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西红花酸酯通过Rho/ROCK/NF-κB信号通路改善心肌缺血。

Crocetin ester improves myocardial ischemia via Rho/ROCK/NF-κB pathway.

作者信息

Huang Zhiheng, Nan Chen, Wang Hanqing, Su Qiang, Xue Wenda, Chen Yanyan, Shan Xin, Duan Jinao, Chen Gang, Tao Weiwei

机构信息

Center for Translational Systems Biology and Neuroscience, School of Basic Biomedical Science, Nanjing University of Chinese Medicine, Nanjing 210023, China.

Medical College of Soochow University, Suzhou 215000, China.

出版信息

Int Immunopharmacol. 2016 Sep;38:186-93. doi: 10.1016/j.intimp.2016.05.025. Epub 2016 Jun 8.

DOI:10.1016/j.intimp.2016.05.025
PMID:27285672
Abstract

Crocetin ester (CE) is the active ingredient of Crocus sativus L. stigmas and Gardenia jasminoides Ellis fruit. The main purpose of the present study was to investigate the protective effect of CE on isoproterenol (ISO)-induced acute myocardial ischemia (AMI) through Rho/ROCK/NF-κB pathway and explore its underlying mechanism. Administration of CE (25 and 50mg/kg) could significantly reduce the serum contents of pro-inflammatory cytokines including tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β) and interleukin-6 (IL-6). In addition, pretreatment with CE attenuated the contents of creatine kinase (CK), malondialdehyde (MDA) and the activities of lactate dehydrogenase (LDH), superoxide dismutase (SOD) in serum. Treatment with CE also improved the histopathological alteration and decreased the ST elevation. Furthermore, CE could ameliorate the cardiac expressions of Cu, Zn-superoxide dismutase (SOD1), MDA5, Rho, ROCK, p-IκB and p-NF-κBp65 in ISO-induced rats. It was assumed that CE might be a new therapeutic candidate for the treatment of AMI possibly through the inhibition of Rho/ROCK/NF-κB pathway.

摘要

西红花酸酯(CE)是藏红花柱头和栀子果实的活性成分。本研究的主要目的是通过Rho/ROCK/NF-κB途径研究CE对异丙肾上腺素(ISO)诱导的急性心肌缺血(AMI)的保护作用,并探讨其潜在机制。给予CE(25和50mg/kg)可显著降低血清中促炎细胞因子的含量,包括肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)和白细胞介素-6(IL-6)。此外,CE预处理可降低血清中肌酸激酶(CK)、丙二醛(MDA)的含量以及乳酸脱氢酶(LDH)、超氧化物歧化酶(SOD)的活性。CE治疗还改善了组织病理学改变并降低了ST段抬高。此外,CE可改善ISO诱导大鼠心脏中铜锌超氧化物歧化酶(SOD1)、MDA5、Rho、ROCK、磷酸化IκB和磷酸化NF-κBp65的表达。推测CE可能是一种通过抑制Rho/ROCK/NF-κB途径治疗AMI的新候选药物。

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