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. 2021 Oct 13;11:20316. doi: 10.1038/s41598-021-99953-y

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Ameliorating effect of ASE on the CCl₄-induced hepatic redox state disturbance. (A) reactive oxygen species (ROS) and total antioxidant capacity (TAC) levels. (B) thiobarbituric acid reactive substances (TBARS) and nitric oxide (NO) levels. (C) reduced glutathione (GSH) level and glutathione peroxidase (GPX) activity. (D) superoxide dismutase (SOD) and myeloperoxidase (MPO) activities. Results are expressed as mean ± S.E of 7 animals. BHT butylated hydroxytoluene, C control untreated rats, V olive oil (vehicle of CCl₄)-administered rats (0.5 ml/kg b.w., ip, 6 times), CCl₄ rats with systemic toxicity induced by CCl₄ injection (1 mL/kg b.w., ip, 6 times), CCl₄-ASE rats with systemic toxicity after their oral treatment with ASE (7.5 g/kg b.w.) for 10 days. ASE normal rats were administered only ASE (7.5 g/kg b.w.) for 10 days. Different letters refer to the significance at P < 0.05; CCl₄-ASE group was compared with the CCl₄ group, while V and ASE groups were individually compared with the C group.