [J]. Int J Dermatol,2017,56(2):232-238.
[2] Lan WJ,Wang HY,Wei L,et al.Evidence that geniposide abrogates norepinephrine-induced hypopigmentation by the activation of GLP-1R-dependent c-kit receptor signaling in melanocyte [J]. J Ethnopharmacol,2008,118(1):154-158.
[3] Nordlund JJ. Vitiligo:a review of some facts lesser known about depigmentation [J]. Indian J Dermatol,2011,56(2):180-189.
[4] Kaspar JW,Niture SK,Jaiswal AK. Nrf2:INrf2(Keap1)signaling in oxidative stress [J]. Free RadicBiol Med,2009, 47(9):1304-1309.
[5] 丁小媛,乔树芳.中药的抗氧化作用治疗白癜风研究进展[J].中国中西医结合皮肤性病学杂志,2014,13(1):66-68.
[6] 张春艳,许爱娥.治疗白癜风的中药外用制剂总结分析[J]中华中医药学刊,2012,30(9):2074-2077.
[7] 赵润英,郝伟,孟祥军,等.阿魏酸川芎嗪对缺血再灌注大鼠心肌细胞凋亡及凋亡相关蛋白表达的影响[J].中国病理生理杂志,2013,29(12):2139-2143.
[8] 石卫州,杨秀芬,程允相,等.活血化瘀类中药及其有效成分对抗氧化酶的影响[J].时珍国医国药,2013,24(2):284-288.
[9] 李伟,王加志,曲岩,等.阿魏酸调节C-KIT/MITF蛋白表达影响黑素生成的实验研究[J].中国医药导报,2017,14(6):28-31.
[10] 赵晓菲,刘国艳.白癜风氧化应激发病机制的研究进展[J].中国麻风皮肤病杂志,2016,32(3):189-191.
[11] 范英姬,刘志军.白癜风的抗氧化治疗[J].中国麻风皮肤病杂志,2015,31(3):160-163.
[12] 石新荣.白癜风的病因病理及中医治疗研究[J].中外医疗,2011(17):133
[13] 方红.白发症与系统疾病[J].中国医学文摘:皮肤科学,2016,33(4):491-495.
[14] 秦思,温炬,郑荣昌,等.氧化应激反应与白癜风的研究进展[J].现代医院,2014,14(2):13-15.
[15] 李伟,李世远,陆健群,等.白癜风患者皮肤组织液氧化-抗氧化物水平比较分析[J].中国皮肤性病学杂志,2012,26(4):303-305.
[16] 曾洲平,林宝珠,葛天华,等.白癜风患者血清和皮肤提取液中氧化与抗氧化能力的比较研究[J].皮肤病与性病,2015,37(3):140-142.
[17] 陈建萍,钟春燕,康云平,等.白癜风患者血清中抗氧化酶及脂质过氧化物的检测分析[J].中国基层医药,2012, 19(20):3104-3105.
[18] 廖永晖,汤雨,千年松,等.氧化应激与细胞凋亡[J].新乡医学院学报,2011,28(1):110-113.
[19] 田军,朱龙飞,坚哲,等.过氧化氢诱导人黑素细胞氧化应激损伤模型的建立[J].实用皮肤病学杂志,2014,7(6):406-405.
[20] Chen W,Jiang Z,Zhang X,et al. N-acetyl-S-(p-chloro?鄄phenylcarbamoyl)cysteine induces mitochondrial-mediated apoptosis and suppresses migration in melanoma cells [J]. Oncol Rep,2015,34(5):2547-2456. |
|
|
|