Abietic acid ameliorates pancreatic injury in acute pancreatitis by modulating MAPK pathway

Purpose: To examine the effect of abietic acid (AA) in the treatment of acute pancreatitis (AP) in mice.Methods: C57BL/6J mice were randomly assigned to 4 groups: sham, AP, AP + 20 mg/kg AA, and AP + 40 mg/kg AA groups. To induce AP mouse model, the mice received intraperitoneal (IP) injections of c...

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Veröffentlicht in:Tropical journal of pharmaceutical research 2023-09, Vol.22 (8), p.1573-1578
Hauptverfasser: Ye, Hailin, Wang, Jun, Mao, Jiaodan, Pan, Debiao
Format: Artikel
Sprache:eng
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Zusammenfassung:Purpose: To examine the effect of abietic acid (AA) in the treatment of acute pancreatitis (AP) in mice.Methods: C57BL/6J mice were randomly assigned to 4 groups: sham, AP, AP + 20 mg/kg AA, and AP + 40 mg/kg AA groups. To induce AP mouse model, the mice received intraperitoneal (IP) injections of cerulein. The extent of pancreatic tissue damage was evaluated by histological examination. Serum ALT, lipase, and amylase levels were determined by commercial kits while TUNEL assay was used to assess the apoptosis of pancreatic cells. The contents of Bax, Caspase-3, Bcl-2, p-ERK/ERK, p-JNK/JNK, and p-P38/P38 in pancreatic tissues were evaluated by western blot while the contents of IL-6, TNF-α, IL-1β, nitrite, MDA, and GSH in the tissues were evaluated by enzyme-linked immunosorbent assay (ELISA) kits.Results: AA relieved pancreatic damage and reduced ALT, lipase, and amylase levels in ceruleintreated AP mouse (p < 0.001). AA repressed apoptosis of pancreatic cells in cerulein-induced AP mouse, and inhibited oxidative stress and inflammatory response in the mice by reducing IL-6, TNF-α, IL-1β, nitrite, and MDA contents; it also enhanced the levels of GSH in the tissues (p < 0.001). In addition, AA inhibited MAPK pathway activity in the mice (p < 0.001).Conclusion: AA ameliorates pancreatic damage, pancreatic cell apoptosis, oxidative stress, and inflammation in cerulein-induced AP mouse by inhibiting MAPK pathway. This study offers a new potential drug for the management of AP and expands the relevant molecular regulatory mechanisms.
ISSN:1596-5996
1596-9827
DOI:10.4314/tjpr.v22i8.7