Fig 2: The LXR agonist T0901317 mitigated endothelial oxidative and nitrative stress in H/SD + HG injury. A, Representative images of dihydroethidium fluorescence (red) staining were used to evaluate oxidative stress. Scale bar: 30 µm. B, Intracellular ROS generation was measured by flow cytometry through the analysis of DHE fluorescence (n = 5). C, Measurement of 3‐NT by ELISA (n = 5). D, Intracellular NOx contents in different groups (n = 5). E, Representative blots of FoxO1, Ac‐FoxO1 (Lys259), NADPH oxidase (NOX4), 3‐nitrotyrosine (3‐NT) and SOD‐2. F‐J, Western blotting was used to analyse the expression of FoxO1, Ac‐FoxO1 (Lys259), 3‐NT, NOX4 and SOD‐2 in each group. (n = 5). *P < .05 between the indicated groups

Fig 3: Pharmacological activation of LXR mimics early-pregnancy lipogenesis in mice. A: expression of lipogenic genes. B: expression of cholesterol homeostatic genes. C: total triglycerides and cholesterol measured in lipid extracts. D: total triglycerides and cholesterol measured in mouse serum. Results are represented as means ± SE (n = 6–8); aP < 0.05, comparison of nonpregnant T0901317-fed groups [days (D) 7–18] vs. nonpregnant group (D0); bP < 0.05, comparison of pregnant T0901317-fed groups (D7-18) vs. pregnant group (D0); cP < 0.05, comparison of pregnant T0901317-fed group vs. corresponding nonpregnant T0901317-fed group. P values were determined by one-way ANOVA with Newman-Keuls post hoc testing.

Fig 4: Fenofibrate increased the expression of PPAR-α and LXR-β in LGs. (A) Gene expression of PPAR-α, LXR-α, and LXR-β in LG. (B) Western blot assay for PPAR-α and LXR-β expression. Images shown are from one experiment representative of three independent experiments. Relative protein level is quantified by ratio of PPAR-α and LXR-β to β-actin. Data are representative of three independent experiments. Data are presented as mean ± SD (n = 3–5, *P < 0.05, **P < 0.01; NS, not significant).

Fig 5: The LXR agonist T0901317 mitigated ischaemic hindlimb oxidative stress and promoted endothelial antioxidant machinery in diabetic mice. A, Representative images are shown of dihydroethidium fluorescence (red) staining which detects ROS generation in the left gastrocnemius on POD 7. Scale bar: 50 µm. B, Quantitative analysis of DHE relative intensity (n = 5). C, Measurement of the oxidative stress‐related indicator malondialdehyde (MDA) in gastrocnemius tissues (n = 6 for each group). D, Representative immunofluorescent staining for endothelial SOD‐2 expression [CD31 and SOD‐2 double‐positive (yellow fluorescence) and DAPI (blue fluorescence)] on POD 7. Scale bar: 50 µm. E, Quantitative analysis of yellow fluorescence IOD (CD31 and SOD‐2 double‐positive) (n = 5). F‐H, Measurement of antioxidant superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH) in gastrocnemius tissues (n = 6 for each group). *P < .05 between the indicated groups