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. 2018 May 31;19(6):1626. doi: 10.3390/ijms19061626

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© 2018 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Hepatoprotective effect on carbon tetrachloride (CCl₄)-induced chronic liver injury in mice. (A) Liver tissue of mice and corresponding hematoxylin-eosin (HE) staining. Groups were as described in “Methods: animal”. The tissue was enlarged locally and diffusion miliary dots were observed in the chronic liver injury (CLI) group; the HE staining was 200×; (B) Body weight gain, liver index, and pathological score. Groups were as described in “Methods: animal”; (C) The activity of alanine transaminase (ALT), aspartate aminotransferase (AST), superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), and catalase (CAT). Groups were as described in “Methods: animal”. Data was the mean ± SD of n = 10 mice/group. * p < 0.05, ** p < 0.01, *** p < 0.001 compared with the control group and ^# p < 0.05, ^## p < 0.01 compared with the CLI group.

Hepatoprotective effect on carbon tetrachloride (CCl₄)-induced chronic liver injury in mice. (A) Liver tissue of mice and corresponding hematoxylin-eosin (HE) staining. Groups were as described in “Methods: animal”. The tissue was enlarged locally and diffusion miliary dots were observed in the chronic liver injury (CLI) group; the HE staining was 200×; (B) Body weight gain, liver index, and pathological score. Groups were as described in “Methods: animal”; (C) The activity of alanine transaminase (ALT), aspartate aminotransferase (AST), superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), and catalase (CAT). Groups were as described in “Methods: animal”. Data was the mean ± SD of n = 10 mice/group. * p < 0.05, ** p < 0.01, *** p < 0.001 compared with the control group and ^# p < 0.05, ^## p < 0.01 compared with the CLI group.