A novel reactive fluorescent probe for cobalt ions was prepared based on integration of thiourea functional groups, coumarin, and naphthalimide fluorophores. There was no fluorescence observed for the probe itself, however, in the presence of cobalt ions, catalytic decomposition occurred for the probe and coumarin molecular fragments were produced that emitted blue fluorescence. This enabled the probe to be used as a ‘turn on’ reagent for detection of cobalt ions. Under physiological pH conditions and in appropriate solvent systems, an obvious fluorescence enhancement for cobalt ions was observed in selective experiments. Competition experiments indicated that cobalt ions could still induce fluorescence enhancement in the presence of other metal ions. Sensitivity experiments showed that the detection limit for cobalt ions was 6.0 nM. Dynamics research demonstrated that the catalytic process was a pseudo‐first‐order reaction and the reaction constant (kobs) was calculated to be 1.49 × 10−2 min−1. In addition, the mechanism of catalytic decomposition could be demonstrated using electrospray ionization mass spectrometry and thin layer chromatography experiments. Cell fluorescence imaging experiments demonstrated that the probe could be used to detect cobalt ions in living HeLa cells.
Endothelial dysfunction is the pathological basis of atherosclerosis. Incomplete understanding of endothelial dysfunction etiology has impeded drug development for this devastating disease despite the currently available therapies. Floralozone, an aroma flavor, specifically exists in rabbit ear grass. Recently, floralozone has been demonstrated to inhibit atherosclerosis, but the underlying mechanisms are undefined. The present study was undertaken to explore whether floralozone pharmacologically targets endothelial dysfunction and therefore exerts therapeutic effects on atherosclerosis. The Na+/H+ exchanger 1 (NHE1), a channel protein, plays a vital role in atherosclerosis. Whether NHE1 is involved in the therapeutic effects of floralozone on endothelial dysfunction has yet to be further answered. By performing oil red staining and hematoxylin–eosin staining, vascular functional study, and oxidative stress monitoring, we found that floralozone not only reduced the size of carotid atherosclerotic plaque but also prevented endothelial dysfunction in atherosclerotic rats. NHE1 expression was upregulated in the inner membrane of carotid arteries and H2O2-induced primary rat aortic endothelial cells. Inspiringly, floralozone prevented the upregulation of NHE1 in vivo and in vitro. Notably, the administration of NHE1 activator LiCl significantly weakened the protective effect of floralozone on endothelial dysfunction in vivo and in vitro. Our study demonstrated that floralozone exerted its protective effect on endothelial dysfunction in atherosclerosis by ameliorating NHE1. NHE1 maybe a drug target for the treatment of atherosclerosis, and floralozone may be an effective drug to meet the urgent needs of atherosclerosis patients by dampening NHE1.
AimThis study aimed to investigate the preventive effect and possible mechanism of amorphous selenium nanoparticles (A-SeQDs) on isocarbophos induced vascular dysfunction.MethodsA-SeQDs was made by auto redox decomposition of selenosulfate precursor. Male rats were given isocarbophos (0.5 mg/kg/2 days) by intragastric administration for 16 weeks to induce vascular dysfunction. During the course, A-SeQDs (50 mg/kg/day) was added to the water from week 5. Then, the rats were killed to observe and test the influence of A-SeQDs on the vascular dysfunction induced by isocarbophos. Finally, human umbilical vein endothelial cells (HUVECs) were treated with 10% DMEM of isocarbophos (100 μM) for 5 days to detect the related indexes. Before the use of isocarbophos treatment, different drugs were given.ResultsA-SeQDs could reduce total carbon dioxide, MDA, VCAM-1, ICAM-1, IL-1, and IL-6 while increasing oxygen saturation, NO content, and SOD activity in rats. A-SeQDs also resulted in relatively normal vascular morphology, and the expression of sodium hydrogen exchanger 1 (NHE1) and caspase-3 decreased in rats. Furthermore, in HUVECs treated with isocarbophos, A-SeQDs maintained mitochondrial membrane potential, inhibited the cleaved caspase-3 expression, and released cytochrome c from mitochondria to cytosol.ConclusionA-SeQDs can inhibit the apoptosis of HUVECs through the mitochondrial pathway, and effectively treat the impairment of vascular endothelial function caused by isocarbophos, which is NHE1-dependent.
Background Floralozone (FL) is medicine with the refreshing aroma of rabbit's ear grass, which can be used to prevent the progression of atherosclerosis and reduces endothelial dysfunction. Vascular endothelial growth factor receptor 1 (VEGFR1) is one of the receptors of vascular endothelial factor (VEGF), which mainly plays a negative role in cardiovascular system regulation mainly by acting as a decoy receptor in endothelial cells. Therefore, the purpose of this study is to evaluate whether FL can down-regulate VEGFR1 expression in treating diabetes-induced heart failure (HF). Methods We used high-sugar and high-fat diet and tail vein injection of streptozotocin (STZ) to establish the rat model of HF. After intragastric administration of FL, the left ventricular function, pathological changes, oxidative stress condition in HF rats were assessed by echocardiography, oxidative stress monitoring, hematoxylin-eosin histological staining, argyrophilic staining, Masson staining, lichen red staining. The expression of VEGFR1 in the myocardial tissue of HF rats was detected by immunohistochemistry, immunofluorescence, western blot and RT-PCR analysis Results The HF model was established successfully. Through intragastric administration of FL, it was observed the cardiac function of HF rats was significantly improved, ventricular remodeling level was reversed, and the ability of antioxidant stress was enhanced. These therapeutic effects were closely connected with the down-regulation of VEGFR1 expression. ZM306416 is an antagonist of VEGFR1, which can up-regulate VEGFR1 expression and inhibit the protective effect of FL in rats with HF. Conclusions These results suggest that FL can play a salutary role in HF rats by down-regulating VEGFR1 expression, inhibiting ventricular remodeling and reducing oxidative stress.
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