RETRACTED: Ketamine reduces lipopolysaccharide-induced high-mobility group box-1 through heme oxygenase-1 and nuclear factor erythroid 2-related factor 2/ p38 mitogen-activated protein kinase

Wang, Fujun; Meng, Yong Hong; Zhang, Yiwei; Zhao, Guoguang; Zheng, Xiaonan; Qi-feng, Xiao; Yu, Yang

doi:10.1016/j.jss.2014.11.031

Cited by 16 publications

(10 citation statements)

References 45 publications

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“…A similar relationship between HMGB1 and JNK was observed when normal human bronchial epithelial cells were cultured with HMGB1 in the presence or absence of SP600125: the HMGB1-induced inflammatory response was suppressed by SP600125 ( Wu et al, 2013 ). By contrast, Wang et al (2015) reported that the MAP kinase p38 mediates the inhibitory effect of ketamine on the LPS-induced secretion of HMGB1 in murine macrophages by upregulating the expression of heme oxygenase-1. Other studies have also shown that several natural products, namely, Dachengqi decoction (a traditional Chinese medicine formula), glycyrrhizin (from licorice root), and the tetrahydroisoquinoline alkaloid THI-28, inhibit HMGB1 release in cellular and animal models of endotoxemia and severe acute pancreatitis by activating p38 signaling ( Kim, Kim & Chang, 2015 ; Chen et al, 2015 ; Kim et al, 2013 ).…”

Section: Discussionmentioning

confidence: 91%

Curcumin longa extract-loaded nanoemulsion improves the survival of endotoxemic mice by inhibiting nitric oxide-dependent HMGB1 release

Ahn

Hwang

Lee

et al. 2017

PeerJ

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BackgroundHigh mobility group box 1 (HMGB1) is a well-known damage-related alarmin that participates in cellular inflammatory responses. However, the mechanisms leading to HMGB1 release in inflammatory conditions and the therapeutic agents that could prevent it remain poorly understood. This study attempted to examine whether the Curcumin longa herb, which is known to have anti-inflammatory property, can modulate cellular inflammatory responses by regulating HMGB1 release.MethodsThe murine macrophage RAW264.7 cells were treated with lipopolysaccharide (LPS) and/or a C. longa extract-loaded nanoemulsion (CLEN). The levels of released HMGB1, nitric oxide (NO) production, inducible NO synthase (iNOS) expression, and phosphorylation of mitogen-activated protein kinases were analyzed in RAW264.7 macrophages. The effects of CLEN on survival of endotoxemic model mice, circulating HMGB1 levels, and tissue iNOS expression were also evaluated.ResultsWe have shown that a nanoemulsion loaded with an extract from the C. longa rhizome regulates cellular inflammatory responses and LPS-induced systemic inflammation by suppressing the release of HMGB1 by macrophages. First, treatment of RAW264.7 macrophages with the nanoemulsion significantly attenuated their LPS-induced release of HMGB1: this effect was mediated by inhibiting c-Jun N-terminal kinase activation, which in turn suppressed the NO production and iNOS expression of the cells. The nanoemulsion did not affect LPS-induced p38 or extracellular signal-regulated kinase activation. Second, intraperitoneal administration of the nanoemulsion improved the survival rate of LPS-injected endotoxemic mice. This associated with marked reductions in circulating HMGB1 levels and tissue iNOS expression.DiscussionThe present study shows for the first time the mechanism by which C. longa ameliorates sepsis, namely, by suppressing NO signaling and thereby inhibiting the release of the proinflammatory cytokine HMGB1. These observations suggest that identification of agents, including those in the herb C. longa, that can inhibit HMGB1 production and/or activity may aid the treatment of endotoxemia.

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Section: Discussionmentioning

confidence: 91%

Curcumin longa extract-loaded nanoemulsion improves the survival of endotoxemic mice by inhibiting nitric oxide-dependent HMGB1 release

Ahn

Hwang

Lee

et al. 2017

PeerJ

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“…Unlike the other HO isoforms, which are constitutively expressed, HO-1 is inducible and can be upregulated by oxidants and inflammatory cytokines [39]. Endogenous HO-1, which is ubiquitously expressed in various cell types, plays an important role in host defense against excessive inflammation and oxidation-related diseases, such as neurodegenerative disease, pulmonary disease, systemic autoimmune disease, and cancer [34,42]. Overexpression of HO-1 inhibits the production of cytokines and ROS, thereby reducing neutrophil infiltration [34].…”

Section: Discussionmentioning

confidence: 99%

Mesenchymal Stem Cells Modified with Heme Oxygenase-1 Have Enhanced Paracrine Function and Attenuate Lipopolysaccharide-Induced Inflammatory and Oxidative Damage in Pulmonary Microvascular Endothelial Cells

