Detection of melatonin protective effects in sepsis via argyrophilic nucleolar regulatory region-associated protein synthesis and TLR4/NF-κB signaling pathway.
Seher YilmazZüleyha DoğanyiğitAslı Okan OflamazŞükrü AteşSümeyye UçarEvrim Suna Arıkan SöylemezPublished in: Chemical biology & drug design (2022)
In this study, the protective effect of melatonin was investigated in lipopolysaccharide induced sepsis model. Twenty-eight rats were randomly divided: Control, Melatonin, LPS and LPS + Melatonin. After LPS application, surgically remove kidney and liver tissues. The level of malondialdehyde (MDA) an oxidative stress marker and the immunoreactivity of Toll-like receptor-4 (TLR4), tumor necrosis factor-α (TNF-α), and transcription factor NF-κB were evaluated immunohistochemically. Expression levels for TLR4, TNF-α, NF-kB, IL-1β (interleukin 1 beta), and IL-6 (interleukin 6) were evaluated. Additionally, Argyrophilic NOR staining was performed in tissues. Vacuolization and inflammation were more intense in the kidney and liver sections in the LPS group compared to the other groups. It was observed that vacuolization and inflammation were decreased in LPS + Melatonin applied groups. It was determined that glomerular damage was increased in the LPS and LPS-melatonin groups, but the damage rate LPS-Melatonin group was decrease in the LPS group. It was determined that the MDA level in tissues of the LPS group was importantly increased compared to other groups. Additionally, TAA/NA ratio statistically significant differences were discovered between the groups. This study supports the potential protective effects of 10 mg/kg melatonin by modulating critical markers of local immune reaction in a model of LPS-induced sepsis.
Keyphrases
- inflammatory response
- lps induced
- toll like receptor
- lipopolysaccharide induced
- oxidative stress
- signaling pathway
- nuclear factor
- transcription factor
- rheumatoid arthritis
- anti inflammatory
- intensive care unit
- pi k akt
- acute kidney injury
- gene expression
- epithelial mesenchymal transition
- dna damage
- immune response
- induced apoptosis
- climate change
- quantum dots
- heat shock protein
- heat shock