Clinical severity of serum S100A12 levels in patients with osteoarthritis and S100A12 open inflammation of osteoarthritis model by NLRP3

Osteoarthritis is a common chronic bone and joint disease, which is characterized by degenerative changes and destruction of articular cartilage, secondary hyperostosis. This study aimed to investigate the clinical severity and mechanism of S100A12 in patients with osteoarthritis. Serum samples were obtained from patients with osteoarthritis or normal volunteer in Minhang Branch of Yueyang Hospital of Integrated Traditional Chinese and Western Medicine affiliated to Shanghai University of Traditional Chinese Medicine (Shanghai, China). C57BL/6J mice performed Resection of the medial collateral ligament and medial meniscus as mice model. MC3T3-E1 cells were induced with 100 ng of LPS as vitro model. The serum level of S100A12 was increased in patients with osteoarthritis. Similarly, S100A12 levels of serum and bone tissue from mice model of osteoarthritis were also higher than those of sham group. Over-expression of S100A12 promoted inflammation levels while down-regulation of S100A12 decreased inflammation levels in in vitro model of osteoarthritis. NLRP3 is an important target of S100A12 in pro-inflammation effects of osteoarthritis. NLRP3 was involved in the effects of S100A12 on inflammation in in vitro model of osteoarthritis. S100A12 also accelerated inflammation by NLRP3 in mice model of osteoarthritis. We conclude that serum S100A12 levels was a possible clinical severity, open inflammation of osteoarthritis model by NLRP3 and its receptors may be effective in preventing the development of osteoarthritis.

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Electrode implantation trauma (EIT) initiates fibrosis by over‐expression of TGF‐β1 and activation of the Wnt/β‐catenin pathway in an in vitro model of cochlear implantation

The FASEB Journal ◽

10.1096/fasebj.27.1_supplement.599.6 ◽

2013 ◽

Vol 27 (S1) ◽

Author(s):

Esperanza Bas Infante ◽

Chhavi Gupta ◽

Bradley Goldstein ◽

Thomas R. Van De Water

Keyword(s):

Cochlear Implantation ◽

In Vitro Model ◽

Electrode Implantation ◽

Over Expression ◽

Vitro Model ◽

Tgf Β1

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Effects of microRNA-208a on inflammation and oxidative stress in ketamine-induced cardiotoxicity through Notch/NF-κB signal pathways by CHD9

Bioscience Reports ◽

10.1042/bsr20182381 ◽

2019 ◽

Vol 39 (5) ◽

Author(s):

Hongjie Yuan ◽

Shibin Du ◽

Youliang Deng ◽

Xiaoqing Xu ◽

Qian Zhang ◽

...

Keyword(s):

Oxidative Stress ◽

In Vitro Model ◽

Epigenetic Modification ◽

Heart Cell ◽

Signal Pathways ◽

Over Expression ◽

Potential Biomarker ◽

Vitro Model ◽

And Oxidative Stress

Abstract Background: MicroRNA can regulate gene expression, and participate in multiple vital activities, such as inflammation, oxidative stress epigenetic modification, cell proliferation, and apoptosis. It plays an important role in the genesis and development of cardiovascular disease. Objective: To assess the role of microRNA-208a in ketamine-induced cardiotoxicity. Methods: All rats were randomly selected into two groups: sham and model groups. After fixed, all rats in the model group was intraperitoneally (IP) injected with 100 mg/kg of ketamine. Heart samples were stained with HE assay. Total RNAs from serum were used to hybridize with the SurePrint G3 Rat Whole Genome GE 8×60 K Microarray G4858A platform. Results: In the rat model with ketamine-induced cardiotoxicity, microRNA-208a expression was increased. Then, over-expression of microRNA-208a increased inflammation and oxidative stress in vitro model. However, down-regulation of microRNA-208a decreased inflammation and oxidative stress in vitro model. Over-expression of microRNA-208a suppressed CHD9 and Notch1, and induced p65 protein expression in vitro model. Overexpression of CHD9 reduced the effects of microRNA-208a on inflammation and oxidative stress in heart cell through Notch/p65 signal pathways. Notch1 activation reduced the effects of microRNA-208a on inflammation and oxidative stress in heart cell through p65 signal pathways. Conclusion: MicroRNA-208a may be a potential biomarker for ketamine-induced cardiotoxicity through inflammation and oxidative stress by Notch/NF-κB signal pathways by CHD9.

