Cellulose nanocrystals (CNCs) have great potential in many areas of research, applications, and future commercialization prospects. Recently, CNCs have emerged as attractive candidates for biomedical applications such as drug and gene delivery systems. As such, cytotoxicity studies have been the major focus in the past decade. However, despite the rod-like nature of CNCs, the potential immune response of surface-modified CNCs is not well investigated. The current study examined the potential immune and antioxidant response induced by CNCs grafted with β-cyclodextrin (CNCs-β-CD) in a human monocyte cell line (THP-1) and a mouse macrophage-like cell line (J774A.1). We analyzed the secretion of the proinflammatory cytokine, interleukin 1β (IL-1β), by ELISA and mitochondria-derived reactive oxygen species (ROS) using fluorescence cell imaging and examined the intracellular levels of proteins involved in the immune and antioxidant response by immunoblotting. Our results indicated a dramatic increase neither in the IL-1β secretion nor in the mitochondria-derived ROS resulting in no changes in the intracellular antioxidant response in THP-1 cells treated with different concentrations of CNCs-β-CD. Overall, CNCs-β-CD is nonimmunogenic and do not induce an increased antioxidant response under the conditions tested and hence has the potential to be used as a drug delivery carrier.
The diabetic heart is at an increased risk for myocardial infarction. The aim of this study was to examine the effect of the superoxide dismutase mimetic EUK‐134 on the susceptibility of the diabetic heart to ischemic/reperfusion injury. Rats were injected with streptozotocin (STZ) or its vehicle (Control) and implanted with an osmotic minipump containing the SOD mimetic EUK‐134 or its vehicle. After 4 weeks, in vivo left ventricular (LV) pressure and contractility were similar in all four groups. Hearts were then isolated and perfused in the Langendorf mode for the measurement of LV pressure and contractility before and after a 30 min global ischemia. Baseline LV pressure was similar in all groups. Following 30 min of ischemia, LV pressure was significantly reduced in the control rats treated with vehicle whereas hearts from STZ rats treated with vehicle or EUK‐134 and control rats treated with EUK‐134 all recovered more quickly and regained normal mechanical function following ischemia/reperfusion. Heart lipid peroxidation was also increased in the vehicle‐treated control rats compared to the other groups. These results suggest that hyperglycemia associated with STZ diabetes and/or treatment with the SOD mimetic EUK‐134 reduce cardiac lipid peroxidation and enhance cardiac mechanical activity after ischemia/reperfusion.
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