枞酸通过调节MAPK通路改善急性胰腺炎的胰腺损伤

IF 0.6 4区 医学 Q4 PHARMACOLOGY & PHARMACY Tropical Journal of Pharmaceutical Research Pub Date : 2023-09-15 DOI:10.4314/tjpr.v22i8.7
Hailin Ye, Jun Wang, Jiaodan Mao, Debiao Pan
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引用次数: 0

摘要

目的:观察枞酸(AA)对小鼠急性胰腺炎(AP)的治疗作用。方法:将C57BL/6J小鼠随机分为4组:假手术组、AP组、AP + 20 mg/kg AA组和AP + 40 mg/kg AA组。为了建立AP小鼠模型,小鼠腹腔注射蓝蛋白。通过组织学检查评估胰腺组织损伤程度。采用商用试剂盒检测血清ALT、脂肪酶和淀粉酶水平,TUNEL法检测胰腺细胞凋亡情况。western blot检测各组胰腺组织中Bax、Caspase-3、Bcl-2、p-ERK/ERK、p-JNK/JNK、p-P38/P38的含量,ELISA试剂盒检测各组组织中IL-6、TNF-α、IL-1β、亚硝酸盐、MDA和GSH的含量。结果:AA减轻了胰脏损伤,降低了酪氨酸处理的AP小鼠的ALT、脂肪酶和淀粉酶水平(p <0.001)。AA通过降低IL-6、TNF-α、IL-1β、亚硝酸盐和MDA含量,抑制丙烯醛诱导的AP小鼠胰腺细胞凋亡,抑制小鼠氧化应激和炎症反应;它还提高了组织中谷胱甘肽的水平(p <0.001)。此外,AA抑制小鼠的MAPK通路活性(p <0.001)。结论:AA可通过抑制MAPK通路改善丙核蛋白诱导的AP小鼠胰腺损伤、胰腺细胞凋亡、氧化应激和炎症反应。本研究为AP的治疗提供了一种新的潜在药物,并扩展了相关的分子调控机制。
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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 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.
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33.30%
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490
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期刊介绍: We seek to encourage pharmaceutical and allied research of tropical and international relevance and to foster multidisciplinary research and collaboration among scientists, the pharmaceutical industry and the healthcare professionals. We publish articles in pharmaceutical sciences and related disciplines (including biotechnology, cell and molecular biology, drug utilization including adverse drug events, medical and other life sciences, and related engineering fields). Although primarily devoted to original research papers, we welcome reviews on current topics of special interest and relevance.
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