Fig. 5
DT-109 inhibits inflammation and oxidative stress.a Coronary arteries were collected and analyzed for inflammation-associated genes. Real-time PCR analysis of NLR family pyrin domain containing 3 (NLRP3), apoptosis-related cysteine peptidase (CASP1), interleukin 18 (IL-18), and IL-1β expressions in the vehicle and DT-109 treated coronary arteries (normalized to 18S; n = 5 for each group). b, c Upon 24 h of ox-LDL induction, protein levels of NLRP3, absent in melanoma 2 (AIM2), PYD and CARD domain containing (ASC), CASP1, and IL-1β were determined by Western blot in A7r5 cells after vehicle or DT-109 treatment (n = 4 for each group). d A7r5 cells were divided into a control group and an ox-LDL-induced group, treated with or without DT-109 (0.02 mM, 0.1 mM, 0.5 mM), and labeled with DCFH-DA to assess superoxide levels (scale bar: 200 μm). e After ox-LDL stimulation, supernatants from A7r5 cells incubated with or without DT-109 (0.5 mM) were collected to analyze glutathione (GSH) and malondialdehyde (MDA) levels (n = 4 for each group). f Detection of GSH and MDA in carotid artery tissue (n = 5 for each group). Data are presented as mean ± SD. Statistical differences were compared using one-way ANOVA with Tukey’s post hoc analysis or Dunn’s test, multiple comparison adjusted p-values were reported
