TNF-a mediated inflammatory macrophage polarization contributes to the pathogenesis of steroid-induced osteonecrosis in mice

Wu, Xinghuo; Xu, Weihua; Feng, Xiaobo; He, Yu; Liu, Xianzhe; Gao, Yong; Yang, Shuai; Shao, Zengwu; Cao, Yang; Ye, Zhewei

doi:10.1177/0394632015593228

Cited by 100 publications

(64 citation statements)

References 32 publications

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“…LPS stimulation releases inflammatory cytokines such as TNF-α, IL-1β, IL-6, and increases their expression levels (Zhang et al, 2011). TNF-α is an important cytokine secreted by macrophages that promotes the activation of neutrophils and the release of other cytokines (Akira et al, 1990; Wu et al, 2015). Similar to TNF-α, IL-1β is also secreted by macrophages and, to some extent, regulates the progress of the inflammatory response (Akira et al, 1990).…”

Section: Discussionmentioning

confidence: 99%

Magnoflorine Ameliorates Lipopolysaccharide-Induced Acute Lung Injury via Suppressing NF-κB and MAPK Activation

Guo

Jiang

et al. 2018

Front. Pharmacol.

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Acute lung injury (ALI) which is featured by a strong pulmonary inflammation, is a major cause of morbidity and mortality in critically ill patients. Magnoflorine, a quaternary alkaloid isolated from Chinese herb Magnolia or Aristolochia, has been reported to have potent anti-inflammatory properties. However, the effect of magnoflorine on lipopolysaccharide (LPS)-induced ALI in mice has not been reported. The purpose of the present study is to investigate the anti-inflammatory effect of magnoflorine on LPS-induced ALI and elucidate its possible molecular mechanisms in RAW264.7 cells. The results of histopathological changes as well as the myeloperoxidase (MPO) activity indicated that magnoflorine significantly alleviated the lung injury induced by LPS. In addition, qPCR results showed that magnoflorine dose-dependently decreased the expression of pro-inflammatory cytokines TNF-α, IL-1β, and IL-6. Immunofluorescence assay also confirmed that the level of Toll-like receptor 4 (TLR4) induced by LPS was inhibited by magnoflorine treatment. Further experiments were performed using Western blotting to detect the expression of related proteins in the NF-κB and MAPK signaling pathways. The results showed that magnoflorine suppressed the levels of phosphorylated p65, IκBα, p38, ERK, and JNK. In conclusion, all data indicate that magnoflorine could protect against LPS-induced inflammation in ALI at least partially by inhibiting TLR4-mediated NF-κB and MAPK signaling pathways.

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Section: Discussionmentioning

confidence: 99%

Magnoflorine Ameliorates Lipopolysaccharide-Induced Acute Lung Injury via Suppressing NF-κB and MAPK Activation

Guo

Jiang

et al. 2018

Front. Pharmacol.

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“…As an initiation factor, TNF-α can induce the expression of the gene itself. In addition, it can then cause waterfall-like chains and a cascading effect (9), prompting the body to release IL-6, IL-8, platelet-activating factor, oxygen-free radicals, prostacyclin, bradykinin etc. The latter has feedback on neutrophils and monocyte-macrophage cell system which further produce more inflammatory mediators, expanding its inflammatory effects and forming a complex and highly coupled network system.…”

