Shaoqing Y, Ruxin Z, Yinjian C, Jianqiu C, Zhiqiang Y, Genhong L
Department of Otolaryngology, Jinan General Hospital of PLA, Shandong, China.
Allergol Immunopathol (Madr). 2009 Jul-Aug;37(4):180-7. doi: 10.1016/j.aller.2009.03.002. Epub 2009 Sep 23.
The present study was designed to explore the possible changes in endogenous hydrogen sulphide (H(2)S), a novel gasotransmitter, on the pathogenesis of allergic rhinitis (AR).
AR guinea pig model was established by nasal ovalbumin sensitisation. Guinea pigs were divided into four groups: Saline control, AR sensitised, sodium hydrosulphide (NaHS) treated, and propargylglycine (PPG) treated group. The frequency of sneezing and nose rubbing was recorded. Leukocyte infiltration in nasal lavage fluid (NLF) and plasma H(2)S level were measured. Expression of Cystathionine-beta-synthase (CBS) and Cystathionine-gamma-lyase (CSE) mRNA as H(2)S-producing enzymes in nasal mucosa was determined by real time Reverse Transcriptase-Polymerase Chain Reaction (RT-PCR).
The frequency of sneezing and nose rubbing, and levels of leukocyte infiltration in NLF were higher than those of control (P<0.01), but plasma H(2)S in sensitised guinea pigs was lower than those of control (P<0.05). From the results of RT-PCR, it was found that the expression of CSE was higher than CBS in nasal mucosa, and in sensitised guinea pigs it was lower than that of control (P<0.05). NaHS successfully increased the level of H(2)S and alleviated the symptoms of AR accompanied by up-regulation of CSE as compared with AR group (P<0.05). PPG significantly suppressed the expression of CSE and decreased the H(2)S level, yet also aggravated the symptoms of AR.
H(2)S level may be negatively correlated with the process of inflammation and positively correlated with expression of CSE in nasal mucosa. The endogenous H(2)S pathway is down-regulated in AR.
本研究旨在探讨新型气体信号分子内源性硫化氢（H₂S）在变应性鼻炎（AR）发病机制中的可能变化。
通过鼻腔卵清蛋白致敏建立AR豚鼠模型。将豚鼠分为四组：生理盐水对照组、AR致敏组、硫氢化钠（NaHS）治疗组和炔丙基甘氨酸（PPG）治疗组。记录打喷嚏和擦鼻的频率。检测鼻灌洗液（NLF）中的白细胞浸润情况及血浆H₂S水平。通过实时逆转录聚合酶链反应（RT-PCR）测定鼻黏膜中作为H₂S生成酶的胱硫醚-β-合酶（CBS）和胱硫醚-γ-裂解酶（CSE）mRNA的表达。
AR致敏组的打喷嚏和擦鼻频率以及NLF中的白细胞浸润水平均高于对照组（P<0.01），但致敏豚鼠的血浆H₂S水平低于对照组（P<0.05）。RT-PCR结果显示，鼻黏膜中CSE的表达高于CBS，且致敏豚鼠中CSE的表达低于对照组（P<0.05）。与AR组相比，NaHS成功提高了H₂S水平并减轻了AR症状，同时CSE表达上调（P<0.05）。PPG显著抑制了CSE的表达并降低了H₂S水平，但也加重了AR症状。
H₂S水平可能与炎症过程呈负相关，与鼻黏膜中CSE的表达呈正相关。AR中内源性H₂S途径下调。
