Increase in dermal collagen fibril diameter and elastogenesis with UVB exposure: an optical and ultrastructural study in albino Balb/c mice.

Cutaneous aging is a complex biological phenomenon, dependent not only on the innate or intrinsic process ("biological clock"), but also on extrinsic elements, primarily chronic sun exposure (photoaging). In order to verify dermal morphological changes in the elastic fiber system and collagen associated with aged skin, we performed a light and electron microscopic study on exposed-shaved albino mice, which were exposed to UVB radiation. The experimental group consisted of 48 exposed animals, randomly distributed in three groups and submitted to different radiation doses (A, 28800 J/m2; B, 57600 J/m2; and C, 86400 J/m2) and studied 0, 30, 60 and 90 days of exposure discontinuation. Nonexposed-shaved and nonexposed-nonshaved animals were included as controls. From the day of exposure discontinuation and subsequently, the elastic system and collagen network were progressively modified. The increase in collagen fibril diameter was prominent in the 60 and 90 day groups (p<0.05), as noticed on electron microscopy. Elastic fiber density also increased after irradiation (p<0.05). On electron microscopy, elastogenesis was seen in the deep dermis. The comparative study among the groups disclosed clear relationship between doses and "elastotic changes". It also showed that chronological aging of mice skin was apparently intensified after UVB exposure. Skin elastogenesis seems to be a major consequence of UVB exposure, apart from elastolysis, and occurs not only in humans but also in hairless mice submitted to continuous, long-term UVB exposure.

Hydralazine reduces myocardial tissue damage in rats submitted to chronic inhibition of systemic nitric oxide synthesis during 4, 14 and 28 days

The aim of the present work was to develop a qualitative chronopathological study concerning abnormalities in myocardium, due to nitric oxide (NO) blockage. We used 60 Wistar normotensive young male rats from several breeds. Groups of rats were submitted to L-Name (L) via oral administration dissolved in water (750mg/l) during days 4, 14 and 28. Other groups were submitted concomitantly to L-Name and hydralazine hydrocloride (L + H) (120mg/l). On days 4 and 14 (L group) we have found myocardial abnormalities and lesions while in L + H we could not identify abnormalities. Considering L group on day 28, the myocardium presented characteristic fibrosis (reactive and reparative), vascular damage with increasing wall thickness due mainly to proliferation of the arterial smooth muscle cell. Total obliteration of vessels was noted only in this period. We also observed reactive fibrosis between muscle cells of the vascular wall and proliferation of cells in the intimal layer. In L + H (day 28), similar vascular abnormalities described for L group (less frequent and less apparent) were also observed. In L + H we did not identify total vascular obstructions. In L + H, infarct areas were not observed. Control groups did not present any abnormalities. Our results support the idea that, at least in some cases, hypertrophy vascular abnormalities and myocardial lesions in arterial hypertension can occur because of the reduction in organic nitric oxide production. Our results also suggested that these morbid processes can be postponed by the use of hydralazine which, however, does not avoid abnormalities after long-term experimental blockage of NO

Quantitave and qualitative interferences of pentoxifillyne on hepatic Schistosoma mansoni granulomas: effects on extracellular matrix and eosinophil population

Mast cells and eosinophils actively participate in tissue repair and are prominent components of Schistosoma mansoni granulomas. Since pentoxifillyne (PTX) is an immunomodulatory and antifibrotic substance, we aimed to characterize, by morphological techniques, the effect of this drug on fibrosis developed inside murine hepatic schistosomal granulomatous reaction, beyond the quantification of eosinophil and mast cell populations. The drug (1 mg/100 g animal weight) was administrated from 35 to 90 days post-infection, when the animals were killed. The intragranulomatous interstitial collagen network was analyzed by confocal laser scanning microscopy, the number of eosinophils and mast cells was quantified and the results were validated by t-student test. Treatment did not interfere on the granuloma evolution but caused a significant decrease in the total and involutive number of hepatic granulomas (p = 0.01 and 0.001, respectivelly), and in the intragranulomatous accumulation of eosinophils (p = 0.0001). Otherwise, the number of mast cells was not significantly altered (p = 0.9); however, it was positively correlated with the number of granulomatous structures (r = 0.955). In conclusion, PTX does not affect development and collagen deposition in S. mansoni murine granuloma, but decreases the intragranulomatous eosinophil accumulation possibly due to its immunomodulatory capability, interfering in cellular recruitment and/or differentiation