Inhibition of TNF-α sepsis of lipopolysaccharide induction using nano cerium oxide system

Ge, Lingqing; Hu, Qiaozhen; Chen, Jing; Shi, Mengrao; Yang, Haojie; Zhu, Guoji

doi:10.1016/j.msec.2017.03.207

Cited by 9 publications

(4 citation statements)

References 53 publications

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“…There are currently three main hypotheses used to explain the pathogenesis of sepsis: i) Pro-inflammatory response; ii) impaired compensatory anti-inflammatory responses; and iii) immune-paralysis, all of which involve the excessive release of inflammatory mediators responsible for the initiation and development of systemic inflammation (1,48). TNF-α was considered to be a central regulator of the immune response and involved in the pathophysiological alterations associated with sepsis (49,50). In addition, TNF-α was demonstrated to promote the release of inflammatory mediators, including IL-6, IL-8, IL-17 and IL-1β, which initiate the host inflammatory response (51,52).…”

Section: Discussionmentioning

confidence: 99%

Long non‑coding RNA‑HOTAIR promotes the progression of sepsis by acting as a sponge of miR‑211 to induce IL‑6R expression

Chen

Zhou

et al. 2019

Exp Ther Med

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Sepsis remains the primary cause of death in intensive care units and multiple long non-coding RNAs (lncRNAs) have been demonstrated to be dysregulated in samples of patients with sepsis. However, whether lncRNA-HOTAIR is involved in the etiology of sepsis remains unclear. The aim of the present study was to investigate the role of HOTAIR in sepsis and to reveal the associated mechanisms. A bioinformatics analysis and dual-luciferase reporter assay was performed to evaluate the interaction between HOTAIR and miR-211, as well as miR-211 and IL-6R. An animal model of sepsis was established in mice via cecal ligation and puncture. Interferon (IFN)-γ, interleukin (IL)-6, IL-17, tumor necrosis factor (TNF)-α, IL-1β, IL-6 receptor (R), microRNA (miR)-211 and HOTAIR expression was measured using reverse transcription-quantitative PCR. Cellular proliferation and apoptosis of monocytes were assessed using cell counting kit-8 assay and flow cytometry, respectively. miR-211 was revealed to be targeted by HOTAIR and IL-6R. The expression of IFN-γ, IL-6, IL-17, TNF-α, IL-1β, IL-6R and HOTAIR was significantly upregulated in the septic mice, whereas miR-211 expression was downregulated. The overexpression of hox transcript antisense RNA (HOTAIR) and knockdown of miR-211 were associated with an increased expression of IFN-γ, IL-6, IL-17, TNF-α, IL-1β and IL-6R in monocytes, while the overexpression of miR-211 exhibited the opposite effect. HOTAIR overexpression and miR-211 knockdown significantly inhibited cellular proliferation and promoted monocyte apoptosis, whereas the overexpression of miR-211 exhibited the opposite effects in monocytes. Therefore, HOTAIR may promote the progression of sepsis by indirectly regulating the expression of IL-6R via miR-211.

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Section: Discussionmentioning

confidence: 99%

Long non‑coding RNA‑HOTAIR promotes the progression of sepsis by acting as a sponge of miR‑211 to induce IL‑6R expression

Chen

Zhou

et al. 2019

Exp Ther Med

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“…Although the effectiveness of NPs for systemic sepsis in mice has been reported in the literature, little has been reported for the treatment of acute pancreatic necrotizing infections. 139,140 4 Summary and outlook AP is a common digestive disease that can be life-threatening in severe cases. Even those who survive may have a poor quality of life with chronic pancreatitis and diabetes for a long time.…”

Section: Nps For Anti-infection Therapy Of Ap Patientsmentioning

confidence: 99%

Section: Treatmentmentioning

confidence: 99%

Application of nanotechnology in the diagnosis and treatment of acute pancreatitis

Jia

et al. 2022

Nanoscale Adv.

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“…Notably, GSK3 disorders are involved in a numbers of diseases, such as diabetes, reperfusion injury, mental stability, cancer, and neurodegenerative diseases [12][13][14][15], which are all related with inflammation. Sepsis leads to systemic inflammation and the destruction of homeostasis in the brain [16,17]. Cognitive and memory impairments occur in rats or mice with endotoxemia in the open-field and Morris water maze experiments [18].…”

Section: Introductionmentioning

confidence: 99%

Isoorientin Inhibits Inflammation in Macrophages and Endotoxemia Mice by Regulating Glycogen Synthase Kinase 3β

Zhao

Tan

et al. 2020

Mediators of Inflammation

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Isoorientin has anti-inflammatory effects; however, the mechanism remains unclear. We previously found isoorientin is an inhibitor of glycogen synthase kinase 3β (GSK3β) in vitro. Overactivation of GSK3β is associated with inflammatory responses. GSK3β is inactivated by phosphorylation at Ser9 (i.e., p-GSK3β). Lithium chloride (LiCl) inhibits GSK3β and also increases p-GSK3β (Ser9). The present study investigated the anti-inflammatory effect and mechanism of isoorientin via GSK3β regulation in lipopolysaccharide- (LPS-) induced RAW264.7 murine macrophage-like cells and endotoxemia mice. LiCl was used as a control. While AKT phosphorylates GSK3β, MK-2206, a selective AKT inhibitor, was used to activate GSK3β via AKT inhibition (i.e., not phosphorylate GSK3β at Ser9). The proinflammatory cytokines TNF-α, IL-6, and IL-1β were detected by ELISA or quantitative real-time PCR, while COX-2 by Western blotting. The p-GSK3β and GSK3β downstream signal molecules, including NF-κB, ERK, Nrf2, and HO-1, as well as the tight junction proteins ZO-1 and occludin were measured by Western blotting. The results showed that isoorientin decreased the production of TNF-α, IL-6, and IL-1β and increased the expression of p-GSK3β in vitro and in vivo, similar to LiCl. Coadministration of isoorientin and LiCl showed antagonistic effects. Isoorientin decreased the expression of COX-2, inhibited the activation of ERK and NF-κB, and increased the activation of Nrf2/HO-1 in LPS-induced RAW264.7 cells. Isoorientin increased the expressions of occludin and ZO-1 in the brain of endotoxemia mice. In summary, isoorientin can inhibit GSK3β by increasing p-GSK3β and regulate the downstream signal molecules to inhibit inflammation and protect the integrity of the blood-brain barrier and the homeostasis in the brain.

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Inhibition of TNF-α sepsis of lipopolysaccharide induction using nano cerium oxide system

Cited by 9 publications

References 53 publications

Long non‑coding RNA‑HOTAIR promotes the progression of sepsis by acting as a sponge of miR‑211 to induce IL‑6R expression

Long non‑coding RNA‑HOTAIR promotes the progression of sepsis by acting as a sponge of miR‑211 to induce IL‑6R expression

Application of nanotechnology in the diagnosis and treatment of acute pancreatitis

Isoorientin Inhibits Inflammation in Macrophages and Endotoxemia Mice by Regulating Glycogen Synthase Kinase 3β

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