Abstract

Geranium schiedeanum has been used in traditional therapies as an antiseptic, antipyretic, and as analgesic. The present study was designed to evaluate the pretreatment with G. schiedeanum total extract (GS) and its active metabolites on stimulating the endogenous antioxidant defense system (EADS): catalase (Cat), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione reduction index (RI GSH/GSSG) in rat liver treated with a sublethal dose (6.6 mmol/Kg) of thioacetamide (TAA) in order to probe the capacity of GS and the active compounds to reduce liver injury. This was assessed by measuring aspartate aminotransferase (AST), alanine aminotransferase (ALT), and total bilirubin (BILT) in rats pretreated or not with TAA, and pretreated or not with GS and its metabolites. The results showed that GS was able to induce the production of EADS enzymes, increasing redox index GSH/GSSG at 24 and 48 h after intoxication, and both the extract and the ellagic acid exhibited a significant reduction of hepatic damage markers. Our data confirmed the hepatoprotective effect of GS and its metabolites, like ellagic acid, support the possible use of this extract in the treatment of liver injury.

Highlights

  • The liver is one of the organs that are most susceptible to damage due to its contact with multiple drugs, environmental toxins, alcohol, etc

  • It is of great importance that the correct use of plants as part of complementary alternative medicine (CAM) be based on phytochemical and biological studies that permit an explanation of the interaction phenomena between plant compounds and physiological responses in live systems

  • The endogenous antioxidant defense system (EADS) is the product of a long evolution in the face of the incessant damage that living beings have faced in the environment

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Summary

Introduction

The liver is one of the organs that are most susceptible to damage due to its contact with multiple drugs, environmental toxins, alcohol, etc. This implies a high worldwide incidence of liver diseases. Due to the high incidence of liver diseases, different experimental models have even greater degree. Due to the high incidence of liver diseases, different experimental models have been designed in order to know the molecular, biochemical, and physiopathological mechanisms by been designed in order to know the molecular, biochemical, and physiopathological mechanisms by which a liver lesion is developed. A frequent model utilized for representing acute damage is a single which a liver lesion is developed. A frequent model utilized for representing acute damage is a single dose of thioacetoamide (TAA). TAA is considered a potent hepatotoxic that causes damage at the centrilobular level; it is fundamentally metabolized in the CYP2E1, localized in the hepatic centrilobular level; it is fundamentally metabolized in the CYP2E1, localized in the hepatic microsomal microsomal space, which is highly reactive and capable of binding covalently to form adducts with space, which is highly reactive and capable of binding covalently to form adducts with the lysine the lysine ε-residues of nuclear proteins, favoring the occurrence of fibrosis, cirrhosis, and cancer [1]

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