Preventive effects of interleukin-6 in lipopolysaccharide/ d -galactosamine induced acute liver injury via regulating inflammatory response in hepatic macrophages

Li, Long; Duan, Chaoli; Zhao, Yan; Zhang, Xiaofang; Yin, Hongyan; Wang, Tianxi; Huang, Caoxin; Liu, Suhuan; Yang, Shuyu; Li, Xuejun

doi:10.1016/j.intimp.2017.08.009

Cited by 37 publications

(31 citation statements)

References 29 publications

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“…Acute liver injury in mice was induced using LPS/D-Gal as previously reported [22]. Briefly, mice were intraperitoneally injected with 10 μg/kg of LPS and 500 mg/kg of D-Gal to induce acute liver injury for 6 h. Successful modeling was confirmed via a pathological examination.…”

Section: Preparing the Inducer Of Acute Liver Injurymentioning

confidence: 99%

RETRACTED ARTICLE: Sedum sarmentosum Bunge extract ameliorates lipopolysaccharide- and D-galactosamine-induced acute liver injury by attenuating the hedgehog signaling pathway via regulation of miR-124 expression

Hao

Liu

et al. 2020

BMC Complement Med Ther

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Background: Sedum sarmentosum is traditionally used to treat various inflammatory diseases in China. It has protective effects against acute liver injury, but the exact mechanism of such effects remains unclear. This study investigated the protective effects of S. sarmentosum extract on lipopolysaccharide (LPS)/D-galactosamine (D-GalN)induced acute liver injury in mice and the mechanism of such effects.Methods: Mice were randomly divided into control, treatment, model, and model treatment groups. Acute liver injury was induced in model mice via intraperitoneal injection of LPS and D-GalN with doses of 10 μg/kg of LPS and 500 mg/kg, respectively. The mRNA expression levels of miR-124, Hedgehog, Patched (Ptch), Smoothened (Smo), and glioma-associated oncogene homolog (Gli) in liver tissues were determined through RT-PCR, and the protein levels of Hedgehog, Ptch, Smo, Gli, P13k, Akt, HMGB1, TLR4, IkB-α, p-IkB-α, and NF-kB65 were evaluated via Western blot analysis. The serum levels of IL-6, TNF-α, CRP, IL-12, and ICAM-1 were determined via ELISA. TLR4 and NF-κBp65 activity and the levels of DNA-bound NF-KB65 and TLR4 in LPS/D-GalN-induced liver tissues were also determined. We recorded the time of death, plotted the survival curve, and calculated the liver index. We then observed the pathological changes in liver tissue and detected the levels of liver enzymes (alanine aminotransferase [ALT] and aspartate transaminase [AST]) in the serum and myeloperoxidase (MPO) and plasma inflammatory factors in the liver homogenate. Afterward, we evaluated the protective effects of S. sarmentosum extracts on acute liver injury in mice.Results: Results showed that after S. sarmentosum extract was administered, the expression level of miR-124 increased in liver tissues. However, the protein expression levels of Hedgehog, Ptch, Smo, Gli, P13k, p-Akt, HMGB1, TLR4, p-IκB-α, and NF-κB65 and the mRNA expression levels of Hedgehog, Ptch, Smo, and Gli decreased. The MPO level in the liver, the IL-6, TNF-α, CRP, IL-12, and MMP-9 levels in the plasma, and the serum ALT and AST levels also decreased, thereby reducing LPS/D-GalN-induced liver injury and improving the survival rate of liver-damaged animals within 24 h.Conclusions: S. sarmentosum extract can alleviate LPS/D-GalN-induced acute liver injury in mice and improve the survival rate of mice. The mechanism may be related to the increase in miR-124 expression, decrease in Hedgehog and HMGB1 signaling pathway activities, and reduction in inflammatory responses in the liver. Hedgehog is a regulatory target for miR-124.

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Section: Preparing the Inducer Of Acute Liver Injurymentioning

confidence: 99%

RETRACTED ARTICLE: Sedum sarmentosum Bunge extract ameliorates lipopolysaccharide- and D-galactosamine-induced acute liver injury by attenuating the hedgehog signaling pathway via regulation of miR-124 expression

Hao

Liu

et al. 2020

BMC Complement Med Ther

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“…The study on mice also showed that the injection of LPS enhanced both: the serum level of IL-1β, IL-6 and TNFα and the gene expression of these cytokines in the hypothalamus [ 24 ], pituitary and peripheral tissue [ 18 ]. Moreover, it was found that an intratracheal injection of LPS also upregulates IL-1β and TNFα expression in rat lung [ 25 ], IL-6 in rat [ 26 ] and mouse [ 27 ] liver.…”

