Abstract
As a well-known hepatoprotective and antioxidant agent, dimethyl diphenyl bicarboxylate (DDB) has frequently been employed to remedy various liver diseases. However, it is still uncertain whether DDB exerts consistent hepatoprotective and antioxidative activities against varying degrees of hepatic damage. Therefore, DDB (100, 25, 5, or 50 mg/kg depending on the model) was administered to animals in four representative models of liver injury (CCl4 chemical acute model, DMN subchronic model, TAA chronic model, and restraint stress psychological acute model). Horizontal comparative analysis indicated that DDB significantly lowered the excess serum AST and ALT levels in the CCl4 and DMN models but not in the TAA and restraint stress models. In accordance with this result, DDB markedly reduced oxidative stress indices (hepatic MDA and ROS) but restored five main antioxidant components (GSH content, GSH-peroxidase, GSH-reductase, SOD, and catalase activity) in the CCl4 and DMN models. DDB failed to normalize oxidative stressors in the restraint stress-induced injury model and restore these five antioxidant components in the TAA model. Overall, our results produced a comprehensive overview of the effects of DDB on oxidative stressors and the main antioxidative components using four animal models. These findings will provide valuable clues to guide therapeutic clinical applications.
Highlights
Accepted: 20 September 2021The liver is a representative metabolic organ that is vulnerable to oxidative stress, and an imbalance in redox homeostasis has been implicated as a pivotal factor for causing numerous liver disorders [1,2,3]
Our results produced a comprehensive overview of the effects of dimethyl diphenyl bicarboxylate (DDB) on oxidative stressors and the main antioxidative components using four animal models
DDB was orally administered at doses of 100 mg/kg, 25 mg/kg, 5 mg/kg and 50 mg/kg in the chemical acute, subchronic, chronic and psychological acute liver injury models, respectively
Summary
Accepted: 20 September 2021The liver is a representative metabolic organ that is vulnerable to oxidative stress, and an imbalance in redox homeostasis has been implicated as a pivotal factor for causing numerous liver disorders [1,2,3]. Various exogenous and endogenous etiologies, such as drugs, xenobiotics and psychogenic stress, lead to liver injury via the excessive accumulation of reactive oxygen species (ROS) and overconsumption of antioxidative ability [2,4,5]. Chemical hepatotoxins, such as carbon tetrachloride (CCl4 ), dimethylnitrosamine (DMN) and thioacetamide (TAA), have been widely used to induce varying degrees of liver injury in antioxidant-related hepatoprotective animal studies [6]. It has long been highly regarded that antioxidants, including N-acetylcysteine, silymarin, and others, are a promising approach to relieve various acute and chronic liver injuries [9,10,11]
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