Loss of angiotensin converting enzyme II (ACE2) accelerates the development of liver injury induced by thioacetamide

Figures

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  Fig. 1.. The changes in body weight and relative liver/body weight ratio of the mice after 8 weeks of TAA administration. The WT and Ace2 KO mice were i.p. injected with TAA or DPBS for 8 weeks, and body weights were measured at the time of each injection. The relative liver/body weight ratio is the final liver weight as a percentage of total body weight. Results are shown as the means ± SD (n=8) for each group. Different letters show a significant difference between the treatment groups (P<0.05).

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  Fig. 2.. Changes in serum AST, ALT and ALP levels of the mice after 8 weeks of TAA administration. The WT and Ace2 KO mice were i.p. injected with 100 and 200 mg/BW of TAA or DPBS for 8 weeks and then serum samples were collected for the assays. Results are shown as the means ± SD (n=8) for each group. Different letters show a significant difference between the treatment groups (P<0.05). (AST: aspartate aminotransferase; ALT: alanine aminotransferase; ALP: alkaline phosphatase)

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  Fig. 3.. Histopathological features of the mice after 8 weeks of TAA administration. All mice were sacrificed and the liver was removed, fixed and embedded in paraffin. Histopathological photomicrographs of the mouse livers were stained with Masson’s trichrome and blue staining shows the fibrosis areas (a). The extracellular matrix (ECM) ratio (blue staining) increased represent by different TAA treatment (b). Scale bars indicate 125 µm.

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  Fig. 4.. Expression levels of inflammation and fibrosis related genes in the mice livers after treatment with TAA. WT and Ace2 KO mice were i.p. injected with TAA or DPBS for 8 weeks, and RNA was then extracted from the liver tissue. Reverse-transcription PCR (RT-PCR) was used to analyze the RNA expression level of inflammatory IL-6 and Tnf genes (a), and fibrosis related Col1a1, Timp1 and Mmp9 genes (b). Gapdh was used as an internal control (IL-6: interleukin-6; Tnf: tumor necrosis factor alpha; Col1a1: collagen type I alpha 1; Timp1: tissue inhibitor of metalloproteinases 1; Mmp9: metalloproteinases 9; Gapdh: glyceraldehyde-3-phosphate dehydrogenase).

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  Fig. 5.. Hepatic MMP-9 activity of the mice given TAA. The WT and Ace2 KO mice were i.p. injected with TAA or DPBS for 8 weeks and total proteins were extracted from liver tissue. MMP-9 activity was analyzed using gelatin zymography (a). The means ± SD (n=4) are shown for each group (b). Different letters show a significant difference between the treatment groups (P<0.05).