Fig 1: TRIM31 knockout in POMC+ neurons aggravates hypothalamic oxidative stress after PM2.5 exposure. (A) MDA, (B) SOD, and (C) GSH in serum were evaluated (n = 15 mice per group). Hypothalamic (D) MDA, (E) SOD, and (F) GSH levels were assessed (n = 15 mice in each). (G) Representative images of DHE staining in hypothalamus were shown (n = 6 mice per group; For each mouse, we recorded 2 fields spanning the entire hypothalamus; Scale bars: 50 µm). (H) ROS production by DHE staining was quantified (n = 6 mice per group). (I,J) RT‐qPCR analysis for the hypothalamic gene expression levels of molecules associated with oxidative stress as displayed (n = 3 mice per group). (K) Western blot for cytoplastic and nuclear Nrf2 protein expression in hypothalamus (n = 4 mice in each). Data are presented as means ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001; Student's t test and one‐way ANOVAs statistics analysis for (A) to (F), (H), and (K); two‐way ANOVAs statistics for (I) and (J).
Fig 2: Effects of TRIM31 in POMC+ neurons on the energy expenditure and glucose metabolism in PM2.5‐exposed mice. (A) VO2 across 48 h monitoring in TRIM31f/f and POMCCre/+;TRIM31flox/flox mice (n = 8 mice for FA‐treated groups; n = 10 mice for PM2.5‐treated groups). (B) Average quantification of VO2 in light and dark cycles of TRIM31f/f and POMCCre/+;TRIM31flox/flox mice (n = 8 mice for FA‐treated groups; n = 10 mice for PM2.5‐treated groups). (C) VCO2 production across 48 h monitoring in TRIM31f/f and POMCCre/+;TRIM31flox/flox mice (n = 8 mice for FA‐treated groups; n = 10 mice for PM2.5‐treated groups). (D) Averages of VCO2 production in light and dark cycles of TRIM31f/f and POMCCre/+;TRIM31flox/flox mice (n = 8 mice for FA‐treated groups; n = 10 mice for PM2.5‐treated groups). (E) Average RER of each group of mice indicated in (A) during light and dark cycles (n = 8 mice for FA‐treated groups; n = 10 mice for PM2.5‐treated groups). (F) VO2 across 48 h monitoring (n = 11 mice for AAV‐Ctrl group; n = 12 mice for AAV‐TRIM31 group). (G) Average quantification of VO2 in light and dark cycles (n = 11 mice for AAV‐Ctrl group; n = 12 mice for AAV‐TRIM31 group). (H) VCO2 production across 48 h monitoring (n = 11 mice for AAV‐Ctrl group; n = 12 mice for AAV‐TRIM31 group). (I) Averages of VCO2 production in light and dark cycles (n = 11 mice for AAV‐Ctrl group; n = 12 mice for AAV‐TRIM31 group). (J) Average RER of each group of mice indicated in (F) during light and dark cycles (n = 11 mice for AAV‐Ctrl group; n = 12 mice for AAV‐TRIM31 group). (K) EE of all groups of mice demonstrated in A) over a 48 h period (n = 8 mice for FA‐treated groups; n = 10 mice for PM2.5‐treated TRIM31f/f and POMCCre/+;TRIM31flox/flox mice). (L) Averages EE in light/dark cycles (n = 8 mice for FA‐treated groups; n = 10 mice for PM2.5‐treated groups). (M,N) EE of all groups of mice over a 48 h period (n = 11 mice for AAV‐Ctrl group; n = 12 mice for AAV‐TRIM31 group). (O) Records of food intake were shown (left panel), and averages of food intake were quantified (right panel) (n = 8 mice for FA‐treated groups; n = 10 mice for PM2.5‐treated groups). (P) Records of food intake were shown (n = 11 mice for AAV‐Ctrl group; n = 12 mice for AAV‐TRIM31 group). (Q) Blood glucose levels of all groups of mice were measured at the shown time points (left panel); and the final fasting blood insulin contents were calculated after PM2.5 exposure for 24 weeks (right panel) in TRIM31f/f and POMCCre/+;TRIM31flox/flox mice (n = 15 mice per group). (R) Blood glucose levels of all groups of mice were measured (right panel); and fasting blood insulin contents were examined after PM2.5 exposure for 24 weeks (right panel) (n = 11 mice for AAV‐Ctrl group; n = 12 mice for AAV‐TRIM31 group). (S) GTT and (T) ITT were conducted in TRIM31f/f and POMCCre/+;TRIM31flox/flox mice after a total of 24 week PM2.5 exposure. AUC for GTT and ITT was quantified (n = 15 mice per group). (U) Examination of serum leptin (left panel) and adiponectin (right panel) levels in TRIM31f/f and POMCCre/+;TRIM31flox/flox mice after FA or PM2.5 exposure (n = 15 mice per group). (V) Serum leptin and adiponectin contents of AAV‐Ctrl and AAV‐TRIM31 mice were calculated after PM2.5 exposure for 24 weeks (n = 8 mice for each group). (W) GTT and (X) ITT were conducted in AAV‐Ctrl and AAV‐TRIM31 mice after a total of 24 week PM2.5 exposure. AUC of each group mice was quantified (n = 7 or 8 mice per group). Data are presented as means ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001; ns, no significant difference; Student's t test and one‐way ANOVAs statistics analysis for (A) to (E), (L), (O), (Q), and (S) to (U); Student's t test analysis for (F) to (J), (N), (P), (R), and (V) to (X).
Fig 3: TRIM31 deficiency in POMC+ neurons accelerates peripheral metabolism disorder in mice after long‐term PM2.5 exposure. (A) Body weights of mice were measured. (B) MBP of each group of mice was recorded. Measurements of (C) liver weights, (D) fat weight, (E) eWAT weight, (F) iWAT weight, and (G) BAT weight from each group of mice were shown (n = 15 mice per group). (H) Images for H&E staining of WAT and liver tissues, and Oil red O staining of liver samples from all groups of mice (n = 6 mice per group; For each mouse, we randomly recorded 6 fields spanning the entire tissue; Scale bars: 50 µm). (I) Quantification for adipocyte area size following H&E staining (n = 6 mice per group). (J) Inflammation score of liver tissues was quantified (n = 6 mice per group). (K) Quantification of fat drop in liver sections of all groups of mice (n = 6 mice per group). (L) Hepatic TG contents were examined (n = 15 mice per group). Data are presented as means ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001; ns, no significant difference; Student's t test and one‐way ANOVAs statistics analysis for (A) to (G), and (I) to (L).
Supplier Page from Biorbyt for Mouse MSH Alpha ELISA Kit
Application Notes: Detection Wavelength: 450 nm