Cyclo­benzaprinium chloride

In the title mol­ecular salt [systematic name: 3-(5H-dibenzo[a,d]cyclo­hepten-5-yl­idene)-N,N-dimethyl­propan­aminium chloride], C20H22N+·Cl−, two cation–anion pairs make up the asymmetric unit. The dihedral angles between the mean planes of the two fused benzene rings of the cation are 49.5 (1) and 50.9 (1)°. The cystal packing is stabilized by N—H⋯Cl hydrogen bonds and weak C—H⋯Cl inter­actions

Cyclo­benzaprinium salicylate

In the title mol­ecular salt [systematic name: 3-(5H-di­benzo[a,d]cyclo­hepten-5-yl­idene)-N,N-dimethyl-1-propanaminium 2-hy­droxy­benzoate], C20H22N+·C7H5O3 −, the benzene rings of the cyclo­benzaprinium cation are inclined with a dihedral angle of 61.66 (7)°. An intra­molecular O—H⋯O hydrogen bond occurs within the salicylate anion, generating an S(6) ring. In the crystal, the cation and anion are linked by an N—H⋯O inter­action

[3-(5-Hy­droxy-5H-dibenzo[a,d]cyclo­hepten-5-yl)prop­yl]dimethyl­ammonium 3-carboxyprop-2-enoate

In the cation of the title salt, C20H24NO+·C4H3O4 −, the N atom in the dimethyl­ammonium group is protonated. The dihedral angle between the mean planes of the two six-membered rings fused to the cyclo­hepten-5-yl ring is 54.4 (1)°. An intra­molecular O—H⋯O hydrogen bond occurs in the anion. The crystal packing is stabilized by inter­molecular O—H⋯O and N—H⋯(O,O) hydrogen bonds and weak C—H⋯O inter­actions, forming a two-dimensional network

Solubility and Permeation of Hydrogen Sulfide in Lipid Membranes

Hydrogen sulfide (H2S) is mainly known for its toxicity but has recently been shown to be produced endogenously in mammalian tissues and to be associated with physiological regulatory functions. To better understand the role of biomembranes in modulating its biological distribution and effects; we measured the partition coefficient of H2S in models of biological membranes. The partition coefficients were found to be 2.1±0.2, 1.9±0.5 and 2.0±0.6 in n-octanol, hexane and dilauroylphosphatidylcholine liposome membranes relative to water, respectively (25°C). This two-fold higher concentration of H2S in the membrane translates into a rapid membrane permeability, Pm = 3 cm s−1. We used a mathematical model in three dimensions to gain insight into the diffusion of total sulfide in tissues. This model shows that the sphere of action of sulfide produced by a single cell expands to involve more than 200 neighboring cells, and that the resistance imposed by lipid membranes has a significant effect on the diffusional spread of sulfide at pH 7.4, increasing local concentrations. These results support the role of hydrogen sulfide as a paracrine signaling molecule and reveal advantageous pharmacokinetic properties for its therapeutic applications

Hydrogen Sulfide Attenuated Tumor Necrosis Factor-α-Induced Inflammatory Signaling and Dysfunction in Vascular Endothelial Cells

S donor) on tumor necrosis factor (TNF)-α-induced human umbilical vein endothelial cells (HUVEC) dysfunction.Application of NaHS concentration-dependently suppressed TNF-α-induced mRNA and proteins expressions of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), mRNA expression of P-selectin and E-selectin as well as U937 monocytes adhesion to HUVEC. Western blot analysis revealed that the expression of the cytoprotective enzyme, heme oxygenase-1 (HO-1), was induced and coincident with the anti-inflammatory action of NaHS. Furthermore, TNF-α-induced NF-κB activation assessed by IκBα degradation and p65 phosphorylation and nuclear translocation and ROS production were diminished in cells subjected to treatment with NaHS.S can exert an anti-inflammatory effect in endothelial cells through a mechanism that involves the up-regulation of HO-1

Release of exogenous γ-[³H]aminobutyric acid during seizure activity in chronically denervated and normal cat cortex

The hypothesis that the seizure susceptibility of chronically denervated cortex is due to interruption of recurrent inhibitory pathways was tested by examining the release of 3H-labeled γ-aminobutyric acid ([3H]GABA) from chronic slabs and normal cortex of cats. Seizure activity was maintained throughout the test periods in both normal and chronically isolated cortex. When methacholine was used to evoke seizure activity, [3H]GABA release was depressed in both normal and epileptic cortex, suggesting that the mechanism of seizure genesis by cholinomimetics involves suppression of inhibitory neuron activity. Pentylenetetrazol-induced seizures evoked a small, equal increase in [3H]GABA efflux from epileptic and normal cortex. Continuous electrical stimulation evoked a large, and again equal increase in [3H]GABA release. Preseizure efflux of [3H]GABA was the same from chronic slabs and normal cortex in all experiments. Since the interruption of recurrent inhibitory pathways by chronic denervation would result in a decreased resting and seizure-evoked release of [3H]GABA, results obtained do not support the above-mentioned hypothesis. </jats:p