Fig 2: IL-6 increased Ucp1 expression in brown adipocytes while downregulating miR-143. (A,B) The miR-143 and Ucp1 mRNA expression in primary brown adipocytes in response to 12 h treatment with various concentrations of IL-6 protein (n = 8). (C,D) Time course of miR-143 and Ucp1 mRNA induction in primary brown adipocytes in response to IL-6 (100 ng/mL) treatment (n = 8). (E,F) The p-STAT3 and STAT3 protein expression levels in primary brown adipocytes treated with or without LMT for 1 h (n = 3). (G,H) The miR-143 and Ucp1, Pgc1a, TNFa, and IL-6 mRNA expression levels in the primary brown adipocytes treated with or without 50 nM LMT for 1h. Data are presented as the mean ± SEM. * p < 0.05 vs. controls; ** p < 0.01 vs. controls. Different letters above bars represent significant differences, with shared letters representing no significant differences, as determined by a two-tailed unpaired Student’s t-test (A–D) or two-way ANOVA followed by Tukey’s post hoc test (F–H).

Fig 3: miR-143KO promotes LPS induced thermogenesis in the BAT. (A) Rectal temperatures of WT and miR-143KO mice treated with 10 μg/kg LPS for 1.5 h. (B,C) Dorsal interscapular surface imaging and temperature. (D) The concentrations of TNFα and IL-6 in the BAT of mice treated with 10 μg/kg LPS for 4 h (n = 6). (E) The inflammation-related mRNA expression levels in the BAT of WT and miR-143KO mice (n = 8). (F,G) The inflammation-related (E) and thermogenic-related (F) mRNA expression levels in the BAT of WT and miR-143KO mice treated with 10 μg/kg LPS for 4 h (n = 6). (H,I) The UCP1 protein levels in the BAT. (J) The mRNA expression levels of TNF-α, IL-6 and UCP1 in the WT and miR-143KO primary brown adipocytes (n = 6). (K–M) The TNFα, IL-6, Ucp1 mRNAs (J), and Ucp1 protein (K,L) expression levels in WT or miR-143KO primary brown adipocytes treated with 0.2 μg/mL LPS. Data are presented as the mean ± SEM. * p < 0.05 vs. controls; ** p < 0.01 vs. controls, as determined by Two-tailed unpaired Student’s t-test.

Fig 4: Low-dose LPS induced fever in mice. (A) Rectal temperatures of mice treated with 10 μg/kg LPS for 1.5 h. (B,C) Dorsal interscapular surface imaging and temperature. (D,E) The inflammation-related (D) and thermogenic-related (E) mRNA expression levels in the BAT of mice treated with 10 μg/kg LPS for 4 h (n = 6). (F,G) The UCP1 protein levels in the BAT. (H–J) The TNFα, IL-6, Ucp1 mRNAs (H), and UCP1 protein (I,J) expression levels in primary brown adipocytes treated with or without 0.2 μg/mL LPS. Data are presented as the mean ± SEM. * p < 0.05 vs. controls; ** p < 0.01 vs. controls, as determined by Two-tailed unpaired Student’s t-test.

Fig 5: IL-6-neutralizing antibody alleviated PM2.5-induced ovarian injury. (A) Scheme of the animal study for assessing whether IL-6-neutralizing antibodies can reverse PM2.5-induced ovarian injury. (B) The serum IL-6 level of mice exposed to PM2.5 with or without IL-6 antibody administration (n = 8 to 10 mice/group, one-way ANOVA). (C) The serum AMH level of mice exposed to PM2.5 with or without IL-6 antibody administration (n = 7 to 9 mice/group, one-way ANOVA). (D) Ovarian H&E staining images of mice exposed to PM2.5 with or without IL-6 antibody administration. (E) Follicle counting results according to ovary serial sections (n = 5 mice/group, one-way ANOVA). (F) The proportion of regular or irregular estrous cycles of mice exposed to PM2.5 with or without IL-6 antibody administration (n = 11 mice/group, chi-square test). (G to I) The serum hormone level of mice exposed to PM2.5 with or without IL-6 antibody administration (n = 8 to 11 mice/group, one-way ANOVA). (J to N) Protein expression of hormone-synthesis-related genes in ovaries from mice exposed to PM2.5 with or without IL-6 antibody administration detected by Western blot (n = 3 biological replicates/group, one-way ANOVA).