This review presents an overview about pharmaceutical and cosmetic topical products containing polymeric nanoparticles (nanospheres and nanocapsules), reporting the main preparation and characterization methods and the studies of penetration and transport of substances through the skin. The penetration and transport extent of those systems through the skin depends on the ingredients chemical composition, on the encapsulation mechanism influencing the drug release, on the size of nanoparticles and on the viscosity of the formulations. The polymeric nanoparticles are able to modify the activity of drugs, delay and control the drug release, and increase the drug adhesivity or its time of permanence in the skin. Briefly, the nanoparticles can be useful as reservoirs of lipophilic drugs to deliver them in the stratum corneum becoming an important strategy to control their permeation into the skin.

https://journals.sagepub.com/doi/pdf/10.1177/117739280700200002

Polymeric Nanoparticles, Nanospheres and Nanocapsules, for Cutaneous Applications

Aclidinium bromide is a novel potent, long-acting inhaled muscarinic antagonist in development for the treatment of chronic obstructive pulmonary disease. Aclidinium showed subnanomolar affinity for the five human muscarinic receptors (M(1)-M(5)). [(3)H]Aclidinium dissociated slightly faster from M(2) and M(3) receptors than [(3)H]tiotropium but much more slowly than [(3)H]ipratropium. Its association rate for the M(3) receptor was similar to [(3)H]ipratropium and 2.6 times faster than [(3)H]tiotropium. Residence half-life of [(3)H]aclidinium at the M(2) receptor was shorter than at the M(3) receptor, demonstrating kinetic selectivity for the M(3) receptor. In isolated guinea pig trachea, aclidinium showed comparable potency to ipratropium and tiotropium, faster onset of action than tiotropium, and duration of action similar to tiotropium and significantly longer than ipratropium. Nebulized aclidinium inhibited bronchoconstriction induced by acetylcholine in guinea pigs in a concentration-dependent manner with an onset of action faster than tiotropium. Duration of action of aclidinium (t(1/2) = 29 h) was much longer than ipratropium (8 h) but shorter than tiotropium (64 h). In dogs, aclidinium induced a smaller and more transient increase in heart rate than tiotropium at comparable supratherapeutic doses. Therefore, under these conditions, aclidinium showed a greater therapeutic index than tiotropium (4.2 versus 1.6). These results indicate that aclidinium is a potent muscarinic antagonist with a fast onset of action, a long duration of effect, and a favorable cardiovascular safety profile.

Characterization of Aclidinium Bromide, a Novel Inhaled Muscarinic Antagonist, with Long Duration of Action and a Favorable Pharmacological Profile

Evidence that tamoxifen is a histamine antagonist.

Involvement of cannabinoid CB2 receptors in the IgE-mediated triphasic cutaneous reaction in mice.

The effect of some drugs on phospholipase A2 (PLA2)-induced histamine release from rat peritoneal mast cells was investigated. 1. PLA2 (Naja naja) caused the release of histamine from rat peritoneal mast cells in a dose related fashion. 2. The release of histamine by PLA2 was decreased by the removal of each of calcium and glucose from the reaction medium (Tyrode's solution). 3. p-Bromophenacyl bromide and mepacrine, PLA2 inhibitors, inhibited the release of histamine caused by PLA2. 4. Cinnarizine and nifedipine, calcium channel blockers, and oxatomide, KC-404, tranilast and disodium cromoglycate, anti-allergic agents, also inhibited the PLA2-induced histamine release. 5. When prednisolone (0.5 mg/kg) was administered i.p. 2, 3 and 4 h prior to the harvest of the mast cells, the amount of histamine released by PLA2 ex vivo was significantly decreased. Hydrocortisone, prednisolone and dexamethasone clearly inhibited the release of histamine from mast cells when they were administered 4 h prior to harvest of the cells.

Pharmacological study of phospholipase A2-induced histamine release from rat peritoneal mast cells.

Reduction of antigen-induced contraction of sensitized guinea-pig tracheal smooth muscle in vitro by calmodulin inhibitors.

