Glaucocalyxin A Ameliorates Myocardial Ischemia-Reperfusion Injury in Mice by Suppression of Microvascular Thrombosis

Liu, Xiaohui; Xu, Dongzhou; Wang, Yuxin; Chen, Ting; Wang, Qi; Zhang, Jian; You, Tao; Zhu, Li

doi:10.12659/msm.898015

Cited by 12 publications

(13 citation statements)

References 34 publications

(42 reference statements)

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“…GLA administration significantly reduces infarct size, improves left ventricular ejection fraction, and left ventricular fractional shortening in mice subjected to myocardial I/R. The protective effect of GLA myocardial I/R injury is proposed to be mediated by the attenuation of microvascular thrombosis 15 . Based on the mechanism investigations, increased production of ROS and ROS-mediated oxidative damage during the I/R process play crucial roles in the development of I/R injury.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, GLA might be an attractive candidate for improving the prognosis of acute MI by controlling cardiac fibrosis 14 . Additionally, GLA was reported to ameliorate myocardial I/R injury in mice through the attenuation of microvascular thrombosis 15 . However, the effects of GLA on I/R-mediated oxidative stress and apoptosis in cardiomyocytes remain unclear.…”

Section: Introductionmentioning

confidence: 99%

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Glaucocalyxin A Protects H9c2 Cells Against Hypoxia/Reoxygenation-Induced Injury Through the Activation of Akt/Nrf2/HO-1 Pathway

et al. 2020

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Myocardial infarction (MI) is one of the most serious cardiovascular diseases associated with myocardial ischemia/reperfusion (I/R) injury. Glaucocalyxin A (GLA) is a biologically active ent-kauranoid diterpenoid that has been found to ameliorate myocardial I/R injury in mice. However, the mechanism has not been fully investigated. In the present study, we aimed to investigate the effect of GLA on rat cardiomyocytes H9c2 cells exposed to hypoxia/reoxygenation (H/R). The results showed that GLA treatment improved cell viability of H/R-stimulated H9c2 cells. Administration with GLA suppressed the H/R-stimulated reactive oxygen species (ROS) production in H9c2 cells. GLA also elevated the activities of antioxidant enzymes, including superoxide dismutase and glutathione peroxidase in H/R-stimulated H9c2 cells. Moreover, GLA prevented H/R-stimulated cell apoptosis in H9c2 cells, as evidenced by increased bcl-2 expression, decreased bax expression, as well as reduced caspase-3 activity. Furthermore, GLA enhanced the activation of protein kinase B (Akt)/nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway in H9c2 cells exposed to H/R. Additionally, treatment with LY294002 reserved the protective effects of GLA on H/R-stimulated oxidative injury in H9c2 cells. In conclusion, these findings suggested that GLA protected H9c2 cells from H/R-stimulated oxidative damage, which was mediated by the Akt/Nrf2/HO-1 signaling pathway. Thus, GLA might be a promising therapeutic agent for the prevention and treatment of myocardial I/R.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Glaucocalyxin A Protects H9c2 Cells Against Hypoxia/Reoxygenation-Induced Injury Through the Activation of Akt/Nrf2/HO-1 Pathway

et al. 2020

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“…Creatine kinase, which located in mitochondria and plasma of tissues including brain tissue, skeletal muscle, and cardiac muscle, is a key kinase correlated with ATP regeneration, intracellular energy transportation and muscle contraction and is widely utilized as a biomarker of myocardial injury [29]. Additionally, an experiment presented that LVEF and LVFS in mice with myocardial I/R injury was improved by treatment [30]. A study revealed that myocardial I/R insult declined LVEF and + dp/dtmax, increased LVEDP, serum CK, LDH, and cTnT levels, also reduced SOD activity and raised MDA level in the myocardial tissue [31].…”

Section: Discussionmentioning

confidence: 99%

LncRNA LINC00461 exacerbates myocardial ischemia-reperfusion injury via microRNA-185-3p/Myd88

