Sesamin protects against DSS-induced colitis in mice by inhibiting NF-κB and MAPK signaling pathways

2021 ◽  
Author(s):  
Shuang Chen ◽  
Chun-Lei Zhang ◽  
Hai-Qing Shen ◽  
Xiao-Fei Zhou ◽  
Jing-He Li ◽  
...  
Keyword(s):  
Protective Effect ◽  
Signaling Pathways ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Experimental Colitis ◽  
Mapk Signaling ◽  
Mapk Signaling Pathways

To investigate the protective effect and mechanisms of sesamin (SES) on dextran sulfate sodium (DSS)-induced experimental colitis in mice.

Protective effect of Lachnum polysaccharide on dextran sulfate sodium-induced colitis in mice

2020 ◽  
Vol 11 (1) ◽  
pp. 846-859 ◽  
Author(s):  
Shuai Zong ◽  
Ziyang Ye ◽  
Xinmiao Zhang ◽  
Hui Chen ◽  
Ming Ye
Keyword(s):  
Endoplasmic Reticulum ◽  
Inflammatory Response ◽  
Endoplasmic Reticulum Stress ◽  
Protective Effect ◽  
Nitrosative Stress ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Experimental Colitis ◽  
Inflammasome Activation ◽  
Excessive Inflammatory Response

Lachnum polysaccharide alleviated dextran sulfate sodium induced experimental colitis through inhibiting excessive inflammatory response, inflammasome activation, endoplasmic reticulum stress and oxidative/nitrosative stress.

scholarly journals Ibudilast Attenuates Folic Acid–Induced Acute Kidney Injury by Blocking Pyroptosis Through TLR4-Mediated NF-κB and MAPK Signaling Pathways

2021 ◽  
Vol 12 ◽  
Author(s):  
Xue Li ◽  
Yu Zou ◽  
Yuan-Yuan Fu ◽  
Jia Xing ◽  
Kai-Yue Wang ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Folic Acid ◽  
Protective Effect ◽  
Signaling Pathways ◽  
Nuclear Translocation ◽  
Kidney Injury ◽  
Mapk Signaling ◽  
Inflammatory Factor ◽  
Anti Inflammatory ◽  
Mapk Signaling Pathways

Folic acid (FA)-induced renal tubule damage, which is characterized by extensive inflammation, is a common model of acute kidney injury (AKI). Pyroptosis, a pro-inflammatory form of cell death due to the activation of inflammatory caspases, is involved in AKI progression. Ibudilast, a TLR4 antagonist, has been used in the clinic to exert an anti-inflammatory effect on asthma. However, researchers have not explored whether ibudilast exerts a protective effect on AKI by inhibiting inflammation. In the present study, ibudilast reversed FA-induced AKI in mice, as indicated by the reduced serum creatinine and urea nitrogen levels, and improved renal pathology, as well as the downregulation of kidney injury marker-1. In addition, ibudilast significantly increased the production of the anti-inflammatory factor IL-10 while suppressing the secretion of the pro-inflammatory cytokine TNF-α and macrophage infiltration. Moreover, in the injured kidney, ibudilast reduced the levels of both inflammasome markers (NLRP3) and pyroptosis-related proteins (caspase-1, IL1-β, IL-18, and GSDMD cleavage), and decreased the number of TUNEL-positive cells. Further mechanistic studies showed that ibudilast administration inhibited the FA-induced upregulation of TLR4, blocked NF-κB nuclear translocation, and reduced the phosphorylation of NF-κB and IκBα, p38, ERK, and JNK. Thus, this study substantiates the protective effect of ibudilast on FA-induced AKI in mice and suggests that protection might be achieved by reducing pyroptosis and inflammation, likely through the inhibition of TLR4-mediated NF-κB and MAPK signaling pathways.

The protective effect of nigeglanine on dextran sulfate sodium‐induced experimental colitis in mice and Caco‐2 cells

2019 ◽  
Vol 234 (12) ◽  
pp. 23398-23408
Author(s):  
Xue‐jiao Gao ◽  
Bin Tang ◽  
Hui‐huang Liang ◽  
Li Yi ◽  
Zi‐gong Wei
Keyword(s):  
Protective Effect ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Experimental Colitis
Sign in / Sign up

Export Citation Format

Share Document