Celastrol inhibits IL-1β-induced inflammation in orbital fibroblasts through the suppression of NF-κB activity

Li, Hong; Yuan, Ya-xiang; Zhang, Yali; He, Qianwen; Xu, Rui‐hua; F, Ge; Wu, Chunxiao

doi:10.3892/mmr.2016.5570

Cited by 22 publications

(27 citation statements)

References 44 publications

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“…In the present study, our results displayed that celastrol treatment significantly decreased mRNA and protein expression of TNF-α and IL-1β in myocardial cells in the condition of H/R. These results are consistent with results of other studies founding that celastrol reduced TNF-β in lung infiltration model and inhibited IL-1β-induced inflammation in orbital fibroblasts ( 25 , 26 ). Therefore, we suggested that celastrol attenuated MIRI by relieving TNF-α- and IL-1β-mediated inflammatory damage to cardiomyocytes.…”

Section: Discussionsupporting

confidence: 93%

Protective effect of celastrol on myocardial ischemia–reperfusion injury

Li¹,

Wu²,

Zou³

et al. 2017

Anatol J Cardiol

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Objective:Celastrol, a major active constituent of Tripterygium wilfordii, has antioxidant, anti-inflammatory, and anticancer effects. However, whether celastrol can exert protective effect on myocardial ischemia–reperfusion injury (MIRI) is unknown. The aim of this study was to test the protective effect of celastrol on MIRI and elucidate its underlying mechanism.Methods:Cardiomyocytes (H9c2 cells) were subjected to hypoxia for 8 h followed by reoxygenation for 4 h to create hypoxia/reoxygenation (H/R) model, an in vitro MIRI model. Celastrol was added to the medium 60 min before the H/R process. Cell viability was detected using MTT assay. Myocardial injury was evaluated by measuring lactate dehydrogenase (LDH) and creatine kinase MB isoenzyme (CK-MB) activity. Changes in mRNA and protein expression of TNF-α, IL-1β, and nuclear factor-KB (NF-KB) were measured with RT-qPCR assay and western blot analysis.Results:Results showed that low-dose celastrol (20 and 50 nM) treatment significantly increased cell viability and decreased LDH and CK-MB activity in the condition of H/R, but high-dose celastrol (200 and 400 nM) resulted in extra injury to cardiomyocytes. Moreover, treatment with 50 nM celastrol significantly downregulated mRNA and protein expression of TNF-α and IL-1β. Meanwhile, NF-KB mRNA and protein in the nucleus were also correspondingly reduced.Conclusion:Our study demonstrated that low-dose celastrol could prevent MIRI in cardiomyocytes by inhibiting the activation of NF-KB, and celastrol may be a potential therapeutic agent for preventing MIRI.

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Section: Discussionsupporting

confidence: 93%

Protective effect of celastrol on myocardial ischemia–reperfusion injury

Li¹,

Wu²,

Zou³

et al. 2017

Anatol J Cardiol

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“…Additionally, Celastrol displays considerable anti-inflammatory activity (De Seabra Rodrigues Dias et al, 2017 ; Zhang et al, 2018 ) and can inhibit cellular inflammation by suppressing NLRP3 activity (Yu et al, 2017 ). Celastrol can also inhibit inflammation by inhibiting the expression of interleukin (IL)-1β (Li et al, 2016b ). Although the anti-inflammatory effects of Celastrol have been studied in many diseases, there are no reports of its anti-inflammatory effects or its molecular mechanisms in COPD.…”

Section: Introductionmentioning

confidence: 99%

Celastrol Alleviates Chronic Obstructive Pulmonary Disease by Inhibiting Cellular Inflammation Induced by Cigarette Smoke via the Ednrb/Kng1 Signaling Pathway

