Therapeutic Potential of Quercetin Loaded Nanoparticles: Novel Insights in Alleviating Colitis in an Experimental DSS Induced Colitis Model.
Safaa I KhaterMarwa M LotfyMaher N AlandiyjanyLeena S AlqahtaniAsmaa W ZagloolFayez AlthobaitiTamer Ahmed IsmailMohamed Mohamed SolimanSaydat SaadDoaa IbrahimPublished in: Biomedicines (2022)
Oxidative stress is considered the main etiologic factor involved in inflammatory bowel disease (IBD). Integration of nanocarriers for natural therapeutic agents with antioxidant and anti-inflammatory potential is a novel promising candidate for curing IBD. Herein, the colonic antioxidant and anti-inflammatory effects of different concentrations of quercetin nanoparticles (QT-NPs) were evaluated using a dextran sulfate sodium (DSS)-induced colitis model. Following colitis induction, the efficacy and mechanistic actions of QT-NPs were evaluated by assessing lesion severity, molecular aids controlling oxidative stress and inflammatory response, and histopathological and immunohistochemistry examination of colonic tissues. Administration of QT-NPs, especially at higher concentrations, significantly reduced the disease activity index and values of fecal calprotectin marker compared to the colitic group. Colonic oxidant/antioxidant status (ROS, H 2 O 2 , MDA, SOD, CAT, GPX and TAC) was restored after treatment with higher concentrations of QT-NPs. Moreover, QT-NPs at levels of 20 mg/kg and, to a lesser extent, 15 mg/kg reduced Nrf2 and HO-1 gene expression, which was in line with decreasing the expression of iNOS and COX2 in colonic tissues. Higher concentrations of QT-NPs greatly downregulated pro-inflammatory cytokines; upregulated genes encoding occludin, MUC-2 and JAM; and restored the healthy architectures of colonic tissues. Taken together, these data suggest that QT-NPs could be a promising alternative to current IBD treatments.
Keyphrases
- anti inflammatory
- oxidative stress
- ulcerative colitis
- gene expression
- drug induced
- disease activity
- oxide nanoparticles
- inflammatory response
- rheumatoid arthritis
- dna damage
- systemic lupus erythematosus
- drug delivery
- induced apoptosis
- ischemia reperfusion injury
- dna methylation
- poor prognosis
- juvenile idiopathic arthritis
- electronic health record
- lipopolysaccharide induced
- cancer therapy
- genome wide
- antiretroviral therapy
- long non coding rna
- transcription factor
- nitric oxide
- heat shock
- risk assessment
- big data
- toll like receptor
- heat stress
- pi k akt