Figure 5.

miR-802 overexpression leads to host lipid accumulation, which can be attenuated by Schistosoma japonicum infection. (A) Mice were randomly divided into four groups: Lv-Ctrl, Lv-miR802, LV-Ctrl+inf+PZQ, and LV-miR802+inf+PZQ groups. Each mouse in the four groups was intravenously administered 5×10⁷ TU lentivirus (LV-Ctrl) or lentivirus-miR-802 (LV-miR802) in 200 µl PBS once a week continuously for four weeks. Data are indicated mean ± s.e.m of 6 mice for each group in one representative experiment; all experiments were repeated twice. *P < 0.05, **P < 0.01, ***P < 0.001. (B) Expression of miR-802 and Prkab1 in the livers of mice from these groups. (C) Dynamic changes in body weight of mice in the LV-Ctrl, LV-miR802, LV-Ctrl+inf+PZQ, and LV-miR802+inf+PZQ groups. (D) Cholesterol, TG, HDL-C, LDL-C levels in the sera of the four groups of mice. (E, F) Representative images of liver sections stained with Oil red. (G, H) The expression of Prkab1, Prkaa1, Prkaa2, phosphorylated AMPK, total ACC, and phosphorylated ACC in the livers from mice in each group. Data are expressed as the mean ± s.e.m. from each group, and are representative of one typical experiment out of three, *P < 0.05, **P < 0.01, ***P < 0.001. (I) qRT-PCR quantification of the expression of lipogenesis-related genes in the livers of mice from each group.