Interleukin-6 (Il6) mRNA levels were dramatically upregulated in pancreas of PGC-1α KO mice after cerulein-induced pancreatitis in comparison with wild-type mice with pancreatitis.
Based on the rigorous investigation of our meta-analysis, it was concluded that serum HMGB1 and IL-6 levels might be used as effective indicators for pancreatic lesions as well as the degree of inflammatory response, owing ultimately to the observations and data analyses, suggesting that serum HMGB1 and IL-6 levels share a close correlation with the severity of pancreatitis..
The severity of pancreatitis was evaluated by serum amylase (AMY), lipase (LIPA), tumor necrosis factor (TNF)‑α, interleukin (IL)‑1β and IL‑6 and assessing the histopathological score.
The preoperative and postoperative inflammatory cytokines such as tumor necrosis factor-α (TNF)-α, interleukin-6 (IL-6) and IL-8, and serum amylase levels were measured, and the incidence of pancreatitis and hyper amylasemia were monitored.
The interplay between LBP, IL-6, hepcidin, and ferritin characterizes metabolic derangements after acute pancreatitis and may play a role in the pathogenesis of new-onset diabetes after pancreatitis.
Therefore, DHA may help prevent the development of pancreatitis by suppressing the activation of NF-κB and PKCδ, expression of IL-6, and oxidative damage to the pancreas.
Administration of MSCs alone significantly reduced pancreatic injury and inflammation, as reflected by reductions in pancreatitis severity scores and serum amylase and lipase levels as well as reducing the serum levels of proinflammatory cytokines (TNF-α, IFN-γ, IL-1β, and IL-6).
We investigated whether pancreatitis-associated ascitic fluid (PAAF) could induce the expression of tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6) in THP-1 cells and the mechanism(s) involved.
When cerulein was administered with LPS, the pancreatic wet weight increased much more than when pancreatitis was induced by cerulein alone in both genotypes, and pretreatment with the anti-IL-6 receptor antibody decreased the pancreatic edema only in human-IL-6 transgenic mice.