Gao

Wang

Fan

et al. 2021

Preprint

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Objective Long non-coding RNA (lncRNA) play critically in myocardial ischemia-reperfusion (I/R) injury. Thus, it was proposed to investigate the mechanism of LINC00461 in the disease through mediating microRNA-185-3p (miR-185-3p)/myeloid differentiation primary response gene 88 (Myd88) axis. Methods Mice with I/R injury were injected with the vectors that altered miR-185-3p and LINC00461 expression. miR-185-3p, LINC00461 and Myd88 expression in mice with I/R injury were measured, as well as cardiac function, hemodynamics, myocardial fibrosis, infarction area, oxidative stress, and cardiomyocyte apoptosis. Results Raised LINC00461 and Myd88 and suppressed miR-185-3p levels were measured in I/R mice. Down-regulating LINC00461 or up-regulating miR-185-3p recovered cardiac function, reduced myocardial collagen hyperplasia, fibrosis and infarction, and attenuated oxidative stress and cardiomyocyte apoptosis in mice with I/R. Conclusion Down-regulation of LINC00461 attenuates myocardial I/R injury via suppressing miR-185-3p-targeted Myd88 expression.

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“…Tumour necrosis factor-α, IL-6, and IL-1β are well-known pro-inflammatory cytokines that are involved in inflammatory responses. 11,13 The results of enzyme-linked immunosorbent assay (ELISA) showed that treatment with H 2 O 2 markedly induced the production of TNFα, IL-6, and IL-1β in HCASMCs; however, this effect was reversed by GLA pretreatment in a dose-dependent manner (Figure 4).…”

Section: Glaucocalyxin a Decreases The Production Of Tumour Necrosimentioning

confidence: 99%

“…Glaucocalyxin A (GLA), an active ent‐kauranoid diterpenoid isolated from Rabdosia japonica var. glaucocalyx , was reported to possess anti‐inflammatory, anti‐tumour, anti‐fibrotic, and cardioprotective activities . In addition, Li et al reported that GLA significantly inhibited platelet activation and thrombus formation.…”

Section: Introductionmentioning

confidence: 99%

Glaucocalyxin A inhibits hydrogen peroxide‐induced oxidative stress and inflammatory response in coronary artery smooth muscle cells

Zhu

Zhang

2020

Clin Exp Pharma Physio

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Atherosclerosis is a complex chronic inflammatory disease that remains one of the leading causes of death and disability worldwide. A previous study reported that glaucocalyxin A (GLA), a natural ent‐Kaurane diterpenoid triptolide, exhibits anti‐atherosclerotic activity. However, the underlying molecular mechanism has not yet been explored. In the present study, we evaluated the anti‐atherosclerotic effect of GLA and the underlying mechanism in vitro. Human coronary artery smooth muscle cells (HCASMCs) were stimulated by hydrogen peroxide (H2O2) to induce oxidative stress and inflammation. The results showed that GLA pretreatment improved the viability of H2O2‐induced HCASMCs. The increased reactive oxygen species production and decreased superoxide dismutase and glutathione peroxidase activities in H2O2‐induced HCASMCs were reversed by GLA pretreatment. In addition, GLA treatment suppressed the H2O2‐induced expression of inducible nitric oxide synthase, NADPH oxidase (NOX) 2, and NOX4 in HCASMCs. Moreover, treatment with GLA reduced the production of several inflammatory cytokines, including tumour necrosis factor‐alpha, interleukin (IL)‐6, and IL‐1β in H2O2‐induced HCASMCs. Furthermore, GLA treatment suppressed the phosphorylation of p38, as well as inactivating the NF‐κB signalling pathway. These findings suggested that GLA protected against H2O2‐induced oxidative stress and inflammation via inhibition of p38 phosphorylation and NF‐κB activation in HCASMCs.

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Glaucocalyxin A Ameliorates Myocardial Ischemia-Reperfusion Injury in Mice by Suppression of Microvascular Thrombosis

Cited by 12 publications

References 34 publications

Glaucocalyxin A Protects H9c2 Cells Against Hypoxia/Reoxygenation-Induced Injury Through the Activation of Akt/Nrf2/HO-1 Pathway

Glaucocalyxin A Protects H9c2 Cells Against Hypoxia/Reoxygenation-Induced Injury Through the Activation of Akt/Nrf2/HO-1 Pathway

LncRNA LINC00461 exacerbates myocardial ischemia-reperfusion injury via microRNA-185-3p/Myd88

Glaucocalyxin A inhibits hydrogen peroxide‐induced oxidative stress and inflammatory response in coronary artery smooth muscle cells

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