Thalidomide as a Potent Inhibitor of Neointimal Hyperplasia After Balloon Injury in Rat Carotid Artery

Park, Seung Jung; Kim, Hyo Soo; Yang, Han Mo; Park, Kyung Woo; Youn, Seock Won; Jeon, Soo In; Kim, Dae–Hee; Koo, Bon Kwon; Chae, In Ho; Choi, Dong Joo; Oh, Byung Hee; Lee, Myoung Mook; Park, Young Bae

doi:10.1161/01.atv.0000124924.21961.c3

Cited by 23 publications

(9 citation statements)

References 34 publications

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“…In this study, the anti-inflammatory and immunomodulatory effects of thalidomide were confirmed through suppression of local and systemic cytokines, particularly TNF-α, IL-1β, and IL-6. These findings are in agreement with other studies that showed that this drug has the ability to downregulate many cytokines 13 , 16 , 22 , 23 . For example, thalidomide enhances the degradation of TNF-α mRNA, thus reducing the release of this proinflammatory cytokine from endotoxin-stimulated macrophages 35 .…”

Section: Discussionsupporting

confidence: 93%

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Immunomodulatory effects of thalidomide in an experimental brain death liver donor model

Santana

Andraus

Silva

et al. 2021

Sci Rep

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Brain death is characterized by a generalized inflammatory response that results in multiorgan damage. This process is mainly mediated through cytokines, which amplify graft immunogenicity. We investigated the immunological response in a brain death liver donor model and analysed the effects of thalidomide, a drug with powerful immunomodulatory properties. Brain death was induced in male Lewis rats. We studied three groups: Control (sham-operated rats in which trepanation was performed without inserting the balloon catheter), BD (rats subjected to brain death by increasing intracranial pressure) and BD + Thalid (BD rats receiving thalidomide after brain death). After 6 h, serum levels of AST, ALT, LDH, and ALP as well as systemic and hepatic levels of TNF-α, IL1-β, IL-6, and IL-10 were analysed. We also determined the mRNA expression of MHC Class I and Class II, NF-κB, and macrophage infiltration. NF-κB was also examined by electrophoretic mobility shift assay. Thalidomide treatment significantly reduced serum levels of hepatic enzymes and TNF-α, IL-1-β, and IL-6. These cytokines were evaluated at either the mRNA expression or protein level in liver tissue. In addition, thalidomide administration resulted in a significant reduction in macrophages, MHC Class I and Class II, and NF-κB activation. This study reveals that thalidomide significantly inhibited the immunologic response and graft immunogenicity, possibly through suppression of NF-κB activation.

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Section: Discussionsupporting

confidence: 93%

“…For the first time, animals subjected to BD were treated with thalidomide, a drug with powerful anti-inflammatory and immunomodulatory effects 22 , 23 . The present study used rats in a BD donor model to investigate the immunological mechanisms involved in this process.…”

Section: Discussionmentioning

confidence: 99%

Immunomodulatory effects of thalidomide in an experimental brain death liver donor model

Santana

Andraus

Silva

et al. 2021

Sci Rep

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“…Moreover, vascular TNF␣ protein levels are decreased upon local thalidomide administration, suggesting that the decrease in neointima formation is due to inhibition of TNF␣ biosynthesis in the injured vessel wall. Recently, Park et al showed a significant reduction in neointima formation and proliferative activity of VSMCs by orally administered thalidomide after carotid artery denudation in Sprague-Dawley rats (27). These results are in concordance with ours.…”

Section: Discussionsupporting

confidence: 91%

Tumor necrosis factor‐α plays an important role in restenosis development

et al. 2005

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Genetic factors appear to be important in the restenotic process after percutaneous coronary intervention (PCI), as well as in inflammation, a pivotal factor in restenosis. TNFalpha, a key regulator of inflammatory responses, may exert critical influence on the development of restenosis after PCI. The GENetic DEterminants of Restenosis (GENDER) project included 3104 patients who underwent a successful PCI. Systematic genotyping for six polymorphisms in the TNFalpha gene was performed. The role of TNFalpha in restenosis was also assessed in ApoE*3-Leiden mice, TNFalpha knockout mice, and by local delivery of a TNFalpha biosynthesis inhibitor, thalidomide. The -238G-1031T haplotype of the TNFalpha gene increased clinical and angiographic risk of restenosis (P=0.02 and P=0.002, respectively). In a mouse model of reactive stenosis, arterial TNFalpha mRNA was significantly time-dependently up-regulated. Mice lacking TNFalpha or treated locally with thalidomide showed a reduction in reactive stenosis (P=0.01 and P=0.005, respectively). Clinical and preclinical data indicate that TNFalpha plays an important role in restenosis. Therefore, TNFalpha genotype may be used as a risk marker for restenosis and may contribute to individual patient screening prior to PCI in clinical practice. Inhibition of TNFalpha may be an anti-restenotic target strategy.

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“…40 Likewise, the anti-inflammatory effect of thalidomide was also found in influenza A (H1N1) virus-induced pulmonary injury in mice by reducing the secretion of pro-inflammatory cytokines. 41 In addition, bGFG is the mostly studied fibrosis-related factor, 42,43 and PQ has been reported to enhance bGFG expression and promote fibrosis in rat lungs, 44 while thalidomide has been reported to inhibit bFGF expression in rats, 45 which was partially in line with our findings. Moreover, considering the teratogenicity 9 and potential side-effects of thalidomide, specifically, rats and cells were treated with thalidomide alone, and it was found that alone administration of thalidomide did not affect the lungs and cells.…”

Section: Discussionsupporting

confidence: 88%

Thal protects against paraquat‐induced lung injury through a microRNA‐141/HDAC6/IκBα‐NF‐κB axis in rat and cell models

Zheng

Zhu

Zhang

et al. 2020

Basic Clin Pharma Tox

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Paraquat (1,1-dichloro-4,4-bipyridine, PQ) is a widely used herbicide in agriculture and with extremely potent toxicity that leads to serious public health problem once misused. By accidental or voluntary ingestion, PQ poisoning results in numerous deaths annually, mainly in developing countries where PQ is more largely used. 2 In oral ingestion cases, the mortality rate is over 90%. 3 PQ poisoning through oral, skin and respiratory tracts contributes to multiple organ failure including lungs, kidneys, liver and nervous system, in which the lung is the primary target organ. 4,5 This phenomenon was attributed to high affinity of PQ to alveolar cells. 6 Therefore, PQ poisonings usually cause acute lung injury and, ultimately, acute respiratory distress syndrome and death. 7 Unfortunately, despite the large volume of studies in the past

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Thalidomide as a Potent Inhibitor of Neointimal Hyperplasia After Balloon Injury in Rat Carotid Artery

Cited by 23 publications

References 34 publications

Immunomodulatory effects of thalidomide in an experimental brain death liver donor model

Immunomodulatory effects of thalidomide in an experimental brain death liver donor model

Tumor necrosis factor‐α plays an important role in restenosis development

Thal protects against paraquat‐induced lung injury through a microRNA‐141/HDAC6/IκBα‐NF‐κB axis in rat and cell models

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