HAGLR aggravates neuropathic pain and promotes inflammatory response and apoptosis of lipopolysaccharide-treated SH-SY5Y cells by sequestering miR-182–5p from ATAT1 and activating NLRP3 inflammasome

2021 ◽  
Vol 145 ◽  
pp. 105001
Author(s):  
QuanYun Zhang ◽  
Li Zhou ◽  
Hong Xie ◽  
HongJin Zhang ◽  
XuZhu Gao
2014 ◽  
Vol 21 (7) ◽  
pp. 831-839 ◽  
Author(s):  
Ji Zhang ◽  
Stefania Echeverry ◽  
Tony Lim ◽  
Seung Lee ◽  
Xiang Shi ◽  
...  

2021 ◽  
Vol 416 ◽  
pp. 115468
Author(s):  
Tao Zheng ◽  
Qibin Wang ◽  
Fang Bian ◽  
Yan Zhao ◽  
Weidong Ma ◽  
...  

2018 ◽  
Vol 15 (1) ◽  
Author(s):  
Zhiqiang Pan ◽  
Qun Shan ◽  
Pan Gu ◽  
Xiao Min Wang ◽  
Lydia Wai Tai ◽  
...  

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Qi Wang ◽  
Bingfeng Lin ◽  
Zhifeng Li ◽  
Jie Su ◽  
Yulin Feng

Gouty arthritis is characterized by the deposition of monosodium urate (MSU) within synovial joints and tissues due to increased urate concentrations. Here, we elucidated the role of the natural compound cichoric acid (CA) on the MSU crystal-stimulated inflammatory response. The THP-1-derived macrophages (THP-Ms) were pretreated with CA and then stimulated with MSU suspensions. The protein levels of p65 and IκBα, the activation of the NF-κB signaling pathway by measuring the expression of its downstream inflammatory cytokines, and the activity of NLRP3 inflammasome were measured by western blotting and ELISA. CA treatment markedly inhibited the degradation of IκBα and the activation of NF-κB signaling pathway and reduced the levels of its downstream inflammatory genes such as IL-1β, TNF-α, COX-2, and PGE2 in the MSU-stimulated THP-M cells. Therefore, we infer that CA effectively alleviated MSU-induced inflammation by suppressing the degradation of IκBα, thereby reducing the activation of the NF-κB signaling pathway and the NLRP3 inflammasome. These results suggest that CA could be a novel therapeutic strategy in averting acute episodes of gout.


2021 ◽  

Introduction: Childhood asthma is one of the most common pediatric diseases, and its incidence is increasing. Annexin A3 (ANXA3) is a member of the Annexin family, a well-known polygenic family of membrane binding proteins. Bioinformation analysis showed that ANXA3 was highly expressed in asthmatic patients, suggesting the effects of ANXA3 on asthma, whereas the mechanism is still unclear. Methods: A inflammatory response model of bronchial epithelial BEAS-2B cells induced by LPS was constructed. Immunoblot and quantitative PCR assays were performed to detect the expression levels of ANXA3 in control or LPS-induced BEAS-2B cells. MTT, flow cytometry (FCM), and Immunoblot assays were respectively conducted to detect the effects of ANXA3 on survival and apoptosis of LPS-induced BEAS-2B cells. qPCR and ELISA assays were performed to detect the expression of TNF-α, IL-6, and IL-8. Additionally, Immunoblot assays were performed to detect the effects of ANXA3 on HIF1α and NLRP3 inflammasome in BEAS-2B cells. Results: We found ANXA3 was overexpressed in LPS-induced BEAS-2B cells. ANXA3 ablation promoted the survival of LPS-induced BEAS-2B cells and suppressed the inflammatory response of LPS-induced BEAS-2B cells. Importantly, we noticed ANXA3 inhibited HIF1α-induced NLRP3 inflammasome activity, and increasing the expression of HIF-α rescued the effects of ANXA3 depletion on asthma. Conclusion: ANXA3 enhanced LPS-triggered inflammation of human bronchial epithelial cells by regulating hypoxia-inducible factor-1α (HIF1α)-mediated NLRP3 inflammasome activation, and thought ANXA3 as a promising molecular target for acute asthma treatment.


Phytomedicine ◽  
2019 ◽  
Vol 59 ◽  
pp. 152785 ◽  
Author(s):  
Yung-Li Hung ◽  
Shu-Chi Wang ◽  
Katsuhiko Suzuki ◽  
Shih-Hua Fang ◽  
Chi-Shuo Chen ◽  
...  

IUBMB Life ◽  
2020 ◽  
Vol 72 (5) ◽  
pp. 1065-1074 ◽  
Author(s):  
Yan Sun ◽  
Yunlong Liu ◽  
Xiaofeng Guan ◽  
Juening Kang ◽  
Xiang Wang ◽  
...  

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