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Nicotinamide phosphoribosyltransferase (NAMPT) maintains mitochondrial function and protects against cerebral ischemic injury by improving energy metabolism. Notoginsenoside R1 (R1), a unique constituent of Panax notoginseng , has been shown to promote the proliferation and tube formation of human umbilical vein endothelial cells. Whether R1 has proangiogenesis on the activation of NAMPT in ischemic stroke remains unclear. The purpose of this study was to investigate the pharmacodynamic effect and mechanism of R1 on angiogenesis after ischemic stroke. We used male Sprague-Dawley (SD) rats subjected to middle cerebral artery occlusion/reperfusion (MCAO/R). R1 was administered via intraperitoneal (i.p.) injection immediately after ischemia induction. The promotion of R1 on angiogenesis were detected by immunofluorescence staining, 3D stereoscopic imaging and transmission electron microscopy detection. HBMEC cells were pretreated with different concentrations of R1 for 12 h before oxygen-glucose deprivation/reoxygenation (OGD/R) exposure. Afterward, scratch assay, EdU staining and tube formation were determined. Western blot analyses of proteins, including those involved in angiogenesis, NAMPT-SIRT1 cascade, VEGFR-2, and Notch signaling, were conducted. We showed that R1 significantly restored cerebral blood flow, improved mitochondrial energy metabolism and promoted angiogenesis. More importantly, incubation with 12.5–50 μM R1 significantly increased the migration, proliferation and tube formation of HBMECs in vitro. The promotion of R1 on angiogenesis were associated with the NAMPT-NAD+-SIRT1 cascade and Notch/VEGFR-2 signaling pathway, which was partially eliminated by inhibitors of NAMPT and SIRT1. We demonstrated that R1 promotes post-stroke angiogenesis via activating NAMPT-NAD+-SIRT1 cascade. The modulation of Notch signaling and VEGFR-2 contribute to the post-stroke angiogenesis. These findings offer insight for exploring new therapeutic strategies for neurorestoration via R1 treatment after ischemic stroke. Schematic diagram of the mechanisms underlying the R1-induced promotion of angiogenesis after ischemia-reperfusion injury. Overall, R1 activates the NAMPT-NAD+-SIRT1 cascade, SIRT1 deacetylates NICD, which led to inhibition of DLL4-Notch signaling. Inhibition of the Dll4-Notch signaling pathway can upregulate the expression of VEGFR-2, thereby promoting angiogenesis after ischemia. [Display omitted] • A new therapeutic strategy in the treatment of ischemic stroke was proposed. • The mechanism relies on the promotion of angiogenesis. • A new method for the detection of energy metabolic molecules were proposed. [ABSTRACT FROM AUTHOR]

The investigations for selective adsorption of dibenzothiophene (DBT) over Ce/Ni-loaded Y zeolites with the emphasis on the effect of Ce as a cocation in the Ni-loaded Y zeolite are carried out in an attempt to produce more effective adsorbents for the desulfurization from transportation fuels. The promotional effects of Ce and coexisting toluene in the model fuel as well as contact time and adsorbent dose on the adsorptive performance were examined. The sulfur uptake strongly depends on the amount of Ce in the zeolite structure. The sorption data is varied according to both Langmuir and Freundlich isotherm models. The maximum sorption capacity by theoretically calculation is 22.2mg/g at 25°C. The Langmuir constants b =5.82mL/mg and the Freundlich constants K =1.042L/mg and 1/n =0.4 are evaluated. Ni/Ce-loaded Y zeolites (NiCeY) and NiY, CeY, NaY zeolites were used as adsorbents for the removal of DBT from model fuel containing 500mg/L sulfur with 5vol% of toluene by a batch method under ambient conditions. NiCeY exhibits higher adsorptive selectivity for DBT than NiY and CeY, indicating that NiCeY is a more effective adsorbent to remove sulfur compounds from transportation fuels. [Copyright &y& Elsevier]