Chlorogenic acid prevents hepatotoxicity in arsenic-treated mice: role of oxidative stress and apoptosis

• Published in: Molecular biology reports 2020-02, Vol.47 (2), p.1161-1171
• Main Authors: Dkhil, Mohamed A., Abdel Moneim, Ahmed E., Bauomy, Amira A., Khalil, Mona, Al-Shaebi, Esam M., Al-Quraishy, Saleh
• Format: Article
• Language: English
• Subjects: Alanine; Alanine transaminase; Alkaline phosphatase; Animal Anatomy; Animal Biochemistry; Animals; Antioxidants - metabolism; Apoptosis; Apoptosis - drug effects; Arsenic; Arsenite; Arsenites - adverse effects; Aspartate transaminase; Bcl-2 protein; Bilirubin; Biomarkers; Biomedical and Life Sciences; Caspase-3; Catalase; Chemical and Drug Induced Liver Injury - diagnosis; Chemical and Drug Induced Liver Injury - etiology; Chemical and Drug Induced Liver Injury - metabolism; Chemical and Drug Induced Liver Injury - prevention & control; Chlorogenic acid; Chlorogenic Acid - pharmacology; Cytokines - metabolism; Degeneration; Disease Models, Animal; Glutathione peroxidase; Glutathione reductase; Heavy metals; Hepatocytes; Hepatocytes - drug effects; Hepatocytes - metabolism; Hepatotoxicity; Histology; Homeostasis; Immunohistochemistry; Inflammation; Inflammation Mediators - metabolism; Life Sciences; Liver; Liver diseases; Liver Function Tests; Male; Metastases; Mice; Morphology; Original Article; Oxidative stress; Oxidative Stress - drug effects; Plant protection; Protective Agents - pharmacology; Sodium Compounds - adverse effects; Superoxide dismutase
• ISSN: 0301-4851; 1573-4978
• DOI: 10.1007/s11033-019-05217-4

Arsenic is a potent and toxic heavy metal found in the environment that causes health problems, including liver disease, in humans and animals. Chlorogenic acid (CA) is the most abundant caffeoylquinic acid isomer present in plants. This study aims to assess how CA protects the liver tissue following sodium arsenite (NaAsO 2 )-induced toxicity in mice. Male Swiss mice were allocated into 5 groups: Control, intragastrically administered CA (200 mg/kg), intragastrically administered NaAsO 2 (5 mg/kg), and two groups administered with CA (100 and 200 mg/kg) and NaAsO 2 . CA was administered 30 min before NaAsO 2 and all the mice were treated daily for 28 days. To investigate the biochemical, histopathological, immunohistochemical, and molecular changes, blood and liver samples were collected. NaAsO 2 treatment increased the liver function biomarkers such as alanine transaminase, aspartate transaminase, alkaline phosphatase, and total bilirubin. Lipid and nitric oxide production was elevated. Glutathione content and the activities of superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase decreased, indicating a disturbance in redox homeostasis. Histopathological examination revealed a granular degeneration of hepatocytes, infiltration of inflammatory cells, and centrilobular hepatocyte necrosis. Furthermore, tumor necrosis factor-α and interleukin-1β were upregulated upon NaAsO 2 treatment, suggesting the induction of inflammation. Moreover, NaAsO 2 triggered apoptosis in the liver by upregulating Bax and caspase-3 and downregulating Bcl-2. However, CA abrogated the biochemical, molecular, and histological changes, reflecting its hepatoprotective role in response to NaAsO 2 treatment. Our findings demonstrate that CA could be a potential therapeutic to minimize NaAsO 2 -induced hepatic injury.