Chen

Zhang

Wang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Bone marrow-derived mesenchymal stem cell (BM-MSC) transplantation has therapeutic effects on endothelial damage during acute lung injury (ALI). Heme oxygenase-1 (HO-1) can restore homeostasis and implement cytoprotective defense functions in many pathologic states. Therefore, we explored whether transduction of HO-1 into BM-MSCs (MSCs-HO-1) would have an increased beneficial effect on lipopolysaccharide (LPS)-induced inflammatory and oxidative damage in human pulmonary microvascular endothelial cells (PVECs). Methods: MSCs were isolated from rat bone marrow and transfected with the HO-1 gene by a lentivirus vector. The phenotype and multilineage differentiation of MSCs were assessed. MSCs or MSCs-HO-1 were co-cultured with PVECs using a transwell system, and LPS was added to induce PVEC injury. The production of reactive oxygen species (ROS), and the activities of lipid peroxide (LPO), malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GPx) in PVECs were determined by flow cytometry and colorimetric assays, respectively. The levels of human PVEC-derived tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-6 in the supernatants of the co-culture system, and the activity of nuclear transcription factor-κB and NF-E2-related factor 2 (Nrf2) in PVECs were examined by enzyme-linked immunosorbent assay (ELISA). The mRNA expression of TNF-α, IL-1β and IL-6 in PVECs was detected by quantitative real-time polymerase chain reaction (qRT-PCR), HO-1 expression and enzymatic activity in PVECs and the influence of zinc protoporphyrin (ZnPP) or HO-1 small interfering RNA on the above inflammatory and oxidative stress markers were evaluated. In addition, the expression of rat MSC-derived hepatocyte growth factor (HGF) and IL-10 was determined by ELISA and qRT-PCR. Results: MSCs showed no significant changes in phenotype or multilineage differentiation after transduction. LPS strongly increased the production of inflammatory and oxidative stress indicators, as well as decreased the levels of antioxidant components and the activity of Nrf2 in PVECs. MSC co-cultivation ameliorated these detrimental effects in PVECs and MSCs-HO-1 further improved the damage to PVECs induced by LPS when compared with MSCs alone. The beneficial effects of MSCs-HO-1 were dependent on HO-1 overexpression and may be attributed to the enhanced paracrine production of HGF and IL-10. Conclusion: MSCs-HO-1 have an enhanced ability to improve LPS-induced inflammatory and oxidative damage in PVECs, and the mechanism may be partially associated with the enhanced paracrine function of the stem cells. These data encourage further testing of the beneficial effects of MSCs-HO-1 in ALI animal models.

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“…In normal human bronchial epithelial cells, SP600125 also inhibited HMGB1-mediated inflammatory responses through the inhibition of JNK signaling [34]. In contrast with these reports, a recent study demonstrated that another MAPK, p38, is implicated in ketamine-mediated inhibition of HMGB1 release induced by LPS through upregulation of HO-1 [35]. In addition, p38-dependent inhibition of HMGB1 release was also demonstrated in cellular or animal models of severe acute pancreatitis and endotoxemia upon administration of the natural products glycyrrhizin, Dachengqi decoction, and the tetrahydroisoquinoline alkaloid THI-28 [36–38].…”

Section: Discussionmentioning

confidence: 99%

A Dalbergia odorifera extract improves the survival of endotoxemia model mice by inhibiting HMGB1 release

Choi

Park

Hwang

et al. 2017

BMC Complement Altern Med

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Background Dalbergia odorifera T. Chen (Leguminosae) is an indigenous medicinal herb that is widely used as a popular remedy in northern and eastern Asia. However, the cellular mechanisms underlying the biological activity of D. odorifera are not fully elucidated.MethodsAnti-inflammatory effect of D. odorifera extract (DOE) was determined through intraperitoneal injection in a mouse model of endotoxemia induced by lipopolysaccharide (LPS). RAW 264.7 cells, a murine macrophage, were also treated with LPS to generate a cellular model of inflammation, and investigated the anti-inflammatory activity and underlying mechanisms of DOE and its constituent isoliquiritigenin.ResultsDOE dose-dependently inhibited LPS-induced release of high mobility group box 1 (HMGB1), a late proinflammatory cytokine, and decreased cytosolic translocation of HMGB1 in RAW264.7 cells. This inhibitory effect of DOE on HMGB1 release was observed in cells treated with DOE before or after LPS treatment, suggesting that DOE is effective for both treatment and prevention. In addition, DOE significantly inhibited LPS-induced formation of nitric oxide (NO) and expression of inducible NO synthase (iNOS) in a dose-dependent manner. These effects of DOE were accompanied by suppression of HMGB1 release triggered by LPS, suggesting a possible mechanism by which DOE modulates HMGB1 release through NO signaling.Isoriquiritigenin, a constituent of DOE, also attenuated LPS-triggered NO formation and HMGB1 release in RAW264.7 cells, indicating that isoriquiritigenin is an indexing molecule for the anti-inflammatory properties of DOE. Furthermore, c-Jun N-terminal kinase, but not extracellular signal-regulated kinase and p38, mediated DOE-dependent inhibition of HMGB1 release and NO/iNOS induction in RAW 264.7 cells exposed to LPS. Notably, administration of DOE ameliorated survival rates in a mouse model of endotoxemia induced by LPS, where decreased level of circulating HMGB1 was observed.ConclusionThese results suggest that DOE confers resistance to LPS-triggered inflammation through NO-mediated inhibitory effects on HMGB1 release.

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RETRACTED: Ketamine reduces lipopolysaccharide-induced high-mobility group box-1 through heme oxygenase-1 and nuclear factor erythroid 2-related factor 2/ p38 mitogen-activated protein kinase

Cited by 16 publications

References 45 publications

Curcumin longa extract-loaded nanoemulsion improves the survival of endotoxemic mice by inhibiting nitric oxide-dependent HMGB1 release

Curcumin longa extract-loaded nanoemulsion improves the survival of endotoxemic mice by inhibiting nitric oxide-dependent HMGB1 release

Mesenchymal Stem Cells Modified with Heme Oxygenase-1 Have Enhanced Paracrine Function and Attenuate Lipopolysaccharide-Induced Inflammatory and Oxidative Damage in Pulmonary Microvascular Endothelial Cells

A Dalbergia odorifera extract improves the survival of endotoxemia model mice by inhibiting HMGB1 release

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