甘草提取物通过抑制自噬和炎症对重症急性胰腺炎所致急性肺损伤的保护作用

Q3 Pharmacology, Toxicology and Pharmaceutics Journal of HerbMed Pharmacology Pub Date : 2023-08-10 DOI:10.34172/jhp.2023.44699
N. EL-Rahmany, E. A. M. Sharaf
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引用次数: 0

摘要

导言:急性胰腺炎(AP)是一种发病率和死亡率都很高的炎症性疾病。本研究旨在评估甘草提取物对精氨酸诱导的大鼠急性胰腺炎及相关肺组织损伤的保护作用。实验方法实验组为健康对照组(G1)、L-精氨酸组(G2)、甘草提取物组(G3)和甘草提取物+L-精氨酸组(保护组;G4)。甘草提取物的保护作用通过测定血清淀粉酶和脂肪酶、氧化应激标志物(丙二醛、一氧化氮和髓过氧化物酶)、炎症生物标志物水平(白细胞介素-6、肿瘤坏死因子-α、toll样受体4和血管细胞粘附分子1)以及通过caspase-3活性和beclin-1表达评估细胞凋亡来评价。此外,还对血红素加氧酶-1(HO-1)进行了免疫组化评估,并对肺部和胰腺组织进行了组织病理学检查。结果显示甘草提取物能明显降低血清淀粉酶、脂肪酶和炎症标志物水平,这表明精氨酸诱导的 AP 存在局部和全身炎症。此外,甘草提取物还能逆转胰腺和肺组织中氧化应激标记物水平的明显升高。此外,甘草提取物还能降低胰腺中贝克莱蛋白-1 和 Caspase-3 的基因表达,从而逆转胰腺自噬失调。结论甘草提取物能调节与急性胰腺损伤相关的氧化损伤和全身炎症。此外,甘草提取物通过其抗氧化、抗炎和抗细胞凋亡作用,明显减少了急性胰腺炎的生化和组织病理学变化,保护了胰腺和肺组织。
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Protective effect of Glycyrrhiza glabra L. root (licorice) extract against severe acute pancreatitis-induced acute lung injury via suppressing autophagy and inflammation
Introduction: Acute pancreatitis (AP) is an inflammatory disease with a high incidence of morbidity and mortality rate. The present study aimed to evaluate the protective effect of licorice extract administration on L-arginine-induced AP and associated lung tissue damage in rats. Methods: The experimental groups were the healthy control group (G1), L-arginine group (G2), licorice extract group (G3), and licorice extract +L-arginine; (protection group; G4). The protective effect of licorice extract was evaluated by measuring serum amylase and lipase, oxidative stress markers (malondialdehyde, nitric oxide, and myeloperoxidase), and inflammatory biomarkers levels (interleukin-6, tumor necrosis factor-alpha, toll-like receptor 4, and vascular cell adhesion molecule 1), as well as apoptosis assessment via caspase-3 activity and beclin-1 expression. Furthermore, an immunohistochemical assessment of heme oxygenase-1 (HO-1) and a histopathological examination of lung and pancreatic tissues were performed. Results: Licorice extract administration significantly reduced serum amylase, lipase, and inflammatory markers levels that pointed to the local and systemic inflammatory condition of AP induced by L-arginine. Moreover, the administration of licorice extract reversed the significant elevation in oxidative stress markers levels in the pancreas and lung tissues. Furthermore, licorice extract downregulated pancreatic gene expression of beclin-1 and caspase-3 which reversed dysregulated pancreatic autophagy. Conclusion: Licorice extract administration causes modulation of oxidative damage and systemic inflammation associated with acute pancreatic damage. Moreover, licorice extract markedly decreases the biochemical and histopathologic changes in AP, preserving the pancreatic and lung tissues through its antioxidant, anti-inflammatory, and antiapoptotic effects.
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来源期刊
Journal of HerbMed Pharmacology
Journal of HerbMed Pharmacology Pharmacology, Toxicology and Pharmaceutics-Drug Discovery
CiteScore
2.50
自引率
0.00%
发文量
49
审稿时长
12 weeks
期刊介绍: Journal of Herbmed Pharmacology (J Herbmed Pharmacol) is the intersection between medicinal plants and pharmacology. This international journal publishes manuscripts in the fields of medicinal plants, pharmacology and therapeutic. This journal aims to reach all relevant national and international medical institutions and persons in electronic version free of charge. J Herbmed Pharmacol has pursued this aim through publishing editorials, original research articles, reviews, mini-reviews, commentaries, letters to the editor, hypothesis, case reports, epidemiology and prevention, news and views. In this journal, particular emphasis is given to research, both experimental and clinical, aimed at protection/prevention of diseases. A further aim of this journal is to emphasize and strengthen the link between herbalists and pharmacologists. In addition, J Herbmed Pharmacol welcomes basic biomedical as well as pharmaceutical scientific research applied to clinical pharmacology. Contributions in any of these formats are invited for editorial consideration following peer review by at least two experts in the field.
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