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اثرات وابسته به زمان نیکوتین بر گلوکز، آلبومین، اوره، اسیداوریک سرم و بافت‌شناسی کبد در موش صحرایی | ||
| فصلنامه علمی زیست شناسی جانوری تجربی | ||
| دوره 13، شماره 2 - شماره پیاپی 50، اسفند 1403، صفحه 67-75 اصل مقاله (1012.55 K) | ||
| نوع مقاله: مقاله پژوهشی | ||
| شناسه دیجیتال (DOI): 10.30473/eab.2025.72323.1965 | ||
| نویسندگان | ||
| پریناز حاجی یوسفی پور؛ مهدی بساکی* ؛ داوود کیانی فرد؛ یوسف پناهی؛ مهری انیسی | ||
| گروه علوم پایه، دانشکده دامپزشکی، دانشگاه تبریز، تبریز، ایران | ||
| چکیده | ||
| نیکوتین یک آلکالوئید طبیعی و عامل اصلی اعتیاد به دخانیات است. نیکوتین با اتصال به گیرنده‌های نیکوتینی استیل‌کولین (nAChRs) مغز را تحریک می‌کند، فشار خون و ضربان قلب را افزایش می‌دهد، سرعت متابولیسم را افزایش می‌دهد، اشتها را سرکوب می‌کند و وزن بدن را تنظیم می‌کند. نیکوتین باعث کاهش وزن، نشت آنزیم، پراکسیداسیون لیپیدی و استرس اکسیداتیو کبد می‌شود. برای بررسی زمانی اثرات نیکوتین بر عملکرد کبد روزانه نیکوتین (mg/kg 2) به‌صورت داخل صفاقی به موش‌ها تزریق شد. 40 نمونه خون در چهار مرحله زمانی، به‌عنوان چهار گروه مستقل، قبل از تزریق نیکوتین و 30 دقیقه، یک هفته و چهار هفته پس از اولین تزریق نیکوتین گرفته شد. گلوکز، آلبومین، اوره و اسید اوریک سرم با روش‌های استاندارد اندازه‌گیری شد. پس از چهار هفته تجویز نیکوتین، نمونه‌های کبد در محلول فرمالدئید 10 درصد تثبیت شدند و قطر ورید مرکزی، هپاتوسیت و سینوزوئید و ضخامت کپسول کبد اندازه‌گیری شد. تجویز کوتاه‌مدت و بلند مدت نیکوتین گلوکز و آلبومین سرم را کاهش داد. تجویز فوری، کوتاه‌مدت و طولانی‌مدت نیکوتین اوره و اسید اوریک سرم را کاهش داد. قطر سلول‌های کبدی و سینوزوئیدها پس از چهار هفته تجویز نیکوتین افزایش یافت. نیکوتین با مکانیسم‌های تنظیمی مختلف سنتز کبدی گلوکز، آلبومین، اوره و اسید اوریک را به‌صورت وابسته به زمان کاهش می‌دهد. بررسی اثرات نیکوتین بر ژن‌ها و آنزیم‌های دخیل در متابولیسم کبد به‌روشن‌ترشدن مکانیسم‌های مولکولی اثرات نیکوتین کمک خواهد کرد. | ||
| کلیدواژه‌ها | ||
| نیکوتین؛ گلوکز؛ آلبومین؛ اوره؛ اسید اوریک؛ کبد | ||
| عنوان مقاله [English] | ||
| Time-dependent effects of nicotine on serum glucose, albumin, urea, uric acid, and liver histology in rat | ||
| نویسندگان [English] | ||
| Parinaz Hajiyousefipour؛ Mehdi Basaki؛ Davoud Kianifard؛ Yousef Panahi؛ Mehri Anisi | ||
| Department of Basic Sciences, Faculty of Veterinary Medicine, University of Tabriz, Tabriz, Iran | ||
| چکیده [English] | ||
| Nicotine is a natural alkaloid and the primary cause of tobacco addiction. Nicotine stimulates the brain, raises blood pressure and heart rate, increases metabolic rate, suppresses appetite, and regulates body weight through binding to nicotinic acetylcholine receptors (nAChRs). Nicotine causes weight loss, enzyme leakage, lipid peroxidation, and oxidative stress in the liver. To investigate the time-dependent effects of nicotine on liver function rats were injected intraperitoneally daily with of nicotine (2 mg/kg). Forty blood samples were taken at four stages, as four independent groups, before nicotine administration and 30 minutes, one week, and four weeks after the first nicotine administration. Serum glucose, albumin, urea, and uric acid were measured by standard methods. After four weeks of nicotine administration, liver samples were fixed in a 10% formaldehyde solution, and diameters of the central vein, hepatocyte, and sinusoid and thickness of the liver capsule were measured. Short and long-term nicotine administration decreased serum glucose and albumin. Serum urea and uric acid decreased following immediate, short-term, and long-term nicotine administration. Also, the diameter of hepatocytes and sinusoids increased after four weeks of nicotine administration. Nicotine reduces hepatic synthesis of glucose, albumin, urea, and uric acid time-dependently through various regulatory mechanisms. Investigating nicotine's effects on the genes and enzymes involved in liver metabolism will help to clarify the molecular mechanisms of nicotine's effects. | ||
| کلیدواژه‌ها [English] | ||
| Nicotine, glucose, albumin, urea, uric acid, liver | ||
| مراجع | ||
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