Interleukin-7 as a potential therapeutic target for alleviating hepatic fibrosis in a mice model induced by carbon tetrachloride: Implications for fitness and exercise

• Cuiyun Liu ^[1] ; Zhiguo Wu ^[1] ; Zhen Gao ^[2] ; Xuebing Yao ^[1] ; Di Jin ^[1] ; Zhiying Song ^[1] ; Shuilin Sun ^[1]
  1. [1] Nanchang University

     Nanchang University

     China

     
  2. [2] Municipal Hospita, Shangrao
• Localización: Revista Internacional de Medicina y Ciencias de la Actividad Física y del Deporte, ISSN-e 1577-0354, Vol. 23, Nº. 90, 2023, págs. 13-24
• Idioma: español
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• Resumen

  • The effects of interleukin-7 (IL-7) on the carbon tetrachloride (CCL4) induced hepatic fibrosis were investigated in this study. Thirty-six female BALB/C mice were randomized into group A (control group) injected with saline, group B (fibrotic model group) and group C (IL-7 intervention group). Histopathological changes were observed by HE, Masson as well as reticular fiber staining. The apoptosis cells and hepatic stellate cell (HSC) were detected from the tissues, and the expressions of Bax and Bcl-2 gene were also detected. The results of histological HE, Masson and reticular fiber staining showed that compared with group B, the degree of inflammation and fibrosis of the tissue were statistically reduced in group C. Compared with sub-group B and C, the degree of reduce inflammation of the liver and inhibit hepatic fibrosis were more obviously with the extension of treatment time. The inflammatory activity and liver fibrosis score were statistical significant between groups (P<0.05), the highest score was group B, followed by group C. The apoptosis cells were similar between fibrotic model group and IL-7 intervention group, while the HSC count was obviously higher in group B compared to the other two groups. The Bax gene was up-regulated when intervened with IL-7 for hepatic fibrosis and Bcl-2 showed to the contrary. IL-7 could inhibit hepatic fibrosis in mice induced by CCL4 and reduce liver inflammation process. The anti-fibrosis mechanism might be involved in inducing apoptosis through P53 pathway regulated Bcl-2 and Bax genes.