Section: Discussionmentioning

confidence: 99%

Effect of Acute and Prolonged Inflammation on the Gene Expression of Proinflammatory Cytokines and Their Receptors in the Anterior Pituitary Gland of Ewes

Wojtulewicz

Krawczyńska

Tomaszewska-Zaremba

et al. 2020

IJMS

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An acute and prolonged inflammation inhibits the reproduction process by the disruption of the neurohormonal activity of the hypothalamic-pituitary-gonadal axis. It is thought that these changes may be caused by proinflammatory cytokines, i.e., interleukin (IL) -1β, IL-6 and tumor necrosis factor (TNF) α. The aim of this study was to determine the effect of an acute and prolonged inflammation on the expression of genes encoding cytokine and their receptors, gonadotropin releasing hormone receptor (GnRHR), beta subunits of luteinizing hormone (LHβ) and follicle-stimulating (FSHβ) in the anterior pituitary (AP). Moreover, the circulating concentration of LH and FSH was also assayed. Two experiments were carried out on adult ewes which were divided into two control groups and treated with lipopolysaccharide (LPS; 400 ng / kg). Acute inflammation was caused by a single injection of LPS into the external jugular vein, while the chronic inflammation was induced by seven times LPS injection (one a day). In both experiments, animals were euthanized 3h after the last LPS / NaCl injection and the blood samples collected 15 min before euthanasia. An acute inflammation stimulates the expression of the IL-1β, IL-6 and TNFα genes and their receptors in the AP of sheep. Prolonged inflammation increased TNFα gene expression and both types of TNFα and IL-6 receptors. Both an acute and prolonged inflammation inhibited LHβ gene expression in the AP and reduced LH level in blood. A sevenfold LPS injection raises FSH concentration. The gene expression of GnRHR was reduced in the ovine AP only after a single injection of endotoxin. Our results suggest that there are important differences in the way how an acute and prolonged inflammation influence proinflammatory cytokines and their receptors gene expression in the AP of anestrous ewes, which could be reflected by differences in the AP secretory activity during these states.

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“…However, TNF-α appears to be the major pro-inflammatory mediator, as macrophage autophagy may inhibit the production of IL-1β. In addition, IL-6 treatment was reported to have a beneficial effect and reduce the expression of TNF-α and MCP-1, and promote macrophage polarization towards M2 in D-GalN/LPS induced liver injury models (89,90). Besides LPS, cytosine-phosphate-guanine DNA and polyinosinic:polycytidylic acid also exert hepatic toxicity mediated by TNF-α in D-GalN-sensitized mice (91).…”

Section: Role Of Macrophages In D-galactosamine-induced Acute Livermentioning

confidence: 99%

Role of macrophages in experimental liver injury and repair in mice (Review)

Dong

Liu

2019

Exp Ther Med

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Liver macrophages make up the largest proportion of tissue macrophages in the host and consist of two dissimilar groups: Kupffer cells (KCs) and monocyte-derived macrophages (MoMø). As the liver is injured, KCs sense the injury and initiate inflammatory cascades mediated by the release of inflammatory cytokines and chemokines. Subsequently, inflammatory monocytes accumulate in the liver via chemokine-chemokine receptor interactions, resulting in massive inflammatory MoMø infiltration. When live r injury ceases, restorative macrophages, derived from recruited inflammatory monocytes (lymphocyte antigen 6 complex, locus C hi monocytes), promote the resolution of hepatic damage and fibrosis. Consequently, a large number of studies have assessed the mechanisms by which liver macrophages exert their opposing functions at different time-points during liver injury. The present review primarily focuses on the diverse functions of macrophages in experimental liver injury, fibrosis and repair in mice and illustrates how macrophages may be targeted to treat liver disease. Contents 1. Introduction 2. Macrophages 3. Role of macrophages in carbon tetrachloride-induced liver injury, fibrosis and repair 4. Role of macrophages in other non-CCl 4 induced liver injury animal models 5. Therapeutic potential of macrophages 6. Conclusions

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Preventive effects of interleukin-6 in lipopolysaccharide/ d -galactosamine induced acute liver injury via regulating inflammatory response in hepatic macrophages

Cited by 37 publications

References 29 publications

RETRACTED ARTICLE: Sedum sarmentosum Bunge extract ameliorates lipopolysaccharide- and D-galactosamine-induced acute liver injury by attenuating the hedgehog signaling pathway via regulation of miR-124 expression

RETRACTED ARTICLE: Sedum sarmentosum Bunge extract ameliorates lipopolysaccharide- and D-galactosamine-induced acute liver injury by attenuating the hedgehog signaling pathway via regulation of miR-124 expression

Effect of Acute and Prolonged Inflammation on the Gene Expression of Proinflammatory Cytokines and Their Receptors in the Anterior Pituitary Gland of Ewes

Role of macrophages in experimental liver injury and repair in mice (Review)

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