Gumral Nurhan, Aslankoc Rahime, Senol Nurgul, Cankara Fatma Nihan
Department of Physiology, Faculty of Medicine, Suleyman Demirel University, Isparta, Turkey.
Department of Nutrition and Dietetics, Faculty of Medicine, Suleyman Demirel University, Isparta, Turkey.
Saudi J Med Med Sci. 2021 May-Aug;9(2):145-151. doi: 10.4103/sjmms.sjmms_387_20. Epub 2021 Apr 29.
Long-term cigarette smoking damages the liver tissue. Alpha-lipoic acid (ALA) is used as a therapeutic agent in a number of conditions and is known to have ameliorative effects against oxidative stress in the liver.
To investigate the ameliorative effects of ALA on cigarette smoke (CS)-induced oxidative liver damage by examining histopathological, immunohistopathological changes and biochemical parameters in an animal model.
Twenty-eight female Sprague-Dawley rats were randomly divided into three groups. In the control group ( = 8), rats were exposed to fresh air twice a day and given 0.1 ml of saline by gavage once a day for 8 weeks. In the smoking group ( = 10), rats were exposed to CS for 1 h in the morning and afternoon and given 0.1 ml of saline by gavage once a day for 8 weeks. In the smoking + ALA group ( = 10), CS exposure was same as the smoking group in addition to 100 mg/kg of ALA per day for 8 weeks through gavage. Oxidative damage in the liver tissue was determined by evaluating malondialdehyde (MDA), catalase (CAT) and superoxide dismutase (SOD) levels. Aspartate aminotransferase (AST), alanine aminotransaminase (ALT), alkaline phosphatase (ALP), direct bilirubin and total bilirubin levels were measured in the blood. Histopathological and immunohistochemical examinations were performed.
MDA ( = 0.011), AST ( = 0.018) and total bilirubin levels ( < 0.001) were increased, while CAT activity ( = 0.009) and the efficiency of SOD ( = 0.010) were decreased in the smoking group compared with the control group. CAT activity was increased ( = 0.017) and AST ( = 0.018) and total bilirubin levels ( < 0.001) were decreased in ALA-treated group compared with the smoking group. We observed vascular dilatation and hemorrhagic areas in the smoking group. TNF-α expression was increased in the smoking group compared with the control group. However, TNF-α expression was high in some preparations in the ALA-treated group.
ALA can enhance antioxidant activity, but studies with different doses of ALA are required to determine the extent of its hepatoprotective effect.
长期吸烟会损害肝组织。α-硫辛酸(ALA)在多种病症中用作治疗剂,并且已知对肝脏中的氧化应激具有改善作用。
通过检查动物模型中的组织病理学、免疫组织病理学变化和生化参数,研究ALA对香烟烟雾(CS)诱导的氧化性肝损伤的改善作用。
28只雌性Sprague-Dawley大鼠随机分为三组。对照组(n = 8),大鼠每天两次暴露于新鲜空气中,每天经口灌胃给予0.1 ml生理盐水,持续8周。吸烟组(n = 10),大鼠每天上午和下午暴露于香烟烟雾中1小时,每天经口灌胃给予0.1 ml生理盐水,持续8周。吸烟+ALA组(n = 10),除每天经口灌胃给予100 mg/kg的ALA持续8周外,香烟烟雾暴露与吸烟组相同。通过评估丙二醛(MDA)、过氧化氢酶(CAT)和超氧化物歧化酶(SOD)水平来确定肝组织中的氧化损伤。测定血液中的天冬氨酸转氨酶(AST)、丙氨酸转氨酶(ALT)、碱性磷酸酶(ALP)、直接胆红素和总胆红素水平。进行组织病理学和免疫组织化学检查。
与对照组相比,吸烟组的MDA(P = 0.011)、AST(P = 0.018)和总胆红素水平(P < 0.001)升高,而CAT活性(P = 0.009)和SOD效率(P = 0.010)降低。与吸烟组相比,ALA治疗组的CAT活性升高(P = 0.017),AST(P = 0.018)和总胆红素水平(P < 0.001)降低。我们在吸烟组中观察到血管扩张和出血区域。与对照组相比,吸烟组的TNF-α表达增加。然而,在ALA治疗组的一些制剂中TNF-α表达较高。
ALA可以增强抗氧化活性,但需要用不同剂量的ALA进行研究以确定其肝保护作用的程度。