Gentianella acuta prevents acute myocardial infarction induced by isoproterenol in rats via inhibition of galectin-3/TLR4/MyD88/NF-кB inflammatory signalling
- 30 April 2020
- journal article
- research article
- Published by Springer Science and Business Media LLC in Inflammopharmacology
- Vol. 29 (1), 205-219
- https://doi.org/10.1007/s10787-020-00708-4
Abstract
Gentianella acuta (G. acuta), as a folk medicine, was used to treat heart disease by the Ewenki people in Inner Mongolia. However, the effect of G. acuta on acute myocardial infarction (AMI) is not clear. To explore the mechanisms of G. acuta on isoproterenol (ISO)-induced AMI, rats were administered G. acuta for 28 days, then injected intraperitoneally with ISO (85 mg/kg) on days 29 and 30. An electrocardiogram helped to evaluate the myocardial injury. Serum lactate dehydrogenase (LDH), creatinine kinase (CK) and aspartate aminotransferase (AST) levels were evaluated, and haematoxylin eosin, Masson’s trichrome staining and terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) staining were used to detect myocardial histological changes. Radioimmunoassay was used to measure serum tumour necrosis factor alpha (TNFα) and interleukin (IL)-6. An enzyme-linked immunosorbent assay kit was used to analyse serum galectin-3 (Gal-3) levels. Immunohistochemistry, Western blotting and reverse transcription polymerase chain reaction were used to examine relevant molecular events. The results revealed that pre-treatment with G. acuta decreased the elevation in the ST segment; reduced serum LDH, CK and AST levels; alleviated cardiac structure disorder; and reduced inflammatory infiltration, abnormal collagen deposition and cardiomyocyte apoptosis that were induced by ISO. Furthermore, pre-treatment with G. acuta inhibited serum Gal-3 levels and Gal-3 expression in heart tissue, and also impeded TLR4/MyD88/NF-кB signalling activation, which ultimately prevented the expression of inflammatory cytokines. The study indicated that pre-treatment with G. acuta protects against ISO-induced AMI, and the protective role may be related to inhibiting Gal-3/TLR4/MyD88/NF-кB inflammatory signalling.Funding Information
- National Natural Science Foundation of China (81573698, 31271466)
- Project of Enhance Scientific Research Capability of Hebei University of Chinese Medicine (3010105231040)
- Project of Basic Scientific Research of Provincial Colleges and Universities of Hebei University of Chinese Medicine (YJZ2019008)
This publication has 38 references indexed in Scilit:
- HIF-1α promotes the keloid development through the activation of TGF-β/Smad and TLR4/MyD88/NF-κB pathwaysCell Cycle, 2019
- Ameliorative effects of cerebrolysin against isoproterenol-induced myocardial injury in male ratsLife Sciences, 2019
- Cardioprotective effects of cerebrolysin on the lesion severity and inflammatory factors in a rat model of isoproterenol-induced myocardial injuryPharmacological Reports, 2019
- Fisetin attenuates isoproterenol-induced cardiac ischemic injury in vivo by suppressing RAGE/NF-κB mediated oxidative stress, apoptosis and inflammationPhytomedicine, 2018
- Thyroid hormones decrease the proinflammatory TLR4/NF-κβ pathway and improve functional parameters of the left ventricle of infarcted ratsMolecular and Cellular Endocrinology, 2018
- Bioactive Constituents from the Whole Plants of Gentianella acuta (Michx.) HultenMolecules, 2017
- Cardioprotective effects of timosaponin B II from Anemarrhenae asphodeloides Bge on isoproterenol-induced myocardial infarction in ratsChemico-Biological Interactions, 2015
- Downregulating galectin-3 inhibits proinflammatory cytokine production by human monocyte-derived dendritic cells via RNA interferenceCellular Immunology, 2015
- The regulation of inflammation by galectin‐3Immunological Reviews, 2009
- The role of IL-6 and STAT3 in inflammation and cancerEuropean Journal of Cancer, 2005