Kininogen-Nitric Oxide Signaling at Nearby Nonexcited Acupoints after Long-Term Stimulation.

Acupuncture treatment is based on acupoint stimulation; however, the biological basis is not understood. We stimulated one acupoint with catgut embedding for 8 weeks and then used isobaric tags for relative and absolute quantitation to screen proteins with altered expression in adjacent acupoints of Sprague Dawley rats. We found that kininogen expression was significantly upregulated in the stimulated and the nonstimulated adjacent acupoints along the same meridian. The enhanced kininogen expression was meridian dependent and was most apparent among small vessels in the subcutaneous layer. Enhanced signals of nitric oxide synthases, cGMP-dependent protein kinase, and myosin light chain were also observed at the nonstimulated adjacent acupoints along the same meridian. These findings uncover biological changes at acupoints and suggest the critical role of the kininogen-nitric oxide signaling pathway in acupoint activation.

(4-Ethyl-cyclo-hex-yl)(4-meth-oxy-phen-yl)methanone.

In the title compound, C16H22O2, the cyclo-hexane ring adopts a chair conformation and its mean plane subtends a dihedral angle of 54.2 (6)° with the benzene ring. The crystal structure is stabilized by van der Waals inter-actions only with no classical inter-molecular hydrogen bonding observed.

Protective effects of ion-imprinted chitooligosaccharides as uranium-specific chelating agents against the cytotoxicity of depleted uranium in human kidney cells.

Occupational internal contamination with depleted uranium (DU) compounds can induce radiological and chemical toxicity, and an effective and specific uranium-chelating agent for clinical use is urgently needed. The purpose of this study was to investigate whether a series of synthesized water-soluble metal-ion-imprinted chitooligosaccharides can be used as uranium-specific chelating agents, because the chitooligosaccharides have excellent heavy metal ion chelation property and the ion-imprinting technology can improve the selective recognition of template ions. DU-poisoned human renal proximal tubule epithelium cells (human kidney 2 cells, HK-2) were used to assess the detoxification of these chitooligosaccharides. The DU-chelating capacity and selectivity of the chitooligosaccharides were determined by inductively coupled plasma-mass spectrometry (ICP-MS). Cell viability, cellular accumulation of DU, membrane damage, DNA damage, and morphological changes in the cellular ultrastructure were examined to assess the detoxification of these chitooligosaccharides. The results showed that the Cu²âº-imprinted chitooligosaccharides, especially the Cu²âº-imprinted glutaraldehyde-crosslinked carboxymethyl chitooligosaccharide (Cu-Glu-CMC), chelated DU effectively and specifically, and significantly reduced the loss of cell viability induced by DU and reduced cellular accumulation of DU in a dose-dependent manner, owing to their chelation of DU outside cells and their prevention of DU internalization. The ultrastructure observation clearly showed that Cu-Glu-CMC-chelated-DU precipitates, mostly outside cells, were grouped in significantly larger clusters, and they barely entered the cells by endocytosis or in any other way. Treatment with Cu-Glu-CMC also increased the activity of antioxidant enzymes, and reduced membrane damage and DNA damage induced by DU oxidant injury. Cu-Glu-CMC was more effective than the positive control drug, diethylenetriaminepentaacetic acid (DTPA), in protection of HK-2 cells against DU cytotoxicity, as a result of its chelation of UO2²âº to prevent the DU internalization and its antioxidant activity.