Procyanidinere therapy of pulmonary fibrosis induced by CdSe nanorods with pulmonary instillation

Background: The CdSe nanorod as a one-dimensional nanostructure has an excellent performance in photoelectric conversion, biological labeling and environmental protection. Thus, it is crucial to investigate its potential adverse health effects at an early stage. Methods: Sprague-Dawley (SD) male rats were exposed to 15 mg/kg CdSe and 200 mg/kg procyanidine (OPC) for 30, 60 and 90 days. Lung tissues were collected on days 30, 60 and 90. Oxidation damages, histopathological analysis, transmission electron microscopy and hydroxyproline level were measured. Results: The lung tissue would be the main target organ after CdSe nanorods entering into biological bodies. Pulmonary instillation of CdSe nanorods could decrease vitality of T-SOD and T-AOC in lung tissues of a rat, increase MDA and hydroxyproline levels and lipid peroxidation products, induce mitochondrial cristae broken and vacuolization, cause inflammatory responses, and finally induce pulmonary fibrosis. The oral administration of procyanidinere could significantly increase the content of antioxidant enzymes, scavenge free radicals, reduce the lipid peroxidation and have protective effects on CdSe nanorods-induced pulmonary fibrosis. Conclusions: CdSe nanorods could induce an extensive inflammatory response, elevate ROS, induce pulmonary fibrosis and reveal time accumulation appearance. OPC has a protective effect on lung injury induced by CdSe nanorods, which might be related to anti-oxidative and anti-inflammatory properties.

Pulmonary instillation of MWCNT increases lung permeability, decreases gp130 expression in the lungs, and initiates cardiovascular IL-6 transsignaling

Pulmonary instillation of multiwalled carbon nanotubes (MWCNT) has the potential to promote cardiovascular derangements, but the mechanisms responsible are currently unclear. We hypothesized that exposure to MWCNT would result in increased epithelial barrier permeability by 24 h postexposure and initiate a signaling process involving IL-6/gp130 transsignaling in peripheral vascular tissue. To test this hypothesis we assessed the impact of 1 and 10 μg/cm2MWCNT on transepithelial electrical resistance (TEER) and expression of barrier proteins and cell activation in vitro using normal human bronchial epithelial primary cells. Parallel studies using male Sprague-Dawley rats instilled with 100 μg MWCNT measured bronchoalveolar lavage (BAL) differential cell counts, BAL fluid total protein, and lung water-to-tissue weight ratios 24 h postexposure and quantified serum concentrations of IL-6, soluble IL-6r, and soluble gp130. Aortic sections were examined immunohistochemically for gp130 expression, and gp130 mRNA/protein expression was evaluated in rat lung, heart, and aortic tissue homogenates. Our in vitro findings indicate that 10 μg/cm2MWCNT decreased the development of TEER and zonula occludens-1 expression relative to the vehicle. In rats MWCNT instillation increased BAL protein, lung water, and induced pulmonary eosinophilia. Serum concentrations of soluble gp130 decreased, aortic endothelial expression of gp130 increased, and expression of gp130 in the lung was downregulated in the MWCNT-exposed group. We propose that pulmonary exposure to MWCNT can manifest as a reduced epithelial barrier and activator of vascular gp130-associated transsignaling that may promote susceptibility to cardiovascular derangements.