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Decreased expression of human aquaporin-5 correlated with mucus overproduction in airways of chronic obstructive pulmonary disease

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Acta Pharmacologica Sinica 2007年第8期28卷 1166-1174页

作者： Ke WANG Yu-lin FENG Fu-qiang WEN~2 Xue-rong CHEN Xue-mei OU Dan XU Jie YANG Zhi-ping DENG Division of Pulmonary Diseases,State Key Laboratory of Biotherapy of China,and Department of Respiratory Medicine,West China Hospital of Sichuan University,Sichuan 610041,China Division of Pulmonary Diseases State Key Laboratory of Biotherapy of Chinaand Department of Respiratory MedicineWest China Hospital of Sichuan UniversitySichuan 610041China

Aim:To investigate the relationship between aquaporin-5(AQP5)expression andmucus overproduction in the airways of Chinese patients with chronic obstruc-tive pulmonary disease(COPD)and the correlation with pulmonary functionchange.Methods:Bronchial tissues were obtained from fiberoptic bronchoscopyand bronchial biopsy in West China Hospital from April to July 2004.Twenty-fivepatients were diagnosed as COPD patients,and another 20 were diagnosed as thecontrol patients.The expressions ofAQP5,mucin 5AC(MUC5AC),and mucin inbronchial tissues were detected by semiquantitative RT-PCR,in situ hybridization,and immunohistochemical and alcian blue-periodic acid-Schiff(AB-PAS)staining,respectively.Results:Compared with the control group,an attenuated expres-sion of AQP5was detected throughout the bronchial tissues from patients withCOPD(P0.05).Simultaneously,increased staining of MUC5AC and mucus in submucosal glandswere noted(P5and increased the staining of MUC5AC and mucus in submucosal glands in theCOPD groups(P0.05).The decreased expression of AQP5mRNA was correlatedwith forced expiratory volume in 1 s(FEV1)/forced vital capacity(FVC)(r=0.60,P50%vital capacity(V50)% predicted value(r=0.55,P5% vital capacity(V25)% predicted value(r=0.45,P5AC mRNA of the epitheliumairways(r=-0.45,P5AC mRNA correlated with the posi-tively AB-PAS-stained area of submucosal glands and correlated negativelywith FEV1/FVC(r=-0.53;P53;P50%predicted value(r=-0.48;P5% predicted value(r=-0.43;P<0.01).Conclusion:The attenuated gene express

关键词： aquaporin-5 mucin 5AC mucin mucus overproduction chronic obstructive pulmonary disease

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Botulinum toxin A inhibits salivary secretion of rabbit submandibular gland

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International Journal of Oral Science 2013年第4期5卷 217-223页

作者： Xiao-Feng Shan Hui Xu Zhi-Gang Cai Li-Ling Wu Guang-Yan Yu Department of Oral and Maxillofacial Surgery Peking University School and Hospital of Stomatology Department of Physiology and Pathophysiology Peking University Health Science Center

Botulinum toxin A （BTXA） has been used in several clinical trials to treat excessive glandular secretion; however, the precise mechanism of its action on the secretory function of salivary gland has not been fully elucidated. In this study, we aimed to investigate the effect of BTXA on secretion of submandibular gland in rabbits and to identify its mechanism of action on the secretory function of salivary gland. At 12 weeks after injection with 5 units of BTXA, we found a significant decrease in the saliva flow from submandibular glands, while the salivary amylase concentration increased. Morphological analysis revealed reduction in the size of acinar cells with intracellular accumulation of secretory granules that coalesced to form a large ovoid structure. Expression of M3-muscarinic acetylcholine receptor （M3 receptor） and aquaporin-5 （AQP5） mRNA decreased after BTXA treatment, and distribution of AQP5 in the apical membrane was reduced at 1, 2 and 4 weeks after BTXA injection. Furthermore, BTXA injection was found to induce apoptosis of acini. These results indicate that BTXA decreases the fluid secretion of submandibular glands and increases the concentration of amylase in saliva. Decreased expression of M3 receptor and AQP5, inhibition of AQP5 translocation, and cell apoptosis might involve in BTXA-reduced fluid secretion of submandibular lands.

