Cardioprotective Effect of Glycyrrhizin on Myocardial Remodeling in Diabetic Rats.
Cardioprotective Effect of Glycyrrhizin on Myocardial Remodeling in Diabetic Rats.
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DOI：
10.3390/biom11040569
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发表时间：
2021-04-13
期刊：
影响因子：
5.5
通讯作者：
Chattopadhyay M
中科院分区：
文献类型：
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作者：
Thakur V;Alcoreza N;Delgado M;Joddar B;Chattopadhyay M
心肌纤维化是长期糖尿病的主要并发症之一。高血压引起的心肌细胞萎缩是糖尿病心脏常见的病理生理指标。本研究旨在观察白藜芦醇苷（GLC）对糖尿病大鼠心肌损伤的保护作用，并评价GLC的抗炎和抗纤维化作用。我们的研究表明，高血糖可加重糖尿病动物的心脏萎缩。在糖尿病发展后8-12周，评价2型糖尿病肥胖大鼠和瘦对照大鼠的心脏损伤和炎症。蛋白质印迹和免疫组化研究表明，糖尿病心脏的间隙连接蛋白连接蛋白-43（CX43）、心脏损伤标记物肌钙蛋白I、心肌特异性电压门控钠通道NaV1.5发生显着改变。此外，在糖尿病心脏中，晚期糖基化终产物的氧化应激介体受体（oxidative stress mediator receptor for advanced glycation end-products，ERK）以及炎症介体磷酸化p38 MAPK和趋化因子受体CXCR 4增加，而核因子红细胞2相关因子2（nuclear factor erythroid-2-related factor 2，Nrf 2）的表达减少，Nrf 2是保护免受氧化损伤的抗氧化蛋白。我们还观察到多效性细胞因子转化生长因子β（TGF-β）在糖尿病心脏中的表达增加。GLC处理后磷酸化p38 MAPK、TGF-β、NaV1.5的表达降低，CX43、CXCR 4、Nrf 2和肌钙蛋白I的表达也发生改变。提示GLC对糖尿病心肌萎缩具有保护作用，其机制可能与激活Nrf 2、抑制CXCR 4/SDF 1和TGF-β/p38 MAPK信号通路有关。
Myocardial fibrosis is one of the major complications of long-term diabetes. Hyperglycemia induced cardiomyocyte atrophy is a frequent pathophysiological indicator of diabetic heart. The objective of this study was to investigate the cardioprotective effect of glycyrrhizin (GLC) on myocardial damage in diabetic rats and assess the anti-inflammatory and anti-fibrotic effect of GLC. Our study demonstrates that hyperglycemia can elevate cardiac atrophy in diabetic animals. Type 2 diabetic fatty and the lean control rats were evaluated for cardiac damage and inflammation at 8–12 weeks after the development of diabetes. Western blot and immunohistochemical studies revealed that gap junction protein connexin-43 (CX43), cardiac injury marker troponin I, cardiac muscle specific voltage gated sodium channel NaV1.5 were significantly altered in the diabetic heart. Furthermore, oxidative stress mediator receptor for advanced glycation end-products (RAGE), as well as inflammatory mediator phospho-p38 MAPK and chemokine receptor CXCR4 were increased in the diabetic heart whereas the expression of nuclear factor erythroid-2-related factor 2 (Nrf2), the antioxidant proteins that protect against oxidative damage was reduced. We also observed an increase in the expression of the pleiotropic cytokine, transforming growth factor beta (TGF-β) in the diabetic heart. GLC treatment exhibited a decrease in the expression of phospho-p38 MAPK, RAGE, NaV1.5 and TGF-β and it also altered the expression of CX43, CXCR4, Nrf2 and troponin I. These observations suggest that GLC possesses cardioprotective effects in diabetic cardiac atrophy and that these effects could be mediated through activation of Nrf2 and inhibition of CXCR4/SDF1 as well as TGF-β/p38MAPK signaling pathway.
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DOI：
10.3109/08977194.2011.595714
发表时间：
2011-10
期刊：
Growth factors (Chur, Switzerland)
影响因子：
--
作者：
Biernacka A;Dobaczewski M;Frangogiannis NG
通讯作者：
Frangogiannis NG
影响因子：
3.7
作者：
Lancefield TF;Patel SK;Freeman M;Velkoska E;Wai B;Srivastava PM;Horrigan M;Farouque O;Burrell LM
通讯作者：
Burrell LM
影响因子：
4.3
作者：
Liang, Bo;Guo, Xiao-Ling;Feng, Zheng-Quan
通讯作者：
Feng, Zheng-Quan
影响因子：
2.7
作者：
Cai, Xiangna;Wang, Xin;Chen, Shuying
通讯作者：
Chen, Shuying
影响因子：
2.5
作者：
Alonzo M;Delgado M;Cleetus C;Kumar SA;Thakur V;Chattopadhyay M;Joddar B
通讯作者：
Joddar B