Section: Discussionmentioning

confidence: 99%

Studies on the Effect of Thymosin Alpha l on Severe Acute Pancreatitis in Rats

Qiu¹,

Z²,

Huang³

et al. 2016

West Indian Med J

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Objective:To observe the effect of thymosin alpha l (Tα1) on severe acute pancreatitis (SAP) in rats. Methods: Twenty-four adult male Sprague-Dawley rats were randomly divided into three groups (eight in each group): control group (Group A), SAP group (Group B) and Tα1 treatment group (Group C). Animal models of SAP were made by retrograde injection of 5% sodium taurocholate into the biliopancreatic duct. Rats in Group C were treated with Tα1 (6 mg/kg) via intraperitoneal administration prior to SAP modelling. Eight rats in each group were sacrificed at 12 hours, respectively, after modelling. The serum levels of amylase, tumour necrosis factor-α (TNF-α), interleukin-lβ (IL-lβ) and interleukin-6 (IL-6) were detected in each group. The pathological scores of the tissue in the pancreas head were observed by light microscopy. Results: The levels of serum amylase of Group B were 6378 ± 538 U/L, which were significantly higher than those (4587 ± 478 U/L) of Group C (p < 0.05). The levels of serum TNF-α of Group B were 360.32 ± 28.67 pg/mL, which were higher than those (269.99 ± 26.11 pg/mL) of Group C (p < 0.05). The levels of serum IL-lβ of Group B were 435.93 ± 36.00 pg/mL, which were higher than those (312.42 ± 17.89 pg/mL) of Group C (p < 0.05). The levels of serum which were higher than those (289.98 ± 23.00 pg/ mL) of Group C (p < 0.05). The pancreatic pathological scores of Group B were 13.34 ± 2.19, which were higher than those (6.39 ± 1.86) of Group C (p < 0.05). Conclusion: Thymosin alpha 1 could decrease proinflammatory cytokines and reduce pancreas injury and had a protective effect in rats with SAP. This provides a new strategy for the clinical treatment of SAP. ReSuMenObjetivo: Observar el efecto de la timosina alfa l (Tα1) sobre la pancreatitis aguda grave (PAG) en ratas. Métodos: Veinticuatro ratas Sprague-Dawley adultas machos fueron divididas aleatoriamente en tres grupos (ocho en cada grupo): grupo de control (grupo A), grupo de PAG (grupo B) yFrom:

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“…TNF-α is a central regulator of inflammation, which exerts various functions in leukemia and normal hematopoietic cells (35). TNF-α is continually expressed in a number of types of leukemia cell (36), and has been demonstrated to upregulate certain molecules involved in cell growth and proliferation via the NF-κB-dependent or -independent pathway in leukemia (37).…”

Section: A B Cmentioning

confidence: 99%

Inhibition of tumor necrosis factor-α enhances apoptosis induced by nuclear factor-κB inhibition in leukemia cells

et al. 2015

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Abstract. Inhibition of nuclear factor-κB (NF-κB) results in antitumor activity in leukemia cells, and may be a potential therapeutic strategy for the treatment of leukemia. However, a significant limitation of NF-κB inhibition in the treatment of leukemia is the low efficiency of this technique. NF-κB inhibitor treatment induces apoptosis in leukemia cells; however, it additionally causes inflammatory molecules to induce increased sensitivity of healthy hematopoietic cells to cell death signals, therefore limiting its clinical applications. Tumor necrosis factor-α (TNF-α) is a key regulator of inflammation, and induces a variety of actions in leukemic and healthy hematopoietic cells. TNF-α induces NF-κB-dependent and -independent survival signals, promoting the proliferation of leukemia cells. However, in healthy hematopoietic cells, TNF-α induces death signaling, an effect which is enhanced by the inhibition of NF-κB. Based on these observations, the present study hypothesized that inhibition of TNF-α signaling may be able to protect healthy hematopoietic cells and other tissue cells, while increasing the anti-leukemia effects of NF-κB inhibition on leukemia cells. The role and underlying molecular mechanisms of TNF-α inhibition in the regulation of NF-κB inhibition-induced apoptosis in leukemia cells was therefore investigated in the present study. The results indicated that inhibition of TNF-α enhanced NF-κB inhibition-induced apoptosis in leukemia cells. It was also revealed that protein kinase B was significant in the regulation of TNF-α and NF-κB inhibition-induced apoptosis. During this process, intrinsic apoptotic pathways were activated. A combination of NF-κB and TNF-α inhibition may be a potential specific and effective novel therapeutic strategy for the treatment of leukemia.

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TNF-a mediated inflammatory macrophage polarization contributes to the pathogenesis of steroid-induced osteonecrosis in mice

Cited by 100 publications

References 32 publications

Magnoflorine Ameliorates Lipopolysaccharide-Induced Acute Lung Injury via Suppressing NF-κB and MAPK Activation

Magnoflorine Ameliorates Lipopolysaccharide-Induced Acute Lung Injury via Suppressing NF-κB and MAPK Activation

Studies on the Effect of Thymosin Alpha l on Severe Acute Pancreatitis in Rats

Inhibition of tumor necrosis factor-α enhances apoptosis induced by nuclear factor-κB inhibition in leukemia cells

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