Wound healing modulation by a latex protein-containing polyvinyl alcohol biomembrane.

In a previous study, we performed the chemical characterization of a polyvinyl alcohol (PVA) membrane supplemented with latex proteins (LP) displaying wound healing activity, and its efficacy as a delivery system was demonstrated. Here, we report on aspects of the mechanism underlying the performance of the PVA-latex protein biomembrane on wound healing. LP-PVA, but not PVA, induced more intense leukocyte (neutrophil) migration and mast cell degranulation during the inflammatory phase of the cicatricial process. Likewise, LP-PVA induced an increase in key markers and mediators of the inflammatory response (myeloperoxidase activity, nitric oxide, TNF, and IL-1ß). These results demonstrated that LP-PVA significantly accelerates the early phase of the inflammatory process by upregulating cytokine release. This remarkable effect improves the subsequent phases of the healing process. The polyvinyl alcohol membrane was fully absorbed as an inert support while LP was shown to be active. It is therefore concluded that the LP-PVA is a suitable bioresource for biomedical engineering.

Neutrophil-infiltrated paw edema induced by mannose-binding Dioclea violacea lectin.

BACKGROUND: The potential edematogenic effect and the pharmacological characterization of a glucose-mannose-binding lectin from Dioclea violacea (DvL) were investigated. METHODS: Paw edema was induced with DvL in control animals, and in animals pretreated with glucocorticoid or with blockers of histamine, nitric oxide synthase, cyclooxygenase, platelet activating factor (PAF), bradykinin and lipoxygenase. RESULTS: DvL-induced paw edema paralleled with an increase in vascular permeability and myeloperoxidase (MPO) activity. DvL-induced edema could be prevented by pre-treatment with the lectin-binding sugar α-D-methyl mannoside. Dexamethasone, meclizine and Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME) inhibited this effect. CONCLUSIONS: DvL induces edema, increase in vascular permeability and neutrophil infiltration. The edematogenic activity involves the lectin mannose-binding sites and is associated with histamine, cytokines and nitric oxide, since it could be treated with meclizine, dexamethasone and L-NAME.

Protein fraction of Calotropis procera latex protects against 5-fluorouracil-induced oral mucositis associated with downregulation of pivotal pro-inflammatory mediators.

Oral mucositis is an important dose-limiting and costly side effect of cancer chemotherapy. Soluble proteins obtained of the latex of Calotropis procera have been extensively characterized as anti-inflammatory in different experimentally induced inflammatory conditions, including arthritis and sepsis. In this study, the phytomodulatory laticifer proteins (LP) were challenged to regress the inflammatory events associated with 5-fluorouracil-induced oral mucositis. We also evaluated the expression of pro-inflammatory cytokines and inducible enzymes, such as cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS). Oral mucositis was induced in hamsters by two injections of 5-fluorouracil (5-FU; 60 and 40 mg/kg, i.p., on experimental days 1 and 2, respectively). LP (5 mg/kg, i.p.) was injected 24 h before and 24 h after mechanical trauma of the cheek pouches. A normal control group received only saline. On day 10, the animals were sacrificed, and the cheek pouches were excised for macroscopic and histopathological analysis, myeloperoxidase activity measurement, and immunohistochemical assessment of tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), iNOS, and COX-2. LP significantly inhibited macroscopic histopathological scores and myeloperoxidase activity compared with the 5-FU control group. 5-Fluorouracil also induced marked immunostaining of TNF-α, IL-1ß, iNOS, and COX-2 on inflamed conjunctive and epithelial tissue compared with the normal control group. Such damage was significantly inhibited (p < 0.05) by LP treatment compared with the 5-FU group. These findings demonstrate an anti-inflammatory effect of LP on 5-FU-induced oral mucositis. The protective mechanism appears to involve inhibition of the expression of iNOS, COX-2, TNF-α, and IL-1ß.