METHODS: A total of 33 sedentary men with metabolic syndrome (age: 46.2 ± 4.6 years; body mass index: 35.4 ± 1.9 kg.m2) were randomly assigned to one of 3 groups: aerobic interval training (n = 12), resistance training (n = 10), or control (n = 11). Participants in the exercise groups completed a 12-week training program, 3 sessions per week, while those in the control group maintained their sedentary lifestyle. The levels of high sensitivity C-reactive protein (hs-CRP), omentin-1, adiponectin, lipid profiles, blood pressure, glucose metabolism, body composition, and peak oxygen uptake (VO2peak) were measured at baseline and after the intervention.

RESULTS: Both aerobic interval training and resistance training significantly improved the levels of omentin-1 and adiponectin, as well as reduced inflammation, as indicated by a decrease in hs-CRP levels. Exercise training also led to significant improvements in lipid profiles, blood pressure, glucose metabolism, and body composition. Specifically, the aerobic interval training group had significantly greater increases in high-density lipoprotein cholesterol and VO2peak, as well as greater reductions in low-density lipoprotein cholesterol, triglycerides, and total cholesterol compared to the resistance training group.

METHODS: cRGD-platelet@MnO/MSN@PPARα/LXRα nanoparticles were synthesized by a chemical method. Dynamic light scattering (DLS) was utilized to detect the size distribution and polydispersity index (PDI) of the nanoparticles. The safety of the nanoparticles was detected by CCK8 in vitro and HE staining and kidney function in vivo. Cell apoptosis was detected by flow cytometry detection and TUNEL staining. Oxidative stress responses (ROS, SOD, MDA, and NOX levels) were tested via a DCFH-DA assay and commercial kits. Immunofluorescence and phagocytosis experiments were used to detect the targeting of nanoparticles. Magnetic resonance imaging (MRI) was used to detect the imaging performance of cRGD-platelet@MnO/MSN@PPARα/LXRα nanoparticles. Using western blotting, the expression changes in LXRα and ABCA1 were identified.

RESULTS: cRGD-platelet@MnO/MSN@PPARα/LXRα nanoparticles were successfully established, with a particle size of approximately 150 nm and PDI less than 0.3, and showed high safety both in vitro and in vivo. cRGD-platelet@MnO/MSN@PPARα/LXRα nanoparticles showed good targeting properties and better MRI imaging performance in AS. cRGD-platelet@MnO/MSN@PPARα/LXRα nanoparticles showed better antioxidative capacities, MRI imaging performance, and diagnostic and therapeutic effects on AS by regulating the expression of LXRα and ABCA1.

Methods: In the experimental study, the rats were randomly divided into four groups of five rats in each and fed with high-fat diet for 12 weeks as follows: One group (normal diet group) was fed with a standard diet, one group was fed with HFD, and two groups were fed with HFD and orally fed with 150 and 450 mg/kg/day HAEM. The serum samples and liver tissues were used for measuring the biochemical and oxidative parameters and histopathological studies. HFD induced hepatosteatosis in rats as evidenced by the altered liver enzymes activity, serum lipid profile and oxidative status.

Results: Serum lipid profile (triglyceride, cholesterol and low-density lipoprotein) in rats fed with HFD + HAEM (150 and 450 mg/kg/day) was significantly decreased. Furthermore, the evaluation of oxidative stress showed a reduction of the malondialdehyde (MDA) level and an increase in ferric-reducing anti-oxidant power. Meanwhile, liver enzyme activities declined in response to HAEM.