et al. 2018

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Chronic obstructive pulmonary disease (COPD) is a debilitating disease caused by chronic exposure to cigarette smoke (CS). Celastrol is a pentacyclic triterpenoid compound exhibits potent antioxidant and anti-inflammatory activities. Also it is presently known to protect against liver damage induced by type II diabetes. However, its role in COPD is unclear. In this study, we investigated the effects of Celastrol on cellular inflammation in mice exposed to CS and Beas-2B cells treated with CS extract (CSE). C57BL/6 mice and Beas-2B cells were randomly divided into three groups: control group, COPD or CSE group, and Celastrol treatment group. The COPD mice models were subjected to smoke exposure and cell models were treated with CSE. Bioinformatics analysis was performed to identify differentially expressed genes following treatment with Celastrol in COPD, the molecular networks was mapped by Cytoscape. The levels of inflammatory cytokinesinterleukin-8, tumor necrosis factor α, monocyte chemoattractant protein-1, and oxidative stress factors superoxide dismutase and catalase were measured by enzyme-linked immunosorbent assay. Hematoxylin and eosin staining to detect the injury of mouse lung tissue. mRNA and protein levels of Ednrb and Kng1 in the tissues and cells were measured by quantitative polymerase chain reaction (PCR) and western blotting, respectively. Apoptosis was measured by flow cytometry and TUNEL staining. Compared to mice in the COPD group, mice treated with Celastrol had significantly reduced levels of inflammatory cytokines interleukin-8, tumor necrosis factor α and monocyte chemoattractant protein-1 in the serum and bronchoalveolar lavage fluid, and significantly increased levels of oxidative stress factors superoxide dismutase and catalase. The same results were obtained at the cellular level using Beas-2B cells. Compared to the model groups, Celastrol reduced lung injury in mice and significantly reduced cellular apoptosis. Bioinformatics analysis showed that Ednrb is a target gene of Celastrol and differentially expressed in COPD. Quantitative PCR analysis showed that Ednrb expression in patients with COPD was significantly increased compared to that in healthy controls. Additionally, Celastrol effectively reduced Ednrb/Kng1 expression in both cell and animal models. Celastrol has a therapeutic effect on COPD and may alleviate COPD by inhibiting inflammation development by suppressing the Ednrb/Kng1 signaling pathway.

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“…Hyperthyroidism patients who met the surgical indications were enrolled in the study. Diagnostic criteria for hyperthyroidism or clinical manifestations of patients with hyperthyroidism were: Hyperphagia, intolerance of heat, palpitations, agitation and other high metabolic syndrome, exophthalmos and varying degrees of goiter ( 6 – 8 ), laboratory tests show high levels of free triiodothyronine FT3 or free thyroid hormone FT4, decreased thyroid hormone TSH levels and anti-thyroid antibody-positive. Indications for surgical treatment for hyperthyroidism: Long-term use of drugs with poor results; secondary hyperthyroidism caused by other factors, moderate or beyond primary hyperthyroidism; hyperthyroidism with oppression; recurrence after drug treatment; bone marrow suppression and other toxic response.…”

Section: Methodsmentioning

confidence: 99%

A retrospective analysis of 1,231 patients with anemia after surgical treatment of hyperthyroidism

Shen

Zhu

et al. 2018

Exp Ther Med

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This study retrospectively analyzed the clinical and pathological data of 1,231 patients affected by anemia after surgical treatment of hyperthyroidism to explore the influencing factors of anemia after surgical treatment of hyperthyroidism. The clinical data of 1,231 patients affected by anemia after surgical treatment of hyperthyroidism from 1987 to 2017 were analyzed. Clinical data included the surgery methods, sex, age and pathological types. SPSS 22.0 statistical software was used for all statistical analyses. Correlation analyses were performed by using logistic regression analysis, and other enumeration data were subjected to χ2 test. p<0.05 was considered to be statistically significant. The occurrence of anemia after surgical treatment of hyperthyroidism was significantly correlated with age and pathological types (p<0.05). Correlation analysis also showed that age and pathological types were significantly correlated with the occurrence of anemia after surgical treatment of hyperthyroidism. Age and pathological types may be the risk factors for anemia in patients with surgical treatment of hyperthyroidism. Age and pathological type were significantly correlated with the occurrence of anemia after surgical treatment of hyperthyroidism, and may be risk factors for this disease.

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Celastrol inhibits IL-1β-induced inflammation in orbital fibroblasts through the suppression of NF-κB activity

Cited by 22 publications

References 44 publications

Protective effect of celastrol on myocardial ischemia–reperfusion injury

Protective effect of celastrol on myocardial ischemia–reperfusion injury

Celastrol Alleviates Chronic Obstructive Pulmonary Disease by Inhibiting Cellular Inflammation Induced by Cigarette Smoke via the Ednrb/Kng1 Signaling Pathway

A retrospective analysis of 1,231 patients with anemia after surgical treatment of hyperthyroidism

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