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. 2022 Jan 26;45(2):812–823. doi: 10.1007/s10753-021-01586-w

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© The Author(s) 2022

Open AccessThis 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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Fig. 4 — Effect of RSV on CCl₄-induced TGF-β synthesis and inflammatory factor expression. Rat HF models were established with or without RSV treatment. Peripheral blood and liver tissues were collected after 3 months. HSCs were isolated from livers 1 month after establishment. A mRNA expression levels of TGF-β in liver tissue were measured by qPCR. B Secretory TGF-β levels in livers were measured by ELISA. C Serum levels of inflammatory factors TNF-α and IL-6 were measured by ELISA. D mRNA levels of TNF-α and IL-6 in liver HSCs were measured by qPCR. A–D Results from three independent experiments are shown as mean ± SD (n = 6 rats per group). More than 12 rats were used for each experiment to make sure that at least 3 rats were survived in the CCl₄ group 3 months after HF development. *p < 0.05, **p < 0.01, and ***p < 0.001.