Cassava biopolymer polyamide hydrogel accelerates healing of induced skin woundsin rats / Hidrogel de biopolímero de poliamido de mandioca acelera o processo de cicatrização em feridas cutâneas induzidas em ratos

This study aimed to macroscopically and microscopically evaluate the healing of skin wounds induced in rats by topical application of cassava polyamide biopolymer hydrogel. In total, 32 rats were used and divided into four groups (n= 8): negative control - saline solution; positive control - use of commercial ointment; experimental group - I - ointment + cassava hydrogel; experimental group - II - cassava hydrogel. A 1cm2 wound induced on the animals dorsum was treated and evaluated. At day 21 post-operation, the animals were sacrificed by anesthetic overdose, and then 1cm2 of cicatricial skin from the wound region was collected. The material was cut to evaluate healing. In the macroscopic evaluation, complete healing was observed at the end of 21 days. Re-epithelialization was observed histologically; the connective tissue in the negative control, positive, and experimental - I groups was characterized by an abundance of collagen fibers, fibroblasts, and blood vessels. In experimental group - II additional healing was observed, as evidenced by the arrangement of collagen fibers and fibroblasts, and the reduction of neoformed vessels. Thus, we concluded that the hydrogel can assist in healing skin wounds, especially in the remodeling phase.(AU)

O objetivo deste estudo foi avaliar macro e microscopicamente a cicatrização de feridas cutâneas induzidas em ratos, a partir da aplicação tópica do hidrogel de biopolímero de poliamido de mandioca. Trinta e dois ratos foram divididos em quatro grupos (n= 8): controle negativo, tratado com solução salina; controle positivo, com pomada comercial; grupo experimental - I, com pomada + hidrogel de mandioca; grupo experimental - II, com hidrogel de mandioca. Feridas induzidas de 1cm 2 no dorso dos animais foram tratadas e avaliadas em intervalos de três a quatro dias. No 21º dia do pós-operatório, os animais foram mortos por aprofundamento anestésico, em seguida foi coletado 1cm 2 de pele da região cicatricial. O material foi cortado, corado pelas técnicas de hematoxilina-eosina e azocarmine-G, para avaliação da cicatrização. Na avaliação macroscópica, foi observada cicatrização completa no final do período de 21 dias. Histologicamente, observou-se reepitelização, o tecido conjuntivo no grupos controle negativo, positivo e experimental - I se caracterizou pela abundância de fibras colágenas, fibroblastos e vasos sanguíneos. No grupo experimental - II, a cicatrização sugere avanço de etapas, evidenciado pelo arranjo das fibras colágenas, pela redução de fibroblastos e dos vasos neoformados. Assim, foi possível concluir que o hidrogel de biopolímero de amido de mandioca pode auxiliar na cicatrização de feridas cutâneas, principalmente na fase de remodelação.(AU)

Effects of the combined artesunate and mefloquine antimalarial drugs on rat embryos.

Artemisinins combination therapy (ACT) is the first choice therapy for falciparum malaria. Data on the safety of ACTs in pregnancy are limited and controversial and the use is not recommended on the first trimester. To evaluate the effects of isolated and combined artesunate (AS)/mefloquine (MQ) on embryo rats, pregnant rats were treated orally with AS (15 and 40 mg/kg body weight (bwt)/day), MQ (30 and 80 mg/kg bwt/day) and AS/MQ (15/30 and 40/80 mg/kg bwt/day) on days 9-11 post coitum (pc). The dams were euthanized on day 12 pc and gestational and embryos histological parameters were evaluated. Embryolethality and histopathological anomalies were significant when AS was given alone or combined with MQ. Combination of AS and MQ did not enhance their toxicity compared to their separate administrations; on the other side, there was a reduction in the toxic effects of the AS when combined with MQ. Isolated MQ did not induce developmental toxicity.

In vivo hydroquinone exposure impairs allergic lung inflammation in rats.

Hydroquinone (HQ) is naturally found in the diet, drugs, as an environmental contaminant and endogenously generated after benzene exposure. Considering that HQ alters the immune system and its several source of exposures in the environment, we hypothesized that prolonged exposure of HQ could affect the course of an immune-mediated inflammatory response. For this purpose, male Wistar rats were intraperitoneally exposed to vehicle or HQ once a day, for 22 days with a 2-day interval every 5 days. On day 10 after exposure with vehicle or HQ, animals were ovalbumin (OA)-sensitized and OA-aerosolized challenged on day 23. HQ exposure did not alter the number of circulating leukocytes but impaired allergic inflammation, evidenced by lower number of leukocytes in the bronchoalveolar lavage fluid 24h after OA-challenge. Reduced force contraction of ex vivo tracheal segments upon OA-challenge and impaired mesentery mast cell degranulation after in situ OA-challenge were also detected in tissues from HQ exposed animals. The OA-specificity on the decreased responses was corroborated by normal trachea contraction and mast cell degranulation in response to compound 48/80. In fact, lower levels of circulating OA-anaphylactic antibodies were found in HQ exposed rats, as assessed by passive cutaneous anaphylaxis assay. The reduced level of OA-anaphylactic antibody was not dependent on lower number or proliferation of lymphocytes. Nevertheless, lower expression of the co-stimulatory molecules CD6 and CD45R on OA-activated lymphocytes from HQ exposed rats indicate the interference of HQ exposure with signaling of the humoral response during allergic inflammation. Together, these data indicate specific effects of HQ exposure manifested during an immune host defense.

Effect of in vivo phenol or hydroquinone exposure on events related to neutrophil delivery during an inflammatory response.

Phenol (PHE) and hydroquinone (HQ) are metabolites of benzene that affect leukocytes after solvent intoxication. Hence, we investigated the effects of PHE or HQ exposure on neutrophil mobilization during an inflammatory response. Male Wistar rats received intraperitoneal injections of PHE, HQ or vehicle only and assays were performed 24 h after the last dose. Quantifications of bone marrow or circulating leukocytes showed that only HQ exposure induced neutrophilia, probably due to the accelerated mobilization from the bone marrow compartment, since reduced numbers of segmented cells in the last phase of maturation were detected there. Intravital microscopy showed that circulating leukocytes of HQ-exposed rats increased their rolling behavior and adherence to the mesenteric postcapillary venule wall in vivo. The enhanced leukocyte-endothelium interaction was not dependent on microvascular reactivity or perivascular mast cell degranulation. Instead, it was the result of neutrophil activation, demonstrated by a decrease in L-selectin and an increase in beta2 integrin expression on neutrophil membranes. This pattern of neutrophil activation may have contributed to the higher number of neutrophils in the subcutaneous inflammatory response of HQ-exposed rats after oyster glycogen injection. Taken together, our results indicate that HQ exposure alters neutrophil mobilization, which results in an exacerbated response after an injury. Although PHE is endogenously metabolized to HQ, PHE exposure only induced an increment in rolling behavior, which was not sufficient to alter the inflammatory response.