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Pancreatic damage induced by cigarette smoke: the specific pathological effects of cigarette smoke in the rat model.
Toxicology Research ( IF 2.1 ) Pub Date : 2016-03-17 , DOI: 10.1039/c5tx00496a
Senay Topsakal 1 , Ozlem Ozmen 2 , Rahime Aslankoc 3 , Demet Hancer Aydemir 4
Affiliation  

In recent years, pancreatic pathologies have become common problems and their etiology and pathogenesis are generally unknown. Studies have shown that smoking may increase the risk of pancreatic disorders but very scant knowledge is available about the pathogenesis of cigarette induced pancreatic pathology. This study aimed to evaluate the oxidative stress status, biochemical, pathological and immunohistochemical findings of rats exposed to cigarette smoke, pathogenesis of smoking related pancreatic damage and usability of Alpha Lipoic Acid (ALA) for amelioration of cigarette smoking induced harmful effects on rat pancreas. Twenty eight female, Sprague Dawley rats were randomly distributed into three groups. The sham group (S) (n = 8), rats were given 0.1 ml of physiological serum by oral gavage for 8 weeks. The cigarette smoke exposed group (CSE) (n = 10), rats were exposed to successive periods of cigarette smoke for 2 hours per day per 8 weeks and given 0.1 ml of physiological serum orally during the study. The cigarette smoke exposed and ALA treated group (CSE + ALA) (n = 10), animals were exposed to cigarette smoke (2 hours per day per 8 weeks) and simultaneously treated with 100 mg per kg per day ALA orally during the study. At the end of the study, the serum samples were collected for insulin, glucagon, glucose and amylase analyses. Tissue samples were collected for biochemical, histopathological and immunohistochemical examinations. Total oxidant status (TOS), total antioxidant status (TAS) levels and oxidative stress index (OSI) were evaluated in the pancreas samples. Immunohistochemical analyses of insulin, glucagon, calcitonin gene related protein (CGRP), active caspase-3, hypoxia inducible factor-1 (Hif-1), Hif-2 and tumor necrosis factor (TNF-α) expressions of pancreas were examined. Cigarette smoke caused statistically significant increase in serum amylase and glucose but decreased insulin levels indicating both endocrine and exocrine cell damage. There were no statistically significant differences in serum glucagon levels between the groups. Histopathological examination of the pancreas exhibited generally normal tissue architecture but slightly degenerative and apoptotic cells were noticed both in the endocrine and exocrine part of the pancreas in the CSE group. Immunohistochemical analyses revealed marked increase in active caspase-3, Hif-1 and Hif-2, CGRP and TNF-α expressions with a slight increase in glucagon immunoreactivity in cells while a marked decrease was observed in insulin expression in some Langerhans islets in the CSE group. ALA ameliorated biochemical and pathological findings in the CSE + ALA group. These findings clearly demonstrated that cigarette smoke can cause damage in both endocrine and exocrine cells in rat pancreas and ALA has an ameliorative effect of cigarette induced lesions.

中文翻译:

香烟烟雾引起的胰腺损伤:香烟烟雾在大鼠模型中的特定病理作用。

近年来,胰腺病理已成为普遍的问题,其病因和发病机理通常是未知的。研究表明,吸烟可能会增加胰腺疾病的风险,但是关于香烟诱发的胰腺病理的发病机理的知识很少。这项研究旨在评估暴露于香烟烟雾的大鼠的氧化应激状态,生化,病理学和免疫组化发现,与吸烟有关的胰腺损伤的发病机制以及α-硫辛酸(ALA)用于改善香烟烟雾对大鼠胰腺的有害影响的可用性。将28只雌性Sprague Dawley大鼠随机分为三组。假手术组(S)(n = 8),通过管饲法给予大鼠0.1ml生理血清8周。香烟烟雾暴露组(CSE)(n = 10),大鼠每8周每天连续2小时暴露于香烟烟雾中,并在研究期间口服0.1 ml生理血清。暴露于香烟烟雾和ALA治疗组(CSE + ALA)(n = 10),使动物暴露于香烟烟雾(每8周每天2小时),并在研究期间同时口服100 mg / kg每天ALA。在研究结束时,收集血清样品进行胰岛素,胰高血糖素,葡萄糖和淀粉酶分析。收集组织样品用于生化,组织病理学和免疫组织化学检查。在胰腺样品中评估了总氧化剂状态(TOS),总抗氧化剂状态(TAS)水平和氧化应激指数(OSI)。胰岛素,胰高血糖素,检测降钙素基因相关蛋白(CGRP),活性caspase-3,缺氧诱导因子-1(Hif-1),Hif-2和肿瘤坏死因子(TNF-α)的表达。香烟烟雾引起血清淀粉酶和葡萄糖的统计学显着增加,但胰岛素水平降低,表明内分泌和外分泌细胞均受损。两组之间的血清胰高血糖素水平无统计学差异。胰腺的组织病理学检查通常显示正常的组织结构,但在CSE组中,胰腺的内分泌和外分泌部分均观察到轻微的变性和凋亡细胞。免疫组织化学分析显示,活性caspase-3,Hif-1和Hif-2明显增加,CSE组中某些朗格汉斯胰岛中的胰高血糖素免疫反应性的CGRP和TNF-α表达略有增加,而胰岛素表达则明显降低。ALA改善了CSE + ALA组的生化和病理学发现。这些发现清楚地表明,香烟烟雾可导致大鼠胰腺内分泌和外分泌细胞受损,ALA具有香烟诱导的病变的改善作用。
更新日期:2019-11-01
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