OBJECTIVETo evaluate the effect of traditional Chinese medicine preparations on bronchial hyperesponsiness (BHR)-induced cough.

METHODSixty patients with cough due to BHR (shown by positive bronchial provocation test) were randomly divided into Chinese medicine group (n = 30) and control group (n = 30) to receive Bufeishenqingre decoction twice a day and 100 mg theophylline sustained-release capsules twice a day for one month, respectively. The changes of the clinical symptoms were observed during the treatment and bronchial infrared imaging was performed before and after the treatment.

RESULTSThe symptoms of patients in the Chinese medicine group were more effectively alleviated than those of the control group (P < 0.05). The difference in the temperature between the bronchial lesions and the surrounding normal mucosa changed more obviously in the Chinese medicine group (P < 0.01).

CONCLUSIONBufeishenqingre decoction can relieve the symptoms and improve the abnormalities in infrared imaging of patients with BHR-induced cough.

Adult ; Bronchial Hyperreactivity ; complications ; drug therapy ; Bronchial Provocation Tests ; Bronchodilator Agents ; administration & dosage ; Cough ; drug therapy ; etiology ; Drugs, Chinese Herbal ; therapeutic use ; Female ; Humans ; Male ; Middle Aged ; Phytotherapy ; Theophylline ; administration & dosage ; Young Adult

Reactive oxygen species (ROS) performs a pivotal function as a signaling mediator in receptor-mediated signaling. However, the sources of ROS in this signaling have yet to be determined, but may include lipoxygenases (LOXs) and NADPH oxidase. The stimulation of lymphoid cells with TNF-alpha, IL-1beta, and LPS resulted in significant ROS production and NF-kappaB activation. Intriguingly, these responses were markedly abolished via treatment with the LOXs inhibitor nordihydroguaiaretic acid (NDGA). We further examined in vivo anti-inflammatory effects of NDGA in allergic airway inflammation. Both intraperitoneal and intravenous NDGA administration attenuated ovalbumin (OVA)-induced influx into the lungs of total leukocytes, as well as IL-4, IL-5, IL-13, and TNF-alpha levels. NDGA also significantly reduced serum levels of OVA-specific IgE and suppressed OVA-induced airway hyperresponsiveness to inhaled methacholine. The results of our histological studies and flow cytometric analyses showed that NDGA inhibits OVA-induced lung inflammation and the infiltration of CD11b+ macrophages into the lung. Collectively, our findings indicate that LOXs performs an essential function in pro-inflammatory signaling via the regulation of ROS regulation, and also that the inhibition of LOXs activity may have therapeutic potential with regard to the treatment of allergic airway inflammation.
Animals ; Antioxidants/metabolism ; Asthma/complications/metabolism/pathology/physiopathology ; Bronchial Hyperreactivity/drug therapy/pathology ; Bronchial Provocation Tests ; Bronchoalveolar Lavage Fluid/cytology ; Cells, Cultured ; Drug Evaluation, Preclinical ; Humans ; Inflammation/*etiology/metabolism ; Jurkat Cells ; Lipoxygenase/*physiology ; Lipoxygenase Inhibitors/pharmacology/therapeutic use ; Lymphocytes/drug effects/metabolism ; Male ; Mice ; Mice, Inbred BALB C ; Nordihydroguaiaretic Acid/pharmacology/therapeutic use ; Reactive Oxygen Species/*adverse effects/*metabolism

Reactive oxygen species (ROS) play a crucial role in acute lung injury. Tissue inflammation, the increased vascular permeability, and plasma exudation are cardinal features of acute lung injury. Angiopoietin-1 (Ang1) has potential therapeutic applications in preventing vascular leakage and also has beneficial effects in several inflammatory disorders. Recently developed COMP-Ang1 is more potent than native Ang1 in phosphorylating tyrosine kinase with immunoglobulin and EGF homology domain 2 receptor in endothelial cells. However, there are no data on effects and related molecular mechanisms of COMP- Ang1 on ROS-induced acute lung injury. We used hydrogen peroxide (H2O2)-inhaled mice to evaluate the effect of COMP-Ang1 on pulmonary inflammation, bronchial hyper-responsiveness, and vascular leakage in acute lung injury. The results have revealed that VEGF expression, the levels of IL-4, TNF-alpha, IL-1 beta, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 in lungs, the levels of hypoxia-inducible factor-1alpha (HIF-1 alpha) and NF-kappa B in nuclear protein extracts, phosphorylation of Akt, and vascular permeability were increased after inhalation of H2O2 and that the administration of COMP-Ang1 markedly reduced airway hyper-responsiveness, pulmonary inflammation, plasma extravasation, and the increases of cytokines, adhesion molecules, and VEGF in lungs treated with H2O2. We have also found that the activation of HIF-1a and NF-kappa B and the increase of phosphoinositide 3-kinase activity in lung tissues after H2O2 inhalation were decreased by the administration of COMP-Ang1. These results suggest that COMP-Ang1 ameliorates ROS-induced acute lung injury through attenuating vascular leakage and modulating inflammatory mediators.
Acute Lung Injury/chemically induced/complications/*drug therapy/metabolism ; Administration, Inhalation ; Airway Resistance/drug effects ; Animals ; Bronchial Hyperreactivity/drug therapy/etiology ; Bronchoalveolar Lavage Fluid ; Capillary Permeability/*drug effects ; Cytokines/antagonists & inhibitors ; Female ; Hydrogen Peroxide/adverse effects ; Hypoxia-Inducible Factor 1, alpha Subunit/antagonists & inhibitors ; Intercellular Adhesion Molecule-1/metabolism ; Mice ; Mice, Inbred BALB C ; NF-kappa B/antagonists & inhibitors ; Pneumonia/*drug therapy/etiology ; Recombinant Fusion Proteins/*administration & dosage ; Vascular Cell Adhesion Molecule-1/metabolism