N-乙酰半胱氨酸联合阿奇霉素对慢性阻塞性肺疾病模型大鼠氧化应激的影响

 目的:探讨N-乙酰半胱氨酸(NAC)联合阿奇霉素(AZI)对慢性阻塞性肺疾病(COPD) 模型大鼠氧化应激的影响。方法:将60只雄性Wistar大鼠随机分为5组,即正常对照(control)组、模型(model)组、AZI治疗组、NAC治疗组和联合治疗组(AZI+NAC组)。采用烟熏联合气管内滴入脂多糖的方法诱导大鼠COPD模型。NAC组和AZI组大鼠每日烟熏前30 min分别给予NAC和AZI灌胃,AZI+NAC组则给予NAC和AZI联合灌胃。第31天行肺功能检测后处死大鼠,提取支气管肺泡灌洗液(BALF)进行细胞计数,并采用ELISA法测定BALF中白细胞介素-8(IL-8)、白细胞介素-17(IL-17)和肿瘤坏死因子-α(TNF-α)的含量。制作肺组织切片及肺匀浆,测定肺匀浆超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)和丙二醛(MDA)水平。结果:与control组对比,其余4组均出现肺功能的下降,组织病理提示炎症细胞浸润、肺泡破坏等表现。与control组比较,其余4组BALF中白细胞总数、单核巨噬细胞、中性粒细胞和淋巴细胞均显著增高(P<0.05);与model组、AZI组、NAC组比较,AZI+NAC组BALF中白细胞总数、中性粒细胞和淋巴细胞均显著下降(P<0.05)。与model组对比,AZI组、NAC组和AZI+NAC组IL-8、IL-17、TNF-α和MDA含量均显著降低(P<0.05),SOD和GSH-Px活性均显著增高(P<0.05);与AZI组和NAC组比较,AZI+NAC组IL-8、IL-17、TNF-α和MDA含量均下降,SOD和GSH-Px活性均增高,差异有统计学显著性(P<0.01)。结论:NAC和AZI均能减轻COPD模型大鼠肺部炎症和氧化损伤,两者联合能增强抗氧化作用,可能更适合COPD的临床治疗。     

特布他林联合N-乙酰半胱氨酸治疗AECOPD的疗效及对患者免疫功能的影响

目的观察特布他林联合N-乙酰半胱氨酸治疗慢性阻塞性肺疾病急性加重(AECOPD)的疗效及对患者免疫功能的影响。方法选取我院60例AECOPD患者,以数字表法随机分为3组,各20例,均接受常规治疗,在此基础上,A组予以特布他林,B组予以N-乙酰半胱氨酸,C组予以特布他林联合N-乙酰半胱氨酸治疗,比较3组治疗前后氧化应激反应[超氧化物转化酶(SOD)与丙二醛(MDA)]、肺功能[用力肺活量(FVC)、1s用力呼气容积(FEV1)与FEV1/FVC]、免疫功能(CD3+、CD4+、CD4+/CD8+)、外周血嗜酸性粒细胞(EOS)计数,观察3组症状改善时间及疗效。结果C组总有效率100.00%,明显高于A组70.00%与B组65.00%(P<0.05);C组治疗后SOD明显高于A组与B组(P<0.05),MDA明显低于A组与B组(P<0.05);C组治疗后FVC、FEV1、FEV1/FVC、CD3+、CD4+、CD4+/CD8+显著高于A组与B组(P<0.05),EOS计数显著低于A组与B组(P<0.05);C组呼吸困难消失、咳嗽消失、喘息改善与哮鸣音消失时间明显短于A组与B组(P<0.05)。结论特布他林联合N-乙酰半胱氨酸可有效改善AECOPD患者免疫功能与肺功能,减轻炎症及氧化应激反应,促进临床症状恢复,获得良好疗效。     

N-乙酰半胱氨酸改善高游离脂肪酸所致大鼠外周胰岛素抵抗

目的 探讨N-乙酰半胱氨酸(NAC)对高游离脂肪酸(FFA)导致的外周胰岛素抵抗的影响及机制.方法 SD大鼠随机分为对照组(NS组,12只)、脂肪乳输注组(FFA组,13只)和脂肪乳 NAC组(NAC组,12只).输注48 h,(1)测血浆硝基酪氨酸,丙二醛(MDA)和还原型谷胱甘肽(GSH)水平;(2)高胰岛素正糖钳夹试验,评价外周胰岛素抵抗程度;(3)实时荧光定量PCR方法测定肌肉组织胰岛素受体底物-1(IRS-1)、胰岛素受体底物-2(IRS-2)mRNA表达.结果 (1)FFA组硝基酪氨酸,MDA高于NS组,GSH低于NS组,NAC分别改善28.6%,33.1%,22.9%(P＜0.05);(2)FFA组葡萄糖输注率(GIR)比NS组降低(P＜0.05),用NAC后GIR升高36.6%(P＜0.05);(3)FFA组肌肉组织IRS-1、IRS-2 mRNA表达比NS组降低87.7%、50.7%(P＜0.05);NAC组肌肉组织IRS-1、IRS-2表达比FFA组增加370.1%、46.2%,(P＜0.05).结论 NAC干预能改善高FFA所致的外周胰岛素信号传导障碍,逆转外周胰岛素抵抗,可能与NAC纠正机体氧化及抗氧化失衡有关.     

