Figure 7.
Figure 7. Overexpression of miR-122 in hepatocytes rescues the hepatic inflammation mediated by IO in vivo. C57BL/6 mice (N = 6) were fed a purified diet with no added iron and subjected to i.p. injection of 20 mg/kg (IA) or 200 mg/kg (IO) dextran-iron. rAAVs with or without a miR-122 transgene were injected via tail vein at day 6. Mice were sacrificed, and liver tissues were harvested at week 4. (A-B) RNA levels of miR-122 (A) and various iron homeostasis-related genes (B) and inflammatory factors were determined by qRT-PCR. (C) The protein levels of CCL2 and NF-κB/p65 were determined by western blot assays. Both representative figures and quantitative data are shown. (D) Immunofluorescence analysis showing the expression of CD68, TNF-α, and IL-1β expression after treatment. Original magnification ×200. (E) The inflammation score in the liver and serum ALT and AST levels were determined. Data were normalized to the IA group and are presented as mean ± SEM. *P < .05; **P < .01 vs IO.

Overexpression of miR-122 in hepatocytes rescues the hepatic inflammation mediated by IO in vivo. C57BL/6 mice (N = 6) were fed a purified diet with no added iron and subjected to i.p. injection of 20 mg/kg (IA) or 200 mg/kg (IO) dextran-iron. rAAVs with or without a miR-122 transgene were injected via tail vein at day 6. Mice were sacrificed, and liver tissues were harvested at week 4. (A-B) RNA levels of miR-122 (A) and various iron homeostasis-related genes (B) and inflammatory factors were determined by qRT-PCR. (C) The protein levels of CCL2 and NF-κB/p65 were determined by western blot assays. Both representative figures and quantitative data are shown. (D) Immunofluorescence analysis showing the expression of CD68, TNF-α, and IL-1β expression after treatment. Original magnification ×200. (E) The inflammation score in the liver and serum ALT and AST levels were determined. Data were normalized to the IA group and are presented as mean ± SEM. *P < .05; **P < .01 vs IO.

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