Fig 1: Phosphorylation levels of AMPK are increased in 3T3-L1 adipocytes when cultured for 15, 30 and 60 min with Glu + PA conditioned media from NOX5-expressing endothelial bEnd.3 cells (A,B). This increase is prevented when IL-6 is immunoprecipitated from the media (C,D). (A,C) Representative images of Western blots for p-AMPK and AMPK. (B,D) p-AMPK and AMPK protein levels of 3T3-L1 adipocytes (n = 6). Results are expressed as mean ± SEM; * p < 0.05, ** p < 0.01, *** p < 0.001: differences relative to Nox5(−)/Glu + PA(−); # p < 0.05, ### p < 0.001: differences relative to Nox5(+)/Glu + PA(−); $ p < 0.05, $$$ p < 0.001: differences relative to Nox5(−)/Glu + PA(+); Statistical test used: ANOVA.
Fig 2: The administration of anti-Myl9/12 Ab ameliorated DSS-induced colitis. (A–C) The rate of survival (A), percent change of body weight on each day relative to those on day 0 (B), and disease activity index (DAI) (C) of the DSS-induced colitis model mice treated with either anti-Myl9/12 Ab or Control Ab (n = 10 per group); *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.001. (D) A representative image showing the gross appearance of the colon from the DSS-induced colitis model mice (upper) and the mice drinking normal water (bottom) treated with either anti-Myl9/12 Ab or Control Ab. Each image included the image from a healthy mouse (Normal colon). The colon length from the mice either at the time of death or on day 15. ***p < 0.001; ****p < 0.001. (E) Hematoxylin and eosin (HE) staining of the colon from a healthy mouse or DSS-induced colitis model mice treated with either anti-Myl9/12 Ab or Control Ab (left). The histological score is determined based on the changes described in Supplementary Table 2. *p < 0.05; **p < 0.01; ****p < 0.001. (F) IL-6, IL-1β, TNFα production in the plasma from DSS-induced colitis model mice treated with either anti-Myl9/12 Ab or Control Ab. *p < 0.05; ****p < 0.0001. ns, not significant.
Fig 3: CBL alleviates neuroinflammation after TBI. CBL significantly reduced hippocampal (a) TNF-α, (b) IL-1β, (c) IL-6, and (d) NF-κB levels at 72 h after TBI (n = 6, P < 0.05, analysis of variance; means ± standard error of mean).
Fig 4: Ferr-1 and 3-MA alleviated the inflammation and oxidative damage of lung tissues in asthma mice. (a) H&E staining was used for the detection of the damage of lung tissues. (b) The expression of LC-3 in lung tissues was detected with immunohistochemistry. (c) The levels of IL-4, IL-5, and IL-13 in lung tissues and BALF were determined with ELISA. (d) The levels of IL-1β, IL-6, and TNF-α in lung tissues and BALF were determined with ELISA. (e) The levels of ROS, SOD, and MDA in lung tissues and BALF were detected with commercial kits. ∗∗∗p < 0.001 vs. the control; #p < 0.05, ##p < 0.01, and ###p < 0.001 vs. the Model. Ferr-1: ferrostatin-1; 3-MA: 3-methyladenine; BALF: bronchoalveolar lavage fluid.
Fig 5: ALI and IL-13 induced the damage of bronchial epithelial cells. (a) CCK-8 was performed for the detection of the viability of these cells. (b–d) The levels of IL-1β, IL-6, and TNF-α in these cells were determined with ELISA. (e–g) The levels of ROS, SOD, and MDA in these cells were detected with commercial kits. (h) The expression of LC-3 in these cells was detected with immunofluorescence. ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001 vs. the control; #p < 0.05, ##p < 0.01, and ###p < 0.001 vs. ALI. ALI: air-liquid interface; CCK-8: cell counting kit-8; ROS: reactive oxygen species; SOD: superoxide dismutase; MDA: malonaldehyde.
Supplier Page from Abcam for Mouse IL-6 ELISA Kit