Skip to main content
. 2016 Feb 18;6:21382. doi: 10.1038/srep21382

Figure 4. Mark4 aggravates inflammation response in mice adipocytes.

Figure 4

(A) Primary adipocytes isolated from WAT of chow fed diet mice were cultured and incubated for 0 h, 12 h, 24 h, 36 h and 48 h in the presence of 5.6 nM, 15 nM and 30 nM glucose. Cell viability was detected by CCK-8 (n = 3). (B) Relative mRNA expression of Caspse3, Bcl-2/Bax, leptin, IL-6, PPARγ and Mark4 of the primary adipocytes incubated for 24 h in the presence of 15 nM glucose (n = 3). (C) Relative activity of ROS, SOD, CAT, MDA, IL-6, TNF-α, MCP-1 and leptin after transfection with HA-Mark4 and sh-Mark4 for 48 h in primary adipocyte. Before transfection, primary adipocytes were treated with 15 nM glucose for 24 h (n = 3). (D) Primary adipocytes were cultured and incubated for 0 h, 12 h, 24 h, 36 h and 48 h in the presence of 100 nM rosiglitazone for 24 h. Relative mRNA expression of PPARγ was detected (n = 3). (E) Relative activity of ROS, SOD, MCP-1 and IL-6 after transfection with HA-Mark4 and sh-Mark4 for 48 h in primary adipocyte. Before transfection primary adipocytes were pretreated with 15 nM glucose or 100 nM rosiglitazone for 24 h (n = 3). Control: no transfection group, HA-Mark4 group: overexpression of Mark4 group, sh-Mark4 group: knock down of Mark4 group. Values are means ± SD. vs. control group, *p < 0.05.