TWIK-related acid-sensitive potassium channels TASK-1 and TASK-3 may participate in the process of the coexistence of asthma and OSA.

OBJECTIVE: To investigate the role of TWIK-related acid-sensitive potassium channels TASK-1 and TASK-3 in the mechanism of asthma combined with obstructive sleep apnea (OSA) in mice. METHOD: C57BL/6 mice were randomly divided into four groups: control group (NS-RA), asthma group (OVA-RA), OSA group (NS-IH), and asthma combined with OSA group (OVA-IH). After monitoring lung function in each group, the expression levels of TASK-1 and TASK-3 mRNA and protein in lung tissues were measured, and the correlation between the changes of both and lung function was analyzed. RESULTS: A total of 64 male mice were studied. Penh, serum IgE concentrations, and the percentage of eosinophils in bronchoalveolar lavage fluid (BALF) were higher in OVA-RA and OVA-IH mice compared with NS-RA (P < 0.05),while the above indexes were slightly elevated in NS-IH mice compared with NS-RA (P > 0.05), where the Penh and the percentage of eosinophils in BALF was higher in OVA-IH mice than NS-IH (P < 0.05).Increased TASK-3 mRNA expression (P < 0.05) as well as TASK-1 and TASK-3 protein expression (P > 0.05) in lung tissues of OVA-RA and NS-IH mice compared with NS-RA, and TASK-3 mRNA expression was slightly more in the OVA-IH group compared with NS-RA (P > 0.05), but less compared with OVA-RA (P < 0.05) or NS-IH (P > 0.05), while TASK-1 and TASK-3 protein expression was increased in the OVA-IH group compared with the remaining three groups, and TASK-3 protein expression was associated with lung function impairment was positively correlated with the degree of lung function impairment (P < 0.05). CONCLUSION: Task-1 and Task-3 may be involved in the pathogenesis of asthma with OSA by affecting lung function.

[The role of toll like receptor-4 signal pathways activation in ischemia-reperfusion injury of island skin flap].

OBJECTIVE: To determine the role of toll like receptor-4 signal pathways activation in ischemia-reperfusion injury of island skin flap. METHODS: A totol of 50 adult male SD rats were randomized into 3 groups: sham-operated group (n=10), ischemia/reperfusion group (n=20) and TLR4 inhibitor-eritoran tetrasodium (E5564)-treated group (n=20). The inguinal island skin flaps models were set up. A bolus of E5564 (5 mg/kg) was infused intravenously 60 min before reper fusionm. TLR4 binding activity in flap tissue was analyzed at 1, 2, 4 and 6 h of reperfusion by immunohistochemical technique and flaps were assessed histologically at 6 h of reperfusion. The viability of flaps was assessed 7 days postoperatively. RESULTS: Exprerssion TLR4 in skin flap tissue was significantly increased in I/R group, compared with E5564-treated group. Immunohistochemical exam showed TLR4 mainly expressed in skin flap vessel wall and PMN membrane. Marked neutrophil infiltration and edema was observed in I/R group, while less neutrophil infiltration was observed in E5564-treated group. In the E5564-treated group, the survival of flaps was (80.31 +/- 11.63)%, which was significantly greater than that in the I/R group (51.70 +/- 7.62)% (P < 0.01). CONCLUSION: After ischemia-reperfusion injury in rats, the expression of TLR4 increased in the skin flap tissue with excessive neutrophil infiltration. Administration of E5564 can significantly improve flap survival by regulating the early activation of TLR4 and suppressing neutrophil infiltration within the flap.