In vivo (lung resistive and viscoelastic pressures and static elastance) and in vitro (tissue resistance, elastance, and hysteresivity) respiratory mechanics were analyzed 1 and 30 days after saline (control) or paraquat (P [10 and 25 mg/kg intraperitoneally]) injection in rats. Additionally, P10 and P25 were treated with methylprednisolone (2 mg/kg intravenously) at 1 or 6 hours after acute lung injury (ALI) induction. Collagen and elastic fibers were quantified. Lung resistive and viscoelastic pressures and static elastance were higher in P10 and P25 than in the control. Tissue elastance and resistance augmented from control to P10 (1 and 30 days) and P25. Hysteresivity increased in only P25. Methylprednisolone at 1 or 6 hours attenuated in vivo and in vitro mechanical changes in P25, whereas P10 parameters were similar to the control. Collagen increment was dose and time dependent. Elastic fibers increased in P25 and at 30 days in P10. Corticosteroid prevented collagen increment and avoided elastogenesis. In conclusion, methylprednisolone led to a complete maintenance of in vivo and in vitro respiratory mechanics in mild lesion, whereas it minimized the changes in tissue impedance and extracellular matrix in severe ALI. The beneficial effects of the early use of steroids in ALI remained unaltered at Day 30.
Complex physical therapy is the main treatment for the secondary lymphedema after breast cancer. The low-level laser therapy (LLLT) has been used in order to stimulate lymphangiogenesis, encourage lymphatic motility, and reduce lymphostatic fibrosis. However, these factors could also favor the development of recurrence and metastasis. The objective of this study is to discuss the use of LLLT in the treatment of lymphedema after breast cancer. This study utilized a systematic review on the use of LLLT in the treatment of lymphedema after breast cancer. Evaluating quality of articles was conducted through the PEDro scale. Of the 41 articles identified, four were considered to be of high methodological quality (score ≥ 5). The low-level laser in the axillary region was performed in all studies. The control group was not similar across studies. The results presented showed that there was a reduction in limb volume in the group subjected to low-power laser when compared with other treatments. No studies have evaluated the risk of metastasis or relapse in the irradiated areas. Because no studies have included the complex physical therapy as the comparison group, we cannot claim that laser treatment is the best efficacy or effectiveness in lymphedema treatment after breast cancer. No studies have evaluated the hypothesis that the LLLT can increase the risk of recurrence or metastasis. Therefore, the questions about the safety of this procedure in cancer patients remain.
Silicosis is an occupational disease triggered by the inhalation of fine particles of crystalline silica and characterized by inflammation and scarring in the form of nodular lesions in the lungs. In spite of the therapeutic arsenal currently available, there is no specific treatment for the disease. Flunisolide is a potent corticosteroid shown to be effective for controlling chronic lung inflammatory diseases. In this study, the effect of flunisolide on silica-induced lung pathological changes in mice was investigated. Swiss-Webster mice were injected intranasally with silica particles and further treated with flunisolide from day 21 to 27 post-silica challenge. Lung function was assessed by whole body invasive plethysmography. Granuloma formation was evaluated morphometrically, collagen deposition by Picrus sirius staining and quantitated by Sircol. Chemokines and cytokines were evaluated using enzyme-linked immunosorbent assay. The sensitivity of lung fibroblasts was also examined in in vitro assays. Silica challenge led to increased leukocyte numbers (mononuclear cells and neutrophils) as well as production of the chemokine KC/CXCL-1 and the cytokines TNF-α and TGF-β in the bronchoalveolar lavage. These alterations paralleled to progressive granuloma formation, collagen deposition and impairment of lung function. Therapeutic administration of intranasal flunisolide inhibited granuloma and fibrotic responses, noted 28 days after silica challenge. The upregulation of MIP-1α/CCL-3 and MIP-2/CXCL-2 and the cytokines TNF-α and TGF-β, as well as deposition of collagen and airway hyper-reactivity to methacholine were shown to be clearly sensitive to flunisolide, as compared to silica-challenge untreated mice. Additionally, flunisolide effectively suppressed the responses of proliferation and MCP-1/CCL-2 production from IL-13 stimulated lung fibroblasts from silica-or saline-challenged mice. In conclusion, we report that intranasal treatment with the corticosteroid flunisolide showed protective properties on pathological features triggered by silica particles in mice, suggesting that the compound may constitute a promising strategy for the treatment of silicosis.
Prophylactic manual needling stimulation of ST36 can mitigate ALI caused by lipopolysaccharide instillation in Wistar rats. Further studies should address the mechanisms of immune system response induced by needle stimulation of ST36 acupoint.
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