N-乙酰半胱氨酸眼液对无痛LASEK术后角膜组织的影响

目的观察N-乙酰半胱氨酸眼液对无痛LASEK术后角膜组织修复的影响。方法采用随机对照方法,将2012年10月01日~12月31日,72例(144眼)无痛LASEK分为对照组,将2013年10月01日~12月31日,79例(158眼)无痛LASEK分为试验组.试验组加用N-乙酰半胱氨酸眼液,其他与对照组相同,用药7d,分别于术后7d、1月,观察丝状角膜炎发生情况。结果丝状角膜炎情况：对照组12眼,试验组2眼,(2=124.19,<0.001),有显著性差异。结论 N-乙酰半胱氨酸眼液有益无痛LASEK术后角膜组织的修复。     

N-乙酰半胱氨酸对碘海醇所致糖尿病大鼠肾损伤的保护作用

目的观察N-乙酰半胱氨酸对碘海醇所致糖尿病大鼠肾损伤的保护作用,从而对临床治疗碘海醇导致的糖尿病肾损伤提供理论依据。方法清洁级糖尿病大鼠45只,体重250～300 g,通过股静脉注射碘海醇法建立糖尿病对比剂肾损伤模型,模型成功后,随机分为碘海醇组(NL组)、N-乙酰半胱氨酸组(NAL组),假手术组(Sham组),分别于建模后24h、48h、72h处死大鼠,观察各组大鼠血肌酐(Scr)和血尿素氮(BUN)的浓度;HE染色观察肾脏病理学变化;ELISA检测血清中总超氧化物歧化酶(T-SOD)、丙二醇(MDA)和谷胱甘肽过氧化物酶(GPX)的含量浓度;TUNEL检测肾上皮细胞凋亡情况;Westernblot检测Bcl-2、Bax、caspase-3蛋白表达。结果 NL组肾损伤严重,细胞凋亡明显,血浆总Scr、BUN、MDA、Bax、caspase-3水平明显升高,T-SOD、GPX、Bcl-2明显降低。N-乙酰半胱氨酸可以减轻碘海醇所致的糖尿病大鼠肾损伤,抑制细胞凋亡,血浆总T-SOD、GPX、Bcl-2明显升高,Scr、BUN、MDA、Bax、caspase-3明显降低。结论 N-乙酰半胱氨酸对糖尿病肾损伤大鼠的保护作用可能与其调控肾脏组织中Bcl-2、Bax及caspase-3蛋白表达介导肾小管上皮细胞凋亡有关。     

N-乙酰半胱氨酸对重症急性胰腺炎大鼠肺损伤作用的实验研究

目的:探讨N-乙酰半胱氨酸(NAC)对重症急性胰腺炎(SAP)大鼠肺损伤的作用。方法:雄性SD大鼠30只,随机分为假手术组(SO组)、SAP组、NAC组。胆胰管逆行注射5%牛磺胆酸钠制备SAP模型,造模后30min腹腔注射5%NAC(0.2ml/100g)干预SAP模型,12h后处死大鼠。检测各组血清淀粉酶(AMY)、肺组织髓过氧化物酶(MPO)、胰腺和肺组织病理学评分、肺组织肿瘤坏死因子-α(TNF-α)和细胞间粘附分子-1(ICAM-1)mRNA表达的变化。结果:与SO组比较,SAP组AMY、MPO、胰腺和肺组织病理学评分明显升高(P<0.01),TNF-α和ICAM-1mRNA表达明显增强(P<0.01);应用NAC处理后,AMY和MPO水平下降,胰腺和肺组织损伤缓解,TNF-α和ICAM-1mRNA表达减弱,与SAP组有明显差异(P<0.01)。结论:NAC对SAP大鼠肺损伤具有保护作用,其机制可能与抑制肺组织TNF-α和ICAM-1mRNA的表达有关。     

N-乙酰半胱氨酸保护PC12细胞对抗化学性低氧诱导的损伤

目的 探讨活性氧( ROS)清除剂N-乙酰半胱氨酸(NAC)能否保护PC12细胞对抗化学性缺氧引起的损伤.方法 应用化学性低氧模拟物氯化钴(CoCl2)处理PC12细胞,建立化学性缺氧损伤PC12细胞的实验模型.在CoCl2处理PC12细胞前60 min将NAC加入培养基中,作为预处理.应用CCK-8比色法检测细胞存活...     

