Accumulating evidence shows that oxidative stress and inflammation contribute to the development of cardiovascular disease. It has been suggested that propolis possesses antioxidant and anti-inflammatory activities. In this study, the antioxidant and anti-inflammatory effects of the main flavonoids of propolis (chrysin, pinocembrin, galangin, and pinobanksin) and propolis extract were researched. The results showed that the cellular ROS (Reactive oxygen species) levels, antioxidant enzymes, Nrf2 (Nuclear factor erythroid 2-related factor 2) nuclear translocation, and the expression of NQO1 (NAD(P)H:quinone oxidoreductase 1) and HO-1 (heme oxygenase 1) were regulated by different concentrations of individual flavonoids and propolis extract, which showed good antioxidant and pro-oxidant effects. For example, ROS levels were decreased; SOD and CAT activities were increased; and the expression of HO-1 protein was increased by chrysin. The results demonstrated that NO (Nitric Oxide), NOS (Nitric Oxide Synthase), and the activation of the NF-κB signaling pathway were inhibited in a dose-dependent manner by different concentrations of individual flavonoids and propolis extract. Moreover, the results revealed that the phytochemicals presented antioxidant effects at lower concentrations but pro-oxidant effects and stronger anti-inflammatory effects at higher concentrations. To maintain the balance of antioxidant and anti-inflammatory effects, it is possible that phytochemicals activate the Nrf2 pathway and inhibited the NF-κB (Nuclear factor kappa B) pathway.

Oxidative stress and inflammation are crucial factors in the development of cardiovascular diseases. In previous research, the oxidative stress and inflammation models have frequently been explored independently. In the current study, we investigated the antioxidant and anti-inflammatory effects of tomato extract and its two main carotenoids (lutein and lycopene) with various concentrations using a rat cardiomyocyte model of co-existing oxidative stress and persistent chronic inflammation. It was discovered that the antioxidant effects of 0.5–5 μM lutein, 0.5–5 μM lycopene, and 50–200 μg/mL tomato extract increased in a dose-dependent manner. However, the pro-oxidation effects emerged by measuring the antioxidant-related indices, including the levels of ROS, SOD, and GPX in H9c2 cells as concentrations exceeded those mentioned above. The anti-inflammatory effects of lutein, lycopene, and tomato extract were simultaneously strengthened with higher concentrations, potentially due to the suppression of the NF-κB signaling pathway. Furthermore, high concentrations of lutein, lycopene, and tomato extract potentially regulated Nrf2/HO-1 and NF-κB signaling pathways dependent on TGF-1β and IL-10 to demonstrate high concentrations of pro-oxidation and anti-inflammation effects. Our findings indicate that the dose–effect regulatory mechanisms of antioxidant and anti-inflammatory properties among lutein, lycopene, and tomato extract will be advantageous in developing more effective therapeutic strategies to prevent cardiovascular diseases.

Antibiotics are the most commonly used clinical drugs for anti-infection, but they can also destroy normal microorganisms and cause intestinal barrier dysfunction. To elucidate the effects and mechanism of a water-soluble polysaccharide from Fagopyrum esculentum Moench bee pollen (WFPP) on intestinal barrier integrity in antibiotic-treated mice, BALB/c mice were exposed to a broad-spectrum antibiotic (ceftriaxone) or not (control), and were administered low-, medium- and high-dose WFFP (100 mg kg⁻¹, 200 mg kg⁻¹ and 400 mg kg⁻¹, respectively) daily by oral gavage for 3 weeks. Mice treated with ceftriaxone displayed symptoms of growth retardation, atrophy of immune organs including thymus and spleen, increased gut permeability, and intestinal barrier damage, which were restored after intervention with WFFP at different doses. Moreover, the beneficial effects of WFFP were closely associated with enhanced intestinal sIgA secretion and reduced inflammatory response. Furthermore 16S rDNA gene sequencing revealed that WFPP elevated microbial diversity and richness and changed the community structure, therefore, alleviating microbiota dysbiosis caused by ceftriaxone. Interestingly, WFPP could modulate the abundance of sIgA secretion-related bacteria (e.g. Proteobacteria) and inflammation-related bacteria (e.g. Enterococcus). Therefore, WFPP can relieve antibiotic-induced microbiota dysbiosis to improve intestinal barrier integrity by increasing intestinal sIgA secretion and inhibiting inflammation.