Journal: Theranostics

Article Title: Depletion of ApoA5 aggravates spontaneous and diet-induced nonalcoholic fatty liver disease by reducing hepatic NR1D1 in hamsters

doi: 10.7150/thno.91084

Figure Lengend Snippet: Cold exposure improves lipid metabolism disorders caused by ApoA5 deficiency. A: The representative images of UCP1 immunohistochemical staining in BAT sections of 3-month old male WT and ApoA5 -/- hamsters on chow diet. B: The body temperature of the hamsters described in (A) (n = 8/group). C: The expression levels of genes involved in thermogenesis in the BAT of the hamsters described in (A) (n = 5-7/group). D-E: Plasma TG (D) and TC (E) were determined from WT and ApoA5 -/- hamsters after cold exposure for 5 days (n = 4-6/group). F-G: The representative images of HE and UCP1 immunohistochemical staining in BAT and eWAT sections of the animals described in (D-E) and quantitative data (n = 4-6/group). H: The representative images of tyrosine hydroxylase (TH) immunofluorescence staining in eWAT sections of the hamsters described in (D-E) and quantitative data (n = 4-6/group). I: The representative images of Oil red O in liver sections of the hamsters described in (D-E) and quantitative data (n = 4-6/group). J-K: Plasma TG (J) and TC (K) were determined from WT and ApoA5 -/- hamsters on HFD after cold exposure for 7 days (n = 3-5/group). L: The representative images of Oil red O in liver sections of the hamsters described in (J-K) and quantitative data (n = 3-5/group). Error bars represent mean ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001; ns, not significant.

Article Snippet: Immunohistochemical staining was performed with UCP1 antibody (1:100 rabbit polyclonal IgG, A5857, ABclonal, China) in BAT and WAT.

Techniques: Immunohistochemical staining, Staining, Expressing, Clinical Proteomics, Immunofluorescence

Journal: Nutrients

Article Title: L-Arabinose Elicits Gut-Derived Hydrogen Production and Ameliorates Metabolic Syndrome in C57BL/6J Mice on High-Fat-Diet

doi: 10.3390/nu11123054

Figure Lengend Snippet: Sequences of oligonucleotide primers targeting indicated genes related to lipid metabolism.

Article Snippet: Antibodies list: CPT1A (A5307, ABclonal, Wuhan, China), UCP1 (A5857, ABclonal), UCP3(A16996, ABclonal), PPARα (sc-9000, Santa Cruz, Dallas, TX, USA), PPARγ (2435S, CST, Danvers, MA, USA), FAS (3189S, CST), SREBP1 (Sc13551, Santa Cruz), PGC-1α (TA319007, Origene, Rockville, MD, USA), NDUFS3 (459130, Invitrogen, Waltham, MA, USA), SDHB (459230, Invitrogen), UQCRC1 (459140, Invitrogen), COX4 (459600, Invitrogen), ATP Synthase Subunit Alpha (459240, Invitrogen), SOD2 (sc-137254, Santa Cruz), β-Actin (3700S, CST), α-Tubulin (3873S, CST).

Techniques: Sequencing, Binding Assay

Journal: Lipids in health and disease

Article Title: Exosomal IL-8 derived from Lung Cancer and Colon Cancer cells induced adipocyte atrophy via NF-κB signaling pathway.

doi: 10.1186/s12944-022-01755-2

Figure Lengend Snippet: Fig. 4 IL-8 in EVs induces lipolysis partly by activating NF-κB signaling pathway. A-C Western blot and the densitometric analysis of phosphorylated-p65, nuclear p65, total p65, UCP1, PGC1α in 3 T3-L1 adipocyte treated with IL-8, LLC-EVs (10 μg), C26-EVs (10 μg) and/or anti-IL-8 (n = 3), as indicated. D The activation of p65 NF-κB (as marked in Green) in 3 T3-L1 adipocytes was confocally imaged upon co-culturing with IL-8 (with and without specific anti-IL-8), LLC-EVs and/or C26-EVs (with and without specific anti-IL-8). The nucleus (Blue) was labeled with DAPI and 10 μg EVs were applied in test. E Oil red O staining assay for above groups. Bar = 100 μm. F Relative levels of glycerol release in cell supernatants upon above treatments. *P < 0.05, **P < 0.01, ***P < 0.001

Article Snippet: The following primary antibodies were used: anti-CXCL15 (ab197016, Abcam, 1:1000); total p65NF-κB (A2547, ABclonal, 1:1000); NF-κB p65-pS536 (3033 T, Cell Signaling Technology, 1:1000);anti-PGC1α (A19674, ABclonal, 1:1000); anti-UCP1 (A5857, ABclonal, 1:1000); anti-αTubulin (66031-1-Ig, Proteintech, 1:1000); anti-LaminB1 (A11495, ABclonal, 1:1000); anti-GAPDH(60004-1-Ig, Proteintech, 1:1000) and anti-Calnexin (2679 T, Cell Signaling Technology, 1:1000).

Techniques: Western Blot, Activation Assay, Labeling, Staining