The Preconditioning of Berberine Suppresses Hydrogen Peroxide-Induced Premature Senescence via Regulation of Sirtuin 1.
The Preconditioning of Berberine Suppresses Hydrogen Peroxide-Induced Premature Senescence via Regulation of Sirtuin 1.
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小檗碱预处理通过调节 Sirtuin 1 抑制过氧化氢诱导的过早衰老
DOI：
10.1155/2017/2391820
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发表时间：
2017
影响因子：
--
通讯作者：
Zhu W
中科院分区：
文献类型：
--
作者：
Zhu X;Yue H;Guo X;Yang J;Liu J;Liu J;Wang R;Zhu W
黄连素（BBR）在中药中的应用历史悠久，对2型糖尿病、动脉粥样硬化等老年性疾病具有一定的保健作用。然而，BBR的抗老化机理尚不完全清楚。采用过氧化氢（H2 O2-）诱导的人二倍体成纤维细胞（HDFs）早衰模型，通过衰老相关β-半乳糖苷酶（SA-β-gal）测定，发现低浓度BBR预处理可对抗HDFs的早衰，并伴有线粒体膜电位的降低和细胞内活性氧（ROS）的产生。此外，低浓度的BBR预处理可以使细胞对随后的H2 O2诱导的细胞周期阻滞和生长抑制的敏感性降低。实验结果进一步表明，低浓度的BBR可以诱导ROS的轻微增加，并上调sirtuin 1（SIRT 1）的表达水平，一个重要的长寿调节因子。BBR预处理后，H2 O2诱导的Chk 2激活明显减弱。提示低浓度BBR预处理可能通过调节SIRT 1对某些衰老相关疾病中氧化应激引起的细胞衰老具有促分裂作用。
With a long history of application in Chinese traditional medicine, berberine (BBR) was reported to exhibit healthspan-extending properties in some age-related diseases, such as type 2 diabetes and atherosclerosis. However, the antiaging mechanism of BBR is not completely clear. By means of hydrogen peroxide- (H2O2-) induced premature cellular senescence model, we found that a low-concentration preconditioning of BBR could resist premature senescence in human diploid fibroblasts (HDFs) measured by senescence-associated β-galactosidase (SA-β-gal), accompanied by a decrease in loss of mitochondrial membrane potential and production of intracellular reactive oxygen species (ROS). Moreover, the low-concentration preconditioning of BBR could make cells less susceptible to subsequent H2O2-induced cell cycle arrest and growth inhibition. Experimental results further showed that the low concentration of BBR could induce a slight increase of ROS and upregulate the expression level of sirtuin 1 (SIRT1), an important longevity regulator. H2O2-induced activation of checkpoint kinase 2 (Chk2) was significantly attenuated after the preconditioning of BBR. The present findings implied that the low-concentration preconditioning of BBR could have a mitohormetic effect against cellular senescence triggered by oxidative stress in some age-related diseases through the regulation of SIRT1.
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DOI：
10.18632/aging.100521
发表时间：
2012-12
期刊：
Aging
影响因子：
--
作者：
Halicka HD;Zhao H;Li J;Lee YS;Hsieh TC;Wu JM;Darzynkiewicz Z
通讯作者：
Darzynkiewicz Z
影响因子：
4.8
作者：
Lan, Fan;Cacicedo, Jose M.;Ido, Yasuo
通讯作者：
Ido, Yasuo
DOI：
10.1073/pnas.92.20.9363
发表时间：
1995-09-26
影响因子：
11.1
作者：
DIMRI, GP;LEE, XH;CAMPISI, J
通讯作者：
CAMPISI, J
影响因子：
5.4
作者：
Gao, N.;Zhao, T-Y;Li, X-J
通讯作者：
Li, X-J
DOI：
10.1016/0005-2728(83)90122-6
发表时间：
1983-01-01
期刊：
BIOCHIMICA ET BIOPHYSICA ACTA
影响因子：
--
作者：
MIKES, V;DADAK, V
通讯作者：
DADAK, V