Triptolide protects mice from ischemia/reperfusion injury by inhibition of IL-17 production

Wu, Caiyan; Xia, Yongxiang; Wang, Ping; Lü, Ling; Zhang, Feng

doi:10.1016/j.intimp.2011.05.015

Cited by 24 publications

(11 citation statements)

References 52 publications

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“…IL‐6 binds to a receptor complex consisting of the ligand‐binding subunit IL‐6R and the signaling subunit gp130 and subsequently activates JAK/STAT3 signaling that is essential for Th17 cell development . Wu et al displayed that triptolide significantly inhibited IL‐6‐induced the differentiation of naïve T cells into Th17 cells in liver IRI . Our data indicated direct targeting of IL6ST by exosomal miR‐1246 resulted in a shift from Th17 cells toward Treg cells.…”

Section: Discussionmentioning

confidence: 52%

Exosomal miR‐1246 derived from human umbilical cord blood mesenchymal stem cells attenuates hepatic ischemia reperfusion injury by modulating T helper 17/regulatory T balance

et al. 2019

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The purpose of this study was to explore the mechanism by which human umbilical cord blood mesenchymal stem cells (hUCB-MSCs)-derived exosomes exerted protective effect in hepatic ischemia/reperfusion injury (IRI). hUCB-MSCs-derived exosomes were administrated into hepatic IRI mice or cocultured with naïve CD4 + T cells exposed to hepatic hypoxia/reoxygenation microenvironment. Hepatic function was assessed by determining serum transaminases. Histological changes were observed using hematoxylin and eosin staining. The proportion of T helper 17 (Th17) and regulatory T (Treg) cells were analyzed by flow cytometry. The concentration of inflammatory cytokines was determined by enzyme-linked immunosorbent assay. The interaction between miR-1246 and interleukin 6 (IL-6) signal transducer (also known as gp130) was verified by luciferase activity assay. The miR-1246 expression, Th17/ Treg-related genes, and gp130-signal transducer and activator of transcription 3 (STAT3) pathway were detected by quantitative real-time polymerase chain reaction and western blotting. hUCB-MSCs-derived exosomes ameliorated IRI-induced hepatic dysfunction and decreased Th17/Treg ratio in CD4 + T cells in vitro, whereas treatment of hUCB-MSCs with miR-1246 inhibitor showed opposite effects, which was mediated via the IL-6-gp130-STAT3 pathway. hUCB-MSCs-derived exosomes could alleviate hepatic IRI through modulating the balance between Tregs and Th17 cells via miR-1246-mediated IL-6-gp130-STAT3 axis. K E Y W O R D Sexosomes, gp130, hepatic injury, ischemia/reperfusion, miR-1246

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Section: Discussionmentioning

confidence: 52%

Exosomal miR‐1246 derived from human umbilical cord blood mesenchymal stem cells attenuates hepatic ischemia reperfusion injury by modulating T helper 17/regulatory T balance

et al. 2019

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“…TL is known as a drug with marked pharmacological activities, including anti-inflammatory and immunomodulatory properties as well as improvement of the microcirculation; it inhibits the proliferation of various types of cancer cell and enhances tumor sensitivity to chemotherapy (10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27). In the present study, the expression patterns of IL-6 in a mouse model of UC model were assessed, as well as association between the anti-colitis effects of TL and IL-6 levels.…”

Section: Introductionmentioning

confidence: 99%

Interleukin 6 inhibition by triptolide prevents inflammation in a mouse model of ulcerative colitis

Zhang

Chen

2017

Experimental and Therapeutic Medicine

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Abstract. The present study aimed to assess interleukin (IL)-6 expression in a murine model of ulcerative colitis (UC) induced by dextran sulfate sodium (DSS) and its potential association with the anti-colitis effects of triptolide (TL). Serum IL-6 levels were measured by ELISA. IL-6 gene expression levels in colonic mucosa specimens were assessed by reverse-transcription quantitative PCR and protein expression was evaluated by western blot analysis and immunohistochemistry. The expression of IL-6 was weak in mucosa specimens from normal control animals and upregulated in DSS-induced mice. In model mice treated with TL (0.4 and 0.6 mg/kg), dexamethasone or mesalazine, IL-6 expression was significantly reduced compared with that in model mice treated with normal saline or propylene glycol (P<0.05), while TL at 0.2 mg/kg did not elicit any significant inhibitory effect. There was no significant difference among TL (0.4 mg/kg and 0.6 mg/kg), mesalazine and dexamethasone treatments (P>0.05) in terms of IL-6 expression or histological score. The results of the present study indicated that IL-6 was overexpressed in a mouse model of UC and was involved in disease progression. In addition, TL exerted therapeutic effects in UC through inhibition of IL-6 expression.

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“…Taken together, the antiinflammatory and immunosuppressive activities of triptolide are mainly mediated by the following mechanisms: (1) Suppressing differentiation, maturation, and trafficking of macrophages and dendritic cells, which play critical roles in inducing both immune response and immune tolerance by processing and presenting antigens to T cells and by producing a variety of inflammatory mediators ; (2) Inhibiting T‐cell and B‐cell proliferation and activation, therefore interfering with cellular and humoral immunity ; (3) Exerting inhibitory effects on a variety of proinflammatory cytokines and mediators, and on the expression of adhesion molecules by endothelial cells . Currently, proinflammatory cytokines and mediators have been found to be suppressed by triptolide including tumor necrosis factor‐α (TNFα), interleukin (IL)‐1, IL‐4, IL‐6, IL‐8, IL‐17, IL‐23, cyclooxygenase (COX)‐2, interferon (IFN)α, and prostaglandin (PG)E 2 . In all cell types examined, triptolide inhibits nuclear factor κB (NFκB) transcriptional activation at a unique step in the nucleus after binding to DNA .…”

Section: Bioactivitymentioning

confidence: 99%

Triptolide with Potential Medicinal Value for Diseases of the Central Nervous System

2012

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Tripterygium wilfordii Hook.f. (TWHF) has a long history as a Traditional Chinese Medicine (TCM) herb that aids in treating inflammatory and autoimmune diseases. The major bioactive component of TWHF is triptolide, which has been recognized to possess a broad spectrum of biological profiles including antiinflammatory, immunosuppressive, antifertility, and antitumor activities, as well as neurotrophic and neuroprotective effects. Limitation of triptolide, such as poor water solubility and severe systemic toxicity, has postponed clinical development and trials; however, the wide range of medicinal value of triptolide has been drawing intensive worldwide attention. In particular, triptolide has been shown to have significant effects on central nervous system (CNS) diseases, such as Parkinson's disease, Alzheimer's disease, spinal cord and brain injury, and multiple sclerosis. This review focuses on the potential therapeutic role of triptolide on CNS diseases, and discusses the structural features, potential modifications, and the other pharmacological activities of triptolide.

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Triptolide protects mice from ischemia/reperfusion injury by inhibition of IL-17 production

Cited by 24 publications

References 52 publications

Exosomal miR‐1246 derived from human umbilical cord blood mesenchymal stem cells attenuates hepatic ischemia reperfusion injury by modulating T helper 17/regulatory T balance

Exosomal miR‐1246 derived from human umbilical cord blood mesenchymal stem cells attenuates hepatic ischemia reperfusion injury by modulating T helper 17/regulatory T balance

Interleukin 6 inhibition by triptolide prevents inflammation in a mouse model of ulcerative colitis

Triptolide with Potential Medicinal Value for Diseases of the Central Nervous System

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