Abstract
Procyanidin B2 has demonstrated several health benefits and medical properties. However, its protective effects against CCl4-induced hepatotoxicity have not been clarified. The present study aimed to investigate the hepatoprotective effects of procyanidin B2 in CCl4-treated mice. Our data showed that procyanidin B2 significantly decreased the CCl4-induced elevation of serum alanine aminotransferase activities, as well as improved hepatic histopathological abnormalities. Procyanidin B2 also significantly decreased the content of MDA but enhanced the activities of antioxidant enzymes SOD, CAT and GSH-Px. Further research demonstrated that procyanidin B2 decreased the expression of TNF-α, IL-1β, cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS), as well as inhibited the translocation of nuclear factor-kappa B (NF-κB) p65 from the cytosol to the nuclear fraction in mouse liver. Moreover, CCl4-induced apoptosis in mouse liver was measured by (terminal-deoxynucleotidyl transferase mediated nick end labeling) TUNEL assay and the cleaved caspase-3. Meanwhile, the expression of apoptosis-related proteins Bax and Bcl-xL was analyzed by Western blot. Results showed that procyanidin B2 significantly inhibited CCl4-induced hepatocyte apoptosis, markedly suppressed the upregulation of Bax expression and restored the downregulation of Bcl-xL expression. Overall, the findings indicated that procyanidin B2 exhibited a protective effect on CCl4-induced hepatic injury by elevating the antioxidative defense potential and consequently suppressing the inflammatory response and apoptosis of liver tissues.
Highlights
The liver is an important metabolic organ with vital roles in several physiological processes, including proteins synthesis, glucose homeostasis and detoxification, as well as utilization and cycling of various nutrients [1]
The serum activities of both alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were significantly increased in the model group compared with those in the normal group (Figure 1A,B)
Administration of procyanidin B2 (100 mg·kg−1) in the procyanidin B2 control group did not alter the level of hepatic markers
Summary
The liver is an important metabolic organ with vital roles in several physiological processes, including proteins synthesis, glucose homeostasis and detoxification, as well as utilization and cycling of various nutrients [1]. CCl4, a chemical hepatotoxin, that produces reactive free radicals trichloromethyl radical (CCl3) and a proxy trichloromethyl radical (CCl3O2) when metabolized, has been frequently used to investigate the hepatoprotective effects of drugs and plant extracts as a solvent for induction of hepatic damage in animal models. CCl4 increases lipid peroxidation and protein oxidation in hepatic cells, as well as induces liver damage and apoptosis [4]. Grape seed procyanidin extract (GSPE) demonstrates various therapeutic properties, such as radical scavenging, and several health benefits, including anti-ulcer, anti-allergy, anti-dental caries, and antitumor activities [5,6]. The hepatoprotective effect of procyanidin B2 has not been fully investigated
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