RESUMEN
Polymeric nanocomposite materials have great potential in the development of tissue-engineered scaffolds because they affect the structure and properties of polymeric materials and regulate cell proliferation and differentiation. In this work, cerium oxide nanoparticles (CeONPs) were incorporated into a chitosan (CS) film to improve the proliferation of multipotent mesenchymal stem cells (MSCs). The citrate-stabilized CeONPs with a negative ζ-potential (-25.0 mV) were precoated with CS to obtain positively charged particles (+20.3 mV) and to prevent their aggregation in the composite solution. The composite CS-CeONP films were prepared in the salt and basic forms using a dry-cast process. The films obtained in both forms were characterized by a uniform distribution of CeONPs. The incorporation of CeONPs into the salt form of CS increased the stiffness of the CS-CeONP film, while the subsequent conversion of the film to the basic form resulted in a decrease in both the Young's modulus and the yield stress. The redox activity (Ce4+ â Ce3+) of cerium oxide in the CS-CeONP film was confirmed by thermal oxidative degradation. In vitro culture of MSCs showed that the CS-CeONP film has good biocompatibility, and in vivo experiments demonstrated its substantial regenerative potential.
Asunto(s)
Cerio , Quitosano , Nanopartículas , Quitosano/química , Nanopartículas/química , Andamios del Tejido/química , Cerio/farmacología , Cerio/químicaRESUMEN
AIMS: The effects of three types of bariatric interventions on myocardial infarct size were tested in the rat model of type 2 diabetes mellitus (T2DM). We also evaluated the effects of bariatric surgery on no-reflow phenomenon and vascular dysfunction caused by T2DM. MAIN METHODS: Rats with T2DM were assigned into groups: without surgery, sham-operated, ileal transposition, Roux-en-Y gastric bypass, and sleeve gastrectomy. Oral glucose tolerance, glucagon-like peptide-1, and insulin levels were measured. Six weeks after surgery, the animals were subjected to myocardial ischemia-reperfusion followed by histochemical determination of infarct size (IS), no-reflow zone, and blood stasis area size. Vascular dysfunction was characterized using wire myography. KEY FINDINGS: All bariatric surgery types caused significant reductions in animal body weight and resulted in T2DM compensation. All bariatric interventions partially normalized glucagon-like peptide-1 responses attenuated by T2DM. IS was significantly smaller in animals with T2DM. Bariatric surgery provided no additional IS limitation compared with T2DM alone. Bariatric surgeries reversed T2DM-induced enhanced contractile responses of the mesenteric artery to 5-hydroxytryptamine. Sleeve gastrectomy normalized decreased nitric oxide synthase contribution to the endothelium-dependent vasodilatation in T2DM. SIGNIFICANCE: T2DM resulted in a reduction of infarct size and no-reflow zone size. Bariatric surgery provided no additional infarct-limiting effect, but it normalized T2DM-induced augmented vascular contractility and reversed decreased contribution of nitric oxide to endothelium-dependent vasodilatation typical of T2DM. All taken together, we suggest that this type of surgery may have a beneficial effect on T2DM-induced cardiovascular diseases.