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Dapk1 promoted inflammation of infantile pneumonia by p38MAPK/NF-κB signaling pathway

10.21203/rs.3.rs-115345/v1 ◽

2020 ◽

Author(s):

Wenbo Zhang

Keyword(s):

Protein Kinase ◽

Signaling Pathway ◽

In Vitro Model ◽

Potential Mechanism ◽

Mice Model ◽

Protein Expressions ◽

Death Associated Protein Kinase ◽

Vitro Model ◽

Induction Model

Abstract Background: The present study was designed to investigate the function of Death associated protein kinase 1 (DAPK1) in infantile pneumonia and explore the potential mechanism of the actions.Methods: Male C57BL/6 mice were injected with 2 mg/kg of LPS for the mice model of infantile pneumonia. A549 cell were treated with 100 ng/ml of LPS for vitro model of infantile pneumonia. Dapk1 mRNA and protein expressions in 6, 12 or 24 h after induction model of mice.Results: Dapk1 gene increased inflammation in vitro model through activation of p38MAPK-mediated NF-κB expression. The inhibition of p38MAPK or NF-κB reduced the pro-inflammation effects of DAPK1 in infantile pneumonia.Conclusions: Our study demonstrates that Dapk1 promoted inflammation of infantile pneumonia by p38MAPK/NF-κB signaling pathway, may be achieved inflammation by activation of p38MAPK/NF-κB signaling pathway

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An in vitro model for investigation of vitamin A effects on wound healing

International Journal for Vitamin and Nutrition Research ◽

10.1024/0300-9831/a000692 ◽

2021 ◽

pp. 1-6

Author(s):

Hoda Keshmiri Neghab ◽

Mohammad Hasan Soheilifar ◽

Gholamreza Esmaeeli Djavid

Keyword(s):

Wound Healing ◽

Endothelial Cell ◽

Vitamin A ◽

In Vitro Model ◽

Cellular Proliferation ◽

Endothelial Cell Migration ◽

Normal Fibroblast ◽

Anti Inflammatory ◽

Vitro Model

Abstract. Wound healing consists of a series of highly orderly overlapping processes characterized by hemostasis, inflammation, proliferation, and remodeling. Prolongation or interruption in each phase can lead to delayed wound healing or a non-healing chronic wound. Vitamin A is a crucial nutrient that is most beneficial for the health of the skin. The present study was undertaken to determine the effect of vitamin A on regeneration, angiogenesis, and inflammation characteristics in an in vitro model system during wound healing. For this purpose, mouse skin normal fibroblast (L929), human umbilical vein endothelial cell (HUVEC), and monocyte/macrophage-like cell line (RAW 264.7) were considered to evaluate proliferation, angiogenesis, and anti-inﬂammatory responses, respectively. Vitamin A (0.1–5 μM) increased cellular proliferation of L929 and HUVEC (p < 0.05). Similarly, it stimulated angiogenesis by promoting endothelial cell migration up to approximately 4 fold and interestingly tube formation up to 8.5 fold (p < 0.01). Furthermore, vitamin A treatment was shown to decrease the level of nitric oxide production in a dose-dependent effect (p < 0.05), exhibiting the anti-inflammatory property of vitamin A in accelerating wound healing. These results may reveal the therapeutic potential of vitamin A in diabetic wound healing by stimulating regeneration, angiogenesis, and anti-inﬂammation responses.

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