Gambogic acid exerts cardioprotective effects in a rat model of acute myocardial infarction through inhibition of inflammation, iNOS and NF‑κB/p38 pathway

Duan, Na; Hou, Ai-jie; Liu, Bo; Miao, Zhimin; Yuan, Long

doi:10.3892/etm.2017.5599

Cited by 4 publications

(3 citation statements)

References 29 publications

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“…p38 has also been linked to cardiac inflammation through its promotion of the expression of regenerating islet-derived 3γ (Reg3γ), a protein associated with cardiac inflammatory signaling [ 70 ]. Moreover, treatment with the anti-inflammatory compound gamboge protects against infarction-induced inflammation by targeting the NF-κB–p38 pathway [ 71 ]. p38α activation is also associated with increased fibrosis during ischemia-induced cardiac remodeling [ 72 ].…”

Section: P38 In Ischemia–reperfusion Injurymentioning

confidence: 99%

p38 MAPK Pathway in the Heart: New Insights in Health and Disease

Romero-Becerra

Santamans

Folgueira

et al. 2020

IJMS

102

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The p38 mitogen-activated kinase (MAPK) family controls cell adaptation to stress stimuli. p38 function has been studied in depth in relation to cardiac development and function. The first isoform demonstrated to play an important role in cardiac development was p38α; however, all p38 family members are now known to collaborate in different aspects of cardiomyocyte differentiation and growth. p38 family members have been proposed to have protective and deleterious actions in the stressed myocardium, with the outcome of their action in part dependent on the model system under study and the identity of the activated p38 family member. Most studies to date have been performed with inhibitors that are not isoform-specific, and, consequently, knowledge remains very limited about how the different p38s control cardiac physiology and respond to cardiac stress. In this review, we summarize the current understanding of the role of the p38 pathway in cardiac physiology and discuss recent advances in the field.

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Section: P38 In Ischemia–reperfusion Injurymentioning

confidence: 99%

p38 MAPK Pathway in the Heart: New Insights in Health and Disease

Romero-Becerra

Santamans

Folgueira

et al. 2020

IJMS

102

View full text Add to dashboard Cite

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“…Gambogic acid (GA), one of the major active ingredients extracted from Chinese medicine gamboges resin, is reported to possess antioxidant, antiinflammatory, and widespread anticancer activities with acceptable side effects (Na, Aijie, Bo, Zhilin, & Long, ; Wei et al, ; Yang & Chen, ). GA is capable of suppressing the growth of a variety of different tumors, such as lung, liver, and prostate cancers (Gu et al, ; Lu et al, ).…”

Section: Introductionmentioning

confidence: 99%

Gambogic acid impairs tumor angiogenesis by targeting YAP/STAT3 signaling axis

Wan

Zhang

Wang

et al. 2019

Phytotherapy Research

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Angiogenesis is central to a wide range of physiological and pathological processes including wound healing, macular degeneration, and cancer. Excessive or inappropriate vascular supply of tumors is one of the main targets for cancer therapy. Recently, critical and selective transcriptional factors such as yes‐associated protein (YAP) that control the expression of angiogenesis factors have gained increasing attention in antiangiogenic therapy. In this study, we have identified and characterized a novel inhibitor of YAP, gambogic acid (GA), which exerted striking antiangiogenic effects both in vitro and in vivo. We demonstrated that GA remarkably inhibited a variety of vascular endothelial growth factor‐induced angiogenesis processes including proliferation, migration, sprouting, and tube formation of endothelial cells in vitro. In addition, GA resulted in decreased neo‐vessel formation in Matrigel plugs of mice and chick chorioallantoic membrane. More importantly, we showed that GA limited tumor growth via preventing tumor angiogenesis and vascular maturation. Further mechanistic studies illustrated that GA directly targeted YAP/STAT3 signaling axis, which is critical for the transcriptional regulation of a series of angiogenic factors. Taken together, these preclinical findings suggest that GA significantly repressed tumor angiogenesis and may serve as a promising drug candidate against cancer.

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“…Myocardial apoptosis induced by AMI may be related to the activation or inhibition of signaling pathways. Na et al has demonstrated that gambogic acid protects against myocardial damage in MI rats by activating NF-κB and p38 pathways [ 16 ]. Liu et al have found that inhibition of AMPK aggravated cell injury in OGD-mediated cardiomyocytes [ 17 ].…”

Section: Introductionmentioning

confidence: 99%

SERPINB1 overexpression protects myocardial damage induced by acute myocardial infarction through AMPK/mTOR pathway

Wang¹,

Hua

Chen

et al. 2022

BMC Cardiovasc Disord

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Background SERPINB1 is involved in the development of a variety of diseases. The purpose of this study was to explore the effect of SERPINB1 on acute myocardial infarction (AMI). Methods Serum SERPINB1 level of AMI patients was measured for receiver operating characteristic curve analysis. The AMI rat model was constructed to observe myocardial damage, and the H9C2 cell oxygen glucose deprivation (OGD) model was constructed to detect cell viability. Transthoracic echocardiography was used to assess the cardiac function. TTC staining and HE staining were used to detect pathologic changes of myocardial tissues. The apoptosis of myocardial tissues and cells were measured by TUNLE staining and flow cytometry assay. CCK-8 assay to measure cell viability. SERPINB1 expression was measured by qRT-PCR. Protein expression was measured by western blot. Results The serum SERPINB1 level was down-regulated in AMI patients. AMI modeling reduced the SERPINB1 expression level, induced inflammatory cells infiltrated, and myocardial apoptosis. OGD treatment inhibited cell viability and promoted apoptosis. The AMPK/mTOR pathway was inhibited in AMI rats and OGD-treated H9C2 cells. Overexpression of SERPINB1 reduced infarct size and myocardial apoptosis of AMI rats, inhibited apoptosis of H9C2 cells, and activated AMPK/mTOR pathway. However, AMPK inhibitor Dorsomorphin reversed the protective effect of SERPINB1 on myocardial cells. Conclusion SERPINB1 overexpression relieved myocardial damage induced by AMI via AMPK/mTOR pathway.

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Gambogic acid exerts cardioprotective effects in a rat model of acute myocardial infarction through inhibition of inflammation, iNOS and NF‑κB/p38 pathway

Cited by 4 publications

References 29 publications

p38 MAPK Pathway in the Heart: New Insights in Health and Disease

p38 MAPK Pathway in the Heart: New Insights in Health and Disease

Gambogic acid impairs tumor angiogenesis by targeting YAP/STAT3 signaling axis

SERPINB1 overexpression protects myocardial damage induced by acute myocardial infarction through AMPK/mTOR pathway

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