In conclusion, the current study investigated a novel regulatory mechanism of the TLR4/NF‑κB pathway in LPS‑stimulated pancreatic cells, which may contribute to pancreatitis.
The regulatory effects of OM on the TLR4/MyD88/NF-κB signaling pathway under the stimulation of lipopolysaccharide (LPS) in MS1 cells were explored to illuminate the potential anti-inflammatory mechanism of OM for pancreatitis treatment.
The distributions of the HY/HY, HY/LY, LY/LY, and LY/LX genotypes of MBL2 gene promoter and 119C>A genotype of the TLR4 gene were similar in patients with mild or severe acute pancreatitis.
Compared with healthy volunteers (5.6%), TLR4 896G allele frequencies was significantly higher in AP patients with pancreatic infection (20%), the incidence of gram-negative infection was significantly higher in AP patients with TLR4 Asp299Gly polymorphism (15 [44%]/34) than that in AP patients without TLR4 polymorphism (15 [18%]/81).
There was no significant correlation between TLR4 polymorphisms and the acute pancreatitis itself, but nonsignificantly increased frequencies of Asp299Gly and Thr399Ile heterozygotes among patients with severe infected pancreatic necrosis could be observed relative to the patients with mild pancreatitis.