To explore the mechanisms of neurogenic inflammation and airway hyperresponsiveness of rat by inhaled sulfur / 中国应用生理学杂志

<p><b>AIM</b>To explore the physiopathological mechanisms of airway injury and the effect on the airway responsiveness of rat by inhaled sulfur dioxide(SO2).</p><p><b>METHODS</b>Sixteen SD male rats were divided randomly into 2 groups (n = 8): the control group and SO2 group. The control group was exposed o pure air. SO2 group was exposed to SO2 of the content 1.0 mg/(m(3) x h) 6h daily for consecutive 3 d. At 4th day, we determined the airway responsiveness, collected the bronchoalveolar lavage fluid (BALF), plasma and lung tissue. Then we counted the total cellular score in BALF, measured the plasma SP content and made the immunohistochemistry staining on the lung tissue (HE and SP methods).</p><p><b>RESULTS</b>Compared with the control group, the total cellular score in BALF and plasma SP content in SO2 group's increased significantly ( P < 0.01). HE staining showed there were a great deal of inflammatory cells infiltration under the tunica mucosa bronchiorum; and SP immunohistochemistry staining indicated there were significant changes in numbers of SP-IR positive fibers of SO2group.</p><p><b>CONCLUSION</b>Exposure to low concentration of SO2 would injure healthy rat's airway, and induce airway hyperresponsiveness, neurogenic inflammation is one of its critical pathophysiological mechanisms.</p>

Respiratory syncytial virus infection enhances airway hyperresponsiveness in guinea pigs and the underlined mechanism / 中国应用生理学杂志

<p><b>AIM</b>To study the relation between Respiratory Syncytial Virus infection and asthma development by measuring airway responsiveness (AR) and M2R function.</p><p><b>METHODS</b>Guinea pigs (n = 34) were randomly divided into 4 groups: Hep-2/NS group (group A, n = 9), RSV/NS group (group B, n =9), Hep-2/OVA group (group C, n = 8) and RSV/OVA group(group D, n = 8). On day 21 after infection we tested AR and M2R. Then counted eosinophils in BALF and observed pathological change.</p><p><b>RESULTS</b>Intraairway pressure(IP mmH20) of group B had no significant difference with group A(P > 0.01), and the extent of IP decrease also had no difference between groups A and B (P > 0. 05), but IP of C group were much higher than group A (P<0.05), with extent of IP decrease lower than group A (P < 0.05). And IP of group D were higher than group C (P < 0.01), with the extent of IP decrease much lower than group C (P < 0.05).</p><p><b>CONCLUSION</b>RSV infection could enhance OVA-induced M2R dysfunction, then develop AHR.</p>

Effect of platelet-activating factor on cell proliferation & NF-kappaB activation in airway smooth muscle cells in rats.

BACKGROUND & OBJECTIVE: Despite the established pro-inflammatory actions of platelet activating factor (PAF) observed on chronic obstructive pulmonary disease (COPD), its action on airway remodeling has been still unclear. It has been reported that nuclear factor-kappa B (NF-kappaB) activity is necessary for ASMC proliferation. Further, PAF has been identified as the proximal inducer of NF-kappaB. The present study was thus aimed to investigate the effect of PAF on airway smooth muscle cells (ASMC) proliferation and to evaluate the potential role of NF-kappaB in this regulation. METHODS: Healthy male Sprague-Dowley rats of 6-8 wk age were used for obtaining ASMCs. 3-(4,5- dimethylthiazole-2-yl)-2,5-diphenyltetrazolium-bromide (MTT) assay was to investigate the effects of PAF on ASMC proliferation and to confirm its optimum concentration for action. Additionally, cell proliferation was also examined using cell cycle assay by flow cytometry and immunocytochemical staining for proliferating cell nuclear antigen (PCNA). And NF-kappaB DNA-binding activity was assayed by electrophoretic mobility shift assay (EMSA). RESULTS: PAF stimulated ASMC proliferation with its peak at 100 nM. At this optimum concentration, PAF significantly increased the cell proliferation index (PI) and the PCNA-positive rate in the ASMCs, as well as NF-kappaB DNA- binding activity. Whereas, 20 mM N-acetylcysteine (NAC) pre-treatment effectively blocked all of these events. INTERPRETATION & CONCLUSION: The present findings demonstrated that PAF could promote ASMC proliferation, suggesting its potential involvement in airway remodeling. Our study also suggested the promising action of 20 mM NAC on the alleviation of airway remodeling due to direct inhibition of ASMC proliferation. The involved mechanism would be relevant to the change of NF-kappaB activation in ASMCs.

Construction of antisense recombinant adenoviral vector for c-myc and its antiproliferative effect on rat lymphocytes / 中国应用生理学杂志

<p><b>AIM</b>To observe the antiproliferative effect of antisense recombinant adenoviral vector for c-myc on rat thymus lymphocytes.</p><p><b>METHODS</b>Antisense and sense bacterial plasmids for c-myc were constructed. Bacterial plasmids and El detected adenoviral plasmid were cotransfected into 293 cells. Recombinant adenoviral vectors were obtained after cotransfection. The antiproliferative effects were assayed by MTS. The expression of c-myc mRNA was detected by RT-PCR.</p><p><b>RESULTS</b>The results showed that antisense recombinant adenoviral vector for c-myc could inhibit rat thymus lymphocytes proliferation. The expression of c-myc mRNA was decreased after antisense recombinant adenoviral vector for c-myc was transfected into cells.</p><p><b>CONCLUSION</b>Recombinant antisense adenoviral vector for c-myc could inhibit rat thymus lymphocytes proliferation.</p>