慢性阻塞性肺疾病患者血清Clara细胞分泌蛋白CC16和SP-D水平与肺功能的关系

目的 研究慢性阻塞性肺疾病的患者血清中Clara细胞分泌蛋白CC16和SP-D水平与患者肺功能的关系.方法 选取在2013年12月至2014年12月之间,随机选择我院呼吸内科住院及门诊受试患者.将患者随机分为三组,A组为COPD的急性加重期(AECOPD)患者组(n=25),B组为COPD稳定期患者组(n=25),C组为非COPD对照组(n=25).收集患者及对照组临床资料和血清标本,采用ELISA法测定血清CC16、SP-D水平.检测受试者第一秒钟用力呼气量占预计值的百分比(FEV1％)、FEV1和用力肺活量的比值(FEVl/FVC)、肺一氧化碳弥散量占预计值百分比(DLCO％).结果 COPD的急性加重期患者血清中Clara细胞分泌蛋白(CC16)水平最低,其次是COPD稳定期患者组,再次是对照组的受试者,其血清中Clara细胞分泌蛋白(CC16)水平最高(P＜0.05).COPD的急性加重期的患者血清中SP-D水平最高,其次是COPD稳定期患者组,再次是对照组的受试者,其血清中SP-D水平最低(P＜0.05).三组慢性阻塞性肺疾病的患者肺功能的变化与血清中CC16和SP-D水平密切相关,Clara细胞分泌蛋白CC16和与患者肺功能的关系:两者间均呈现出高度的一致性,呈正相关关系;SP-D水平与患者肺功能的关系:两者间均呈现出高度的反向性,呈负相关关系(P＜0.05).结论 COPD患者血清CC16降低而SP-D水平升高,Clara细胞分泌蛋白CC16和与患者肺功能呈正相关关系;SP-D水平与患者肺功能呈负相关关系.     

NAC减轻香烟烟雾致COPD大鼠的肺组织损伤北大核心CSCD

目的:分析N-乙酰半胱氨酸(NAC)对香烟烟雾致慢性阻塞性肺疾病(COPD)大鼠肺组织细胞凋亡的保护作用及机制。方法:采用简单随机分组将36只SD大鼠分为对照组、模型组和NAC组,12只/组,造模大鼠采用烟熏联合脂多糖制备大鼠COPD模型。造模后,NAC组灌胃NAC(400 mg/kg),持续灌胃30 d。检测大鼠第0.3秒用力呼气量(FEV_(0.3))、FEV_(0.3)/用力肺活量(FVC)、最大呼气流量(PEF);检测大鼠血清TNF-α、IL-6、IL-8、肺组织MDA、SOD和GSH-Px水平;检测B细胞淋巴瘤2(Bcl-2)、Bcl-2相关X蛋白(Bax)、cleaved Caspase-3、雷帕霉素靶蛋白/S6激酶1(mTOR/S6K1)信号通路表达;HE和TUNEL染色观察肺组织损伤。结果:与对照组相比,模型组大鼠FEV_(0.3)、FEV_(0.3)/FVC和PEF水平明显降低(P<0.05),IL-6、IL-8、TNF-α和MDA水平升高(P<0.05),SOD和GSH-Px活性明显降低(P<0.05),细胞凋亡率升高(P<0.05),cleaved Caspase-3、Bcl-2和Bax表达上调(P<0.05);与模型组相比,NAC组大鼠IL-6、IL-8、TNF-α和MDA水平降低(P<0.05),SOD和GSH-Px活性升高(P<0.05),细胞凋亡率降低(P<0.05),cleaved Caspase-3和Bax表达下调(P<0.05),Bcl-2、p-mTOR/mTOR、p-S6K1/S6K1表达上调(P<0.05)。HE染色结果表明,NAC组大鼠肺组织病理变化明显减轻。结论:NAC可抑制香烟烟雾致COPD大鼠的肺组织细胞凋亡,保护肺组织损伤,其作用机制可能与激活mTOR/S6K1信号通路有关。     

N-乙酰半胱氨酸拮抗6-羟基多巴胺对骨髓基质细胞的毒性作用

背景：内源性6-羟基多巴胺能参与氧化应激,N-乙酰半胱氨酸能有效抗氧化和清除自由基。 目的：探讨6-羟基多巴胺对骨髓基质细胞的毒性作用及N-乙酰半胱氨酸对其的拮抗作用。 方法：在体外培养SD大鼠骨髓基质细胞,取第3代骨髓基质细胞分别加入终浓度为0,0.05,0.1 g/L的6-羟基多巴胺和终浓度为0,0.075,0.3,1.2,4.8 g/L的N-乙酰半胱氨酸。 结果与结论：MTT检测发现0.05和0.1 g/L 6-羟基多巴胺可以明显降低骨髓基质细胞的细胞活性,而加入6-羟基多巴胺的同时加入0.3 g/L N-乙酰半胱氨酸可以显著抑制6-羟基多巴胺的毒性作用。提示抗氧化剂N-乙酰半胱氨酸可以影响6-羟基多巴胺的作用。     

Inhaled LPS induces blood release of Clara cell specific protein (CC16) in human beings

BACKGROUND: Animal models of lung inflammation have validated the plasma 16-kd Clara cell protein (CC16) as a peripheral marker of the permeability of the alveolocapillary barrier. OBJECTIVE: We investigated in human beings whether inhaled LPS induced a rise in airways permeability measured by the plasma changes in CC16. METHODS: The CC16 was measured in plasma from 15 subjects exposed to LPS by inhalation, during which the kinetics and the dose-response relationship of LPS-induced CC16 were evaluated