Fahad S Al Amri, Norah M Alzamil, Bahjat Al-Ani, Hind Zafrah, Nervana M Bayoumy, Mohamed Abd Ellatif, Samaa S Kamar, Saeed M Alqahtani, Abeer I Omar, Asmaa M ShamsEldeen
{"title":"急性胰腺炎胰腺腺泡细胞中糖蛋白酶原颗粒的失调:维生素E和二甲双胍的不同保护作用。","authors":"Fahad S Al Amri, Norah M Alzamil, Bahjat Al-Ani, Hind Zafrah, Nervana M Bayoumy, Mohamed Abd Ellatif, Samaa S Kamar, Saeed M Alqahtani, Abeer I Omar, Asmaa M ShamsEldeen","doi":"10.1080/13813455.2025.2518366","DOIUrl":null,"url":null,"abstract":"<p><p>We investigated whether induction of acute pancreatitis (AP) can cause dysregulation in the glycoprotein zymogens, following episodes of nitrosative stress, which may be differentially protected by vitamin E and metformin. AP was induced in rats by L-arginine (2.5 g/kg) injections (two doses given at 1-h interval). The protective groups were pre-treated with either vitamin E (60 mg/kg) or metformin (50 mg/kg) prior to L-arginine injections and continued on these medications until being sacrificed. AP markedly decreased the density of zymogen granules in pancreatic acinar cells (44.5 ± 2.2% in control versus 9.2 ± 1.9% in AP), alongside tissue damage and a significant (<i>p</i> < 0.0001) increase in biomarkers of nitrosative stress (iNOS), inflammation (IL-6 and TNF-α mRNA), and pancreatic injury (amylase, lipase, LDH, and MPO). All these parameters were significantly (<i>p</i> ≤ 0.0005) protected by vitamin E and metformin, with vitamin E providing greater protection for pancreatic glycoprotein zymogens and serum amylase. Thus, AP is associated with the destruction of the glycoprotein zymogens, which is differentially protected by vitamin E and metformin.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"1-10"},"PeriodicalIF":2.7000,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Dysregulation of the glycoprotein zymogen granules in pancreatic acinar cells in acute pancreatitis: differential protection by vitamin E and metformin.\",\"authors\":\"Fahad S Al Amri, Norah M Alzamil, Bahjat Al-Ani, Hind Zafrah, Nervana M Bayoumy, Mohamed Abd Ellatif, Samaa S Kamar, Saeed M Alqahtani, Abeer I Omar, Asmaa M ShamsEldeen\",\"doi\":\"10.1080/13813455.2025.2518366\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>We investigated whether induction of acute pancreatitis (AP) can cause dysregulation in the glycoprotein zymogens, following episodes of nitrosative stress, which may be differentially protected by vitamin E and metformin. AP was induced in rats by L-arginine (2.5 g/kg) injections (two doses given at 1-h interval). The protective groups were pre-treated with either vitamin E (60 mg/kg) or metformin (50 mg/kg) prior to L-arginine injections and continued on these medications until being sacrificed. AP markedly decreased the density of zymogen granules in pancreatic acinar cells (44.5 ± 2.2% in control versus 9.2 ± 1.9% in AP), alongside tissue damage and a significant (<i>p</i> < 0.0001) increase in biomarkers of nitrosative stress (iNOS), inflammation (IL-6 and TNF-α mRNA), and pancreatic injury (amylase, lipase, LDH, and MPO). All these parameters were significantly (<i>p</i> ≤ 0.0005) protected by vitamin E and metformin, with vitamin E providing greater protection for pancreatic glycoprotein zymogens and serum amylase. Thus, AP is associated with the destruction of the glycoprotein zymogens, which is differentially protected by vitamin E and metformin.</p>\",\"PeriodicalId\":8331,\"journal\":{\"name\":\"Archives of Physiology and Biochemistry\",\"volume\":\" \",\"pages\":\"1-10\"},\"PeriodicalIF\":2.7000,\"publicationDate\":\"2025-06-16\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Archives of Physiology and Biochemistry\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1080/13813455.2025.2518366\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"ENDOCRINOLOGY & METABOLISM\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Archives of Physiology and Biochemistry","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/13813455.2025.2518366","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"ENDOCRINOLOGY & METABOLISM","Score":null,"Total":0}
Dysregulation of the glycoprotein zymogen granules in pancreatic acinar cells in acute pancreatitis: differential protection by vitamin E and metformin.
We investigated whether induction of acute pancreatitis (AP) can cause dysregulation in the glycoprotein zymogens, following episodes of nitrosative stress, which may be differentially protected by vitamin E and metformin. AP was induced in rats by L-arginine (2.5 g/kg) injections (two doses given at 1-h interval). The protective groups were pre-treated with either vitamin E (60 mg/kg) or metformin (50 mg/kg) prior to L-arginine injections and continued on these medications until being sacrificed. AP markedly decreased the density of zymogen granules in pancreatic acinar cells (44.5 ± 2.2% in control versus 9.2 ± 1.9% in AP), alongside tissue damage and a significant (p < 0.0001) increase in biomarkers of nitrosative stress (iNOS), inflammation (IL-6 and TNF-α mRNA), and pancreatic injury (amylase, lipase, LDH, and MPO). All these parameters were significantly (p ≤ 0.0005) protected by vitamin E and metformin, with vitamin E providing greater protection for pancreatic glycoprotein zymogens and serum amylase. Thus, AP is associated with the destruction of the glycoprotein zymogens, which is differentially protected by vitamin E and metformin.
期刊介绍:
Archives of Physiology and Biochemistry: The Journal of Metabolic Diseases is an international peer-reviewed journal which has been relaunched to meet the increasing demand for integrated publication on molecular, biochemical and cellular aspects of metabolic diseases, as well as clinical and therapeutic strategies for their treatment. It publishes full-length original articles, rapid papers, reviews and mini-reviews on selected topics. It is the overall goal of the journal to disseminate novel approaches to an improved understanding of major metabolic disorders.
The scope encompasses all topics related to the molecular and cellular pathophysiology of metabolic diseases like obesity, type 2 diabetes and the metabolic syndrome, and their associated complications.
Clinical studies are considered as an integral part of the Journal and should be related to one of the following topics:
-Dysregulation of hormone receptors and signal transduction
-Contribution of gene variants and gene regulatory processes
-Impairment of intermediary metabolism at the cellular level
-Secretion and metabolism of peptides and other factors that mediate cellular crosstalk
-Therapeutic strategies for managing metabolic diseases
Special issues dedicated to topics in the field will be published regularly.