Quinic acid ameliorates ulcerative colitis in rats, through the inhibition of two TLR4-NF-κB and NF-κB-INOS-NO signaling pathways.
Maryam Ghasemi-DehnooZahra LorigooiniHossein Amini-KhoeiMilad Sabzevary-GhahfarokhiMahmoud Rafieian-KopaeiPublished in: Immunity, inflammation and disease (2023)
QA ameliorated UC through the inhibition of two TLR4-NF-κB and NF-κB-INOS-NO signaling pathways, which results in the reduction of colitis complications, including oxidative stress, inflammation, apoptosis and histopathological injuries in rats. Therefore it can be concluded, that QA exerts its therapeutic effects through antiapoptotic, antioxidant, and anti-inflammatory properties.
Keyphrases
- oxidative stress
- signaling pathway
- pi k akt
- lps induced
- nuclear factor
- induced apoptosis
- inflammatory response
- ulcerative colitis
- toll like receptor
- anti inflammatory
- diabetic rats
- dna damage
- ischemia reperfusion injury
- cell cycle arrest
- immune response
- epithelial mesenchymal transition
- cell death
- endoplasmic reticulum stress
- risk factors
- nitric oxide synthase
- cell proliferation
- nitric oxide
- heat shock protein