Relaxin ameliorates high glucose-induced cardiomyocyte hypertrophy and apoptosis via the Notch1 pathway.
Relaxin ameliorates high glucose-induced cardiomyocyte hypertrophy and apoptosis via the Notch1 pathway.
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松弛素可以通过Notch1途径改善高葡萄糖诱导的心肌细胞肥大和凋亡。
DOI：
10.3892/etm.2017.5448
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发表时间：
2018-01
影响因子：
2.7
通讯作者：
Xiao H
中科院分区：
文献类型：
--
作者：
Wei X;Yang Y;Jiang YJ;Lei JM;Guo JW;Xiao H
本研究旨在探讨松弛素（RLX）在高糖（HG）诱导的心肌细胞肥大和凋亡中的作用及其可能的分子机制。将H9 c2细胞暴露于33 mmol/l HG（含或不含RLX（100 nmol/ml））。检测心肌细胞活力、凋亡、氧化应激、细胞肥大以及Notch 1、hes 1、心钠素（ANP）、脑钠素（BNP）、锰超氧化物歧化酶（MnSOD）、细胞色素C和caspase-3的水平。与HG组相比，RLX能显著提高H9 c2细胞的存活率，并呈时间和剂量依赖性，同时能显著减少H9 c2细胞的凋亡。RLX还能显著抑制活性氧和丙二醛的生成，提高SOD活性。此外，与正常组相比，HG组ANP、BNP、细胞色素C和caspase-3水平升高，Notch 1、hes 1和MnSOD水平降低。然而，Notch抑制剂DAPT几乎取消了RLX的保护作用。这些结果表明，RLX保护心肌细胞从HG诱导的肥大和凋亡部分通过Notch 1依赖的途径，这可能与减少氧化应激。
The present study aimed to investigate the role of relaxin (RLX) on high glucose (HG)-induced cardiomyocyte hypertrophy and apoptosis, as well as the possible molecular mechanism. H9c2 cells were exposed to 33 mmol/l HG with or without RLX (100 nmol/ml). Cell viability, apoptosis, oxidative stress, cell hypertrophy and the levels of Notch1, hairy and enhancer of split 1 (hes1), atrial natriuretic polypeptide (ANP), brain natriuretic peptide (BNP), manganese superoxide dismutase (MnSOD), cytochrome C and caspase-3 were assessed in cardiomyocytes. Compared with the HG group, the viability of H9c2 cells was increased by RLX in a time- and dose-dependent manner, and was accompanied with a significant reduction in apoptosis. Furthermore, RLX significantly suppressed the formation of reactive oxygen species and malondialdehyde, and enhanced the activity of SOD. In addition, the levels of ANP, BNP, cytochrome C and caspase-3 were increased and Notch1, hes1 and MnSOD were inhibited in the HG group compared with those in the normal group. However, the Notch inhibitor DAPT almost abolished the protective effects of RLX. These results suggested that RLX protected cardiomyocytes from HG-induced hypertrophy and apoptosis partly through a Notch1-dependent pathway, which may be associated with reducing oxidative stress.
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DOI：
10.1042/cs20130105
发表时间：
2013-12
期刊：
Clinical science (London, England : 1979)
影响因子：
--
作者：
Bitto A;Irrera N;Minutoli L;Calò M;Lo Cascio P;Caccia P;Pizzino G;Pallio G;Micali A;Vaccaro M;Saitta A;Squadrito F;Altavilla D
通讯作者：
Altavilla D
DOI：
10.2147/dmso.s30968
发表时间：
2013
期刊：
Diabetes, metabolic syndrome and obesity : targets and therapy
影响因子：
--
作者：
Chavali V;Tyagi SC;Mishra PK
通讯作者：
Mishra PK
影响因子：
24.3
作者：
Dabral, Swati;Tian, Xia;Schermuly, Ralph Theo
通讯作者：
Schermuly, Ralph Theo
影响因子：
20.1
作者：
Urbanek K;Cabral-da-Silva MC;Ide-Iwata N;Maestroni S;Delucchi F;Zheng H;Ferreira-Martins J;Ogórek B;D'Amario D;Bauer M;Zerbini G;Rota M;Hosoda T;Liao R;Anversa P;Kajstura J;Leri A
通讯作者：
Leri A
影响因子：
9.5
作者：
Pei, Haifeng;Yu, Qiujun;Tao, Ling
通讯作者：
Tao, Ling