Fig 1: Col XV promotes adipose inflammation. (A) Relative mRNA and protein expression levels of inflammation marker genes IL6, MCP1, TNFa in mice adipocytes in control group, pc-Col XV group and sh-Col XV group with or without TM (1µM) (n = 4). (B) Relative protein expression levels of IRE1a, TNFa, IL6, IL1ß in different groups in adipocytes pretreated with or without TM (n = 4). (C) Relative protein expression levels of IRE1a, TNFa, IL6 in different groups in adipocytes treated with or without 4PBA (2ug/mL) (n = 4). (D) Relative Col XV mRNA level in iWAT of treatment group mice (n = 4). (E) Images of hematoxylin and eosin staining of white adipose tissue in different groups (n = 4). Scale bar, 100 µm. (F) Representative images of Masson’s trichrome staining in iWAT Arrowheads indicate collagen fibers (n = 4). Scale bar, 100 µm. (G) Images of immunohistochemical staining for F4/80 and TNFa of adipose tissue in different groups (n = 4). Scale bar, 200 µm. (H) Fluorescence staining of NLRP3 in adipocytes in different groups (n = 4). Scale bar, 100 µm. Values are means ± SEM. # or * p < 0.05 compared with the control group.
Fig 2: Effect of PTEN expression on cytokine expression. Serum concentrations of (A) TNF-a and (B) IL-6 were measured using ELISA for rat cardiomyocytes treated with septic shock serum and transfected with siR-NC or siR-PTEN. *P<0.05 vs. siR-NC group. PTEN, phosphatase and tensin homolog; TNF-a, tumor necrosis factor-a; IL-6, interleukin-6; siR, short interfering RNA; NC, negative control.
Fig 3: DMRT2 is downregulated in insulin-resistant adipocyte model. (A) 3T3-L1 preadipocytes were induced toward adipogenesis and the formation of lip droplets in preadipocytes and adipocytes was confirmed using oil O red staining. (B) The mRNA expression levels of Fabp4 and PPARγ in preadipocytes and adipocytes were examined using qRT-PCR. Then, the insulin-resistant adipocyte model was established in differentiated adipocytes as described and examined for Fabp4 and PPARγ mRNA levels (C), glucose uptake ability (D), and triglyceride content (E); cellular membrane-located GLUT4 levels in control or insulin-resistant (IR) adipocytes by immunofluorescent (IF) staining (F); membrane protein levels of GLUT4 in control or IR adipocytes by immunoblotting (G); the protein levels of Akt and p-Akt in control or IR adipocytes by immunoblotting (H); the mRNA expression of TNF-α and IL-6 in control or IR adipocytes by qRT-PCR (I); the secretion levels of TNF-α and IL-6 in control or IR adipocytes by ELISA (J); and the protein levels of DMRT2 in control or IR adipocytes by immunoblotting (K). *P < 0.05, **P < 0.01.
Fig 4: Complement and cytokine assay and biochemical analysis of organ functions following multiple transfusions.(A) Timeline of the three succeeding blood transfusions. (B) Life span of PKH-26–labeled native and engineered RBCs after blood transfusion in vivo. (C) Serum levels of complement 3 and complement 4 after multiple transfusions. (D) Serum levels of TNF-a and IL-6 after multiple transfusions. (E) Biochemical analysis of liver function after multiple transfusions. ALT (U/l), AST (U/l), ALP (U/l), TBIL (µM), DBIL (µM). (F) Biochemical analysis of kidney function after multiple transfusions. CREA (µM), BUN (mM), UA (µM).
Fig 5: Ad-TGF-ß3 Reduced the Inflammatory Factors IL-6, TNF-a, COX2, and IL-1ß during Flexor Tendon Healing. Concentration of IL-6 (A), TNF-a (B), COX2 (C), and IL-1ß (D) in the flexor tendon healing tissues at given-days. *P < 0.05, vs. vehicle group. n = 6 for each group
Supplier Page from Abcam for Mouse IL-6 ELISA Kit