Dapsone reduced acetic acid-induced inflammatory response in rat colon tissue through inhibition of NF-kB signaling pathway

2019 ◽  
Vol 41 (6) ◽  
pp. 607-613 ◽  
Author(s):  
Amir Rashidian ◽  
Asma Rashki ◽  
Alireza Abdollahi ◽  
Nazgol-Sadat Haddadi ◽  
Mohsen Chamanara ◽  
...  
Keyword(s):  
Acetic Acid ◽  
Inflammatory Response ◽  
Signaling Pathway ◽  
Rat Colon ◽  
Colon Tissue

Thymol reduces acetic acid-induced inflammatory response through inhibition of NF-kB signaling pathway in rat colon tissue

2019 ◽  
Vol 27 (6) ◽  
pp. 1275-1283 ◽  
Author(s):  
Mohsen Chamanara ◽  
Alireza Abdollahi ◽  
Seyed Mahdi Rezayat ◽  
Mamoud Ghazi-Khansari ◽  
Ahmadreza Dehpour ◽  
...  
Keyword(s):  
Acetic Acid ◽  
Inflammatory Response ◽  
Signaling Pathway ◽  
Rat Colon ◽  
Colon Tissue

scholarly journals Protective Effect of Methane-Rich Saline on Acetic Acid-Induced Ulcerative Colitis via Blocking the TLR4/NF-κB/MAPK Pathway and Promoting IL-10/JAK1/STAT3-Mediated Anti-inflammatory Response

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Guanghui Wang ◽  
Bing Xu ◽  
Feiyu Shi ◽  
Mengfan Du ◽  
Yaguang Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ulcerative Colitis ◽  
Acetic Acid ◽  
Inflammatory Response ◽  
Protective Effect ◽  
Signaling Pathway ◽  
Tissue Damage ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Anti Inflammatory

Ulcerative colitis (UC) is an inflammation-related disease involved in uncontrolled inflammation and oxidative stress and is characterized by high recurrence and relapse risk. As a rising star in gas medicine, methane owns the properties of anti-inflammation, antioxidation, and antiapoptosis. Based on the possible mechanism, we aimed to investigate the effect of methane on UC. Methane-rich saline (MRS) was introduced here, and UC was induced by acetic acid. All the C57BL/6 mice were allocated into groups as follows: control group, colitis model group, colitis treated with salazosulfapyridine (SASP) group, and colitis treated with MRS (1 or 10 ml/kg) groups. Tissue damage, the degree of inflammation, oxidative stress, and apoptosis were evaluated in the study, as well as the TLR4/NF-κB/MAPK and IL-10/JAK1/STAT3 signaling pathways for further exploration of the potential mechanism. The results showed that MRS (1) alleviated tissue damage caused by acetic acid, (2) controlled acetic acid-induced inflammation, (3) inhibited acetic acid-caused oxidative stress, (4) reduced colonic cell apoptosis due to acetic acid, (5) suppressed the TLR-4/NF-κB/MAPK signaling pathway, and (6) activated IL-10/JAK1/STAT3 anti-inflammatory response to improve the injury induced by acetic acid. We conclude that MRS has a protective effect on acetic acid-induced ulcerative colitis in mice via blocking the TLR4/NF-κB/MAPK signaling pathway and promoting the IL-10/JAK1/STAT3-mediated anti-inflammatory response.

scholarly journals Umbelliferone ameliorates ulcerative colitis induced by acetic acid via modulation of TLR4/NF-κB-p65/iNOS and PPARγ/SIRT1 signaling pathways in rats

2021 ◽  
Author(s):  
Basel A Abdel-Wahab ◽  
Saad A Alkahtani ◽  
Abdulsalam A Alqahtani ◽  
Emad H.M. Hassanein
Keyword(s):  
Ulcerative Colitis ◽  
Acetic Acid ◽  
Inflammatory Response ◽  
Signaling Pathways ◽  
Signaling Pathway ◽  
Therapeutic Potential ◽  
Tissue Injury ◽  
Oxidative Injury ◽  
Control Group ◽  
Anti Inflammatory

Abstract Ulcerative colitis (UC) is a common chronic, idiopathic inflammatory bowel disease associated with inflammatory perturbation and oxidative stress. Umbelliferone (UMB) is a potent anti-inflammatory and antioxidant coumarin derivative. Depending on the possible mechanisms, we aimed to explore and elucidate the therapeutic potential of UMB on UC-inflammatory response and oxidative injury-induced via intrarectal administration of acetic acid (AA). Rats were assigned into four groups: control group, UMB (30 mg/kg) treated group, colitis model group (2 ml of AA; 3% v/v), and colitis treated with UMB groups. Our results exhibited that UMB improved macroscopic and histological tissue injury caused by the AA. Mechanistically, UMB reduced the elevated TNF-α, IL-6, MPO and VCAM-1 via effective downregulation of TLR-4, NF-κB and iNOS signaling pathway, thereby mediated potent anti-inflammatory effects. Moreover, UMB administration resulted in effective up-regulation of both PPARγ and SIRT1 signaling pathways, thereby inhibited both oxidative injury and inflammatory response. Conclusively, UMB protected against AA-induced UC in rats through suppressing of the TLR4/NF-κB-p65/iNOS signaling pathway and promoting the PPARγ/SIRT1 signaling. Indeed, our data proved the effectiveness of UMB in UC and introduced it as a potential therapeutic beneficial applicant for clinical application.

scholarly journals Retraction: Salvianolic acid B inhibits inflammatory response and cell apoptosis via the PI3K/Akt signaling pathway in IL-1β-induced osteoarthritis chondrocytes

RSC Advances ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 4441-4441
Author(s):  
Laura Fisher
Keyword(s):  
Inflammatory Response ◽  
Signaling Pathway ◽  
Cell Apoptosis ◽  
Akt Signaling ◽  
Salvianolic Acid B ◽  
Signalling Pathway ◽  
Akt Signaling Pathway ◽  
Salvianolic Acid ◽  
Osteoarthritis Chondrocytes

Retraction of ‘Salvianolic acid B inhibits inflammatory response and cell apoptosis via the PI3K/Akt signalling pathway in IL-1β-induced osteoarthritis chondrocytes’ by Bin Zhu et al., RSC Adv., 2018, 8, 36422–36429, DOI: 10.1039/C8RA02418A.

scholarly journals Cichoric Acid Ameliorates Monosodium Urate-Induced Inflammatory Response by Reducing NLRP3 Inflammasome Activation via Inhibition of NF-kB Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Qi Wang ◽  
Bingfeng Lin ◽  
Zhifeng Li ◽  
Jie Su ◽  
Yulin Feng
Keyword(s):  
Inflammatory Response ◽  
Signaling Pathway ◽  
Nlrp3 Inflammasome ◽  
Gouty Arthritis ◽  
Inflammasome Activation ◽  
Cichoric Acid ◽  
Monosodium Urate ◽  
Protein Levels ◽  
Nlrp3 Inflammasome Activation ◽  
Tnf Α

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.

Sign in / Sign up

Export Citation Format

Share Document