关键词： aquaporin-5 apoptosis botulinum toxin A M3-muscarinic acetylcholine receptor submandibular gland

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H_2S Protecting against Lung Injury following Limb Ischemia-reperfusion by Alleviating Inflammation and Water Transport Abnormality in Rats

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Biomedical and Environmental Sciences 2014年第6期27卷 410-418页

作者： QI Ying Chun CHEN Wen LI Xiao Ling WANG Yu Wei XIE Xiao Hua Department of Comprehensive Surgery in South Building Chinese People's Liberation Army General HospitalChinese People's Liberation Army Medical School

Objective To investigate the effect of H2S on lower limb ischemia-reperfusion （LIR） induced lung injury and explore the underlying mechanism. Methods Wistar rats were randomly divided into control group, IR group, IR＋ Sodium Hydrosulphide （NariS） group and IR＋ DL-propargylglycine （PPG） group. IR group as lung injury model induced by LIR were given 4 h reperfusion following 4 h ischemia of bilateral hindlimbs with rubber bands. NariS （0.78 mg/kg） as exogenous H2S donor and PPG （60 mg/kg） which can suppress endogenous H2S production were administrated before LIR, respectively. The lungs were removed for histologic analysis, the determination of wet-to-dry weight ratios and the measurement of mRNA and protein levels of aquaporin-1 （AQP1）, aquaporin-5 （AQP5） as indexes of water transport abnormality, and mRNA and protein levels of Toll-like receptor 4 （TLR4）, myeloid differentiation primary-response gene 88 （MyD88） and p-NF-KB as indexes of inflammation. Results LIR induced lung injury was accompanied with upregulation of TLR4-Myd88-NF-κB pathway and downregulation of AQP1/AQP5. NariS pre-treatment reduced lung injury with increasing AQP1/AQP5 expression and inhibition of TLR4-Myd88-NF-KB pathway, but PPG adjusted AO.PJAO.Ps and TLR4 pathway to the opposite side and exacerbated lung injury. Conclusion Endogenous H2S, TLR4-Myd88-NF-κB pathway and AQP1/AQP5 were involved in LIR induced lung injury. Increased H2S would alleviate lung injury and the effect is at least partially depend on the adjustment of TLR4-Myd88-NF-κB pathway and AQP1/AQP5 expression to reduce inflammatory reaction and lessen pulmonary edema.

关键词： Hydrogen sulfide Limb Ischemia-reperfusion Toll-like receptors Nuclear Factor-κB aquaporin-i aquaporin-5

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Dexmedetomidine Alleviates Pulmonary Edema by Upregulating AQP1 and AQP5 Expression in Rats with Acute Lung Injury Induced by Lipopolysaccharide

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2015年第5期35卷 684-688页

作者：姜远旭戴中亮张雪萍赵伟黄强高利昆 Department of Anesthesiology Shenzhen People's Hospital Department of Anesthesiology Zhujiang HospitalNanfang Medical University Department of Pathology Shenzhen People's Hospital

This study aims to elucidate the mechanisms by which dexmedetomidine alleviates pulmonary edema in rats with acute lung injury induced by lipopolysaccharide （LPS）. Male Wistar rats were randomly divided into five groups： normal saline control （NS） group, receiving intravenous 0.9% normal saline （5 mL/kg）; LPS group, receiving intravenous LPS （10 mg/kg）; small-dose dexmedetomidine （S） group, treated with a small dose of dexmedetomidine （0.5 μg·kg^-1·h^-1）; medium-dose dexmedetomidine （M） group, treated with a medium dose of dexmedetomidine （2.5 μg·kg^-1·h^-1）; high-dose dexmedetomidine （H） group, treated with a high dose of dexmedetomidine （5μg·kg^-1·h^-1）. The rats were sacrificed 6 h after intravenous injection of LPS or NS, and the hmgs were removed for evaluating histological characteristics and determining the lung wet/dry weight ratio （W/D）. The levels of tumor necrosis factor-alpha （TNF-α） and interleukin-1β （IL-1β） in the lung tissues were assessed by enzyme-linked immunosorbent assay （ELISA）. The mRNA and protein expression levels of aquaporin-1 （AQP1） and aquaporin-5 （AQP5） were detected by RT-PCR, immunohistochemistry, and Western blot- ting. The lung tissues from the LPS groups were significantly damaged, which were less pronounced in the H group but not in the small-dose dexmedetomidine group or medium-dose dexmedetomidine group. The W/D and the concentrations of TNF-α and IL-1β in the pulmonary tissues were increased in the LPS group as compared with those in NS group, which were reduced in the H group but not in S group or M group （P〈0.01）. The expression of AQP1 and AQP5 was lower in the LPS group than in the NS group, and significantly increased in the H group but not in the S group or M group （P〈0.01）. Our findings suggest that dexmedetomidine may alleviate pulmonary edema by increasing the expression of AQP-1 and AQP-5.

关键词： dexmedetomidine acute lung injury lung edema aquaporin-1 aquaporin-5

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