Previous　studies　have　reported　that　the　mice　passively　sensitized　with　anti－DNP　IgE　antibody exhibited　IgRmediated　biphasic　cutaneous　reaction　with　an　immediate　phase　response（IPR）at　l　h　and a　late　phase　response（LPR）at24h　after　the　challenge　of　DNFB（dinitrofluorobenzene）．We　recently found　that　the　third　phase　inflammatory　response　with　intense　and　persisting　infiltration　of　eosinophils， named　very　late　phase　response（vLPR），was　induced　following　IPR　and　LPR　in　response　to　DNFB　in passively　sensitized　mice，and　that　the　peak　response　of　vLPR　was　on　the8th　day　after　the　challenge． The　inhibitory　effect　of　Kampo　medicines　on　the　triphasic　cutaneous　inflammatory　reaction　was　divided into　several　groups　in　terms　of　their　inhibition　rate　of　ear　swelling．Among　the　formulations，Tokaku－ joki－to（Tao－He－Cheng－Qi－Tang）was　effective　at　inhibiting　IPR，LPR　and　vLPR（＋／＋／＋group） and　scratching　behavior　in　IPR．The　Inhibitory　effect　of　Tokaku－joki－to　on　triphasic　cutaneous　reaction primarily　depends　on　its　composed　cmde　dmgs，Glycyrrhizae　Radix　and　Cimamomi　Cortex．These

Effect of Some Kampo Medicines, Including Tokaku-joki-to(Tao-He-Cheng-Qi-Tang), on IgE-mediated Triphasic Skin Reaction in Passively Sensitized Mice.

The effects of 11-oxo-11H-pyrido[2,1-b]quinazoline-2-carboxylic acid (Sm 857) on immediate type, particularly type I allergic reactions were investigated and the following results were obtained. 48-h homologous passive cutaneous anaphylaxis (PCA) in rats was inhibited by oral administration of Sm 857 from the 4th h to the 30th min before antigen challenge and by intravenous administration from the 2nd h to just before antigen challenge. 48-h homologous PCA in rats was inhibited dose-dependently by oral administration of Sm 857 at 1-50 mg/kg 30 min before antigen challenge. On the other hand, the intravenous administration 10 min before antigen challenge showed similar dose-dependent effects on PCA and the effects were significant at doses of 0.5-2 mg/kg. The oral administration of Sm 857 for 1-4 weeks reduced the PCA inhibitory effect in comparison with single administration. Sm 857 injected intravenously twice at intervals of 15-120 min showed no change in inhibitory effect. The PCA inhibitory effect of Sm 857 in adrenalectomized rats was reduced markedly when compared with that in sham-operated rats. On the other hand, adrenalectomy had no influence on the inhibitory effect of tranilast. Sm 857, tranilast and ketotifen inhibited histamin-induced capillary permeability in rats and, in particular, the effect of ketotifen was conspicuous. Sm 857, tranilast and ketotifen significantly inhibited antigen-induced histamine release from the peritoneal cavity of passively sensitized rats. Release of slow reacting substance of anaphylaxis (SRS-A), on the other hand, was inhibited significantly by Sm 857 and ketotifen. Sm 857 showed a tendency to inhibit antigen-induced histamine release from the lung tissue of passively sensitized guinea pigs and significantly inhibited SRS-A release. Sm 857 inhibited histamine- and leukotriene D4 (LTD4)-induced contraction in the lung parenchyma and the tracheal muscle. However, the drug had no effect on contraction of the ileum. Sm 857 showed a tendency to inhibit the Schultz-Dale reaction in the lung parenchyma ana the ileum. Both oral and intravenous administration of Sm 857 showed an inhibitory effect on experimental asthma in guinea pigs, which was similar to that of tranilast.

Effects of the New Antiallergic Drug 11-Oxo-11H-Pyrido[2,1-b]quinazoline-2-carboxylic Acid on Immediate Allergic Reactions.

Interleukin-4 Is Involved in Allergen-induced Airway Eosinophilic Inflammation and Bronchial Hyperresponsiveness Independent of Genetic Background.

In order to characterize nephrotoxic serum nephritis accelerated with rabbit γ-globulin in mice, histopathological studies were carried out 15 days after NTS injection, the time when increases in urinary protein and serum cholesterol and a decrease in serum albumin were apparent. Characteristic changes were widespread thickening of glomerular capillary walls and widening of mesangial areas, owing to deposits of mesangial matrixlike substances. The mesangial interposition into subendothelial areas and the resultant narrowing of the capillary lumen were shown ultrastructurally. In severely affected glomeruli, a hyaline nodular lesion was observed. Visceral epithelial cells demonstrated fusion of the foot processes, microvilli formation, occasional proliferation, and enlargement. Parietal epithelial cells proliferated, forming a cellular crescent. Based on these characteristics, it appears this nephritic model shares a common pathology with human membranoproliterative glomerulonephritis type 1 and crescentic glomerulonephritis and can be considered an appropriate model for producing severe nephritis for short periods.

Pathological studies on nephrotoxic serum nephritis accelerated with rabbit γ-globulin in mice.

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