Protective Effect and Mechanism of MyD88 Inhibitor in Acute Pancreatitis Associated Gastric Injury
10.3870/j.issn.1672-0741.25.02.002
- VernacularTitle:MyD88抑制剂对急性胰腺炎相关性胃损伤的保护作用及机制研究
- Author:
Hao WANG
1
;
Jianhua LIU
;
Jian YOU
Author Information
1. 武汉市第四医院普通外科胃肠外科,武汉 430030
- Publication Type:Journal Article
- Keywords:
MyD88 inhibitor;
gastric injury associated with acute pancreatitis;
p65 phosphorylation;
inflammatory factor
- From:
Acta Medicinae Universitatis Scientiae et Technologiae Huazhong
2025;54(2):198-202
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the inhibitory effect of MyD88 inhibitor St-2825 on inflammatory pathways and its protective efficacy on gastric tissue in sodium taurocholate-induced acute pancreatitis-associated gastric injury.Methods An a-cute pancreatitis rat model was established by subcapsular pancreatic injection of sodium taurocholate.Rats were randomly di-vided into normal control group(Group C,received saline+saline treatment),acute pancreatitis group(Group P,received sodium taurocholate+saline treatment),and intervention group(Group T,received sodium taurocholate+MyD88 inhibitor St-2825 treatment),with 16 rats in each group,48 rats in total.Pancreatic and gastric tissue samples were collected at 2 h and 6 h post-modeling.The samples were paraffin-embedded,sectioned,and stained with hematoxylin-eosin(HE)for comparative pathological scoring.Serum levels of tumor necrosis factor-α(TNF-α),interleukin-1(IL-1),and interleukin-6(IL-6)were measured by ELISA.Immunofluorescence staining was performed to assess immune cell infiltration in gastric tissues.Western blot was used to determine the protein expression of MyD88 and the phosphorylation ratio of p65 in the TLR/MyD88/NF-κB p65 signaling pathway in rat gastric tissues.Results In sodium taurocholate-induced acute pancreatitis-associated gastric injury rats,both pancreatic and gastric pathological scores were increased progressively over time.The plasma levels of TNF-α,IL-1 and IL-6 were significantly elevated.During pancreatic injury,gastric tissues exhibited markedly increased infiltration of neutrophils,mac-rophages,dendritic cells and T lymphocytes.The upregulated MyD88 in tissues stimulated NF-κB pathway activation,leading to phosphorylated p65 nuclear translocation and downstream inflammatory factors transcription.MyD88 inhibitor St-2825 inter-vention effectively blocked p65 phosphorylation and nuclear translocation,attenuated downstream inflammatory responses,and reduced immune cell infiltration in gastric tissues.Conclusion Gastric tissues undergo progressive damage during pancreatic in-jury.The MyD88 inhibitor St-2825 attenuates inflammatory responses and mitigates immune cell infiltration in acute pancreati-tis-associated gastric injury,thereby exerting protective effects.
