Protective effect of alpha lipoic acid against liver damage induced by cigarette smoke: An in vivo study

• Main Authors: Nurhan Gumral, Rahime Aslankoc, Nurgul Senol, Fatma Nihan Cankara
• Format: Article
• Language: English
• Published: Wolters Kluwer Medknow Publications 2021-01-01
• Series: Saudi Journal of Medicine and Medical Sciences
• Subjects: alpha-lipoic acid; inflammation; liver; oxidative stress; smoking
• Online Access: http://www.sjmms.net/article.asp?issn=1658-631X;year=2021;volume=9;issue=2;spage=145;epage=151;aulast=Gumral

Background: 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. Objective: 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. Materials and Methods: Twenty-eight female Sprague–Dawley rats were randomly divided into three groups. In the control group (n = 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 (n = 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 (n = 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. Results: MDA (P = 0.011), AST (P = 0.018) and total bilirubin levels (P < 0.001) were increased, while CAT activity (P = 0.009) and the efficiency of SOD (P = 0.010) were decreased in the smoking group compared with the control group. CAT activity was increased (P = 0.017) and AST (P = 0.018) and total bilirubin levels (P < 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. Conclusions: ALA can enhance antioxidant activity, but studies with different doses of ALA are required to determine the extent of its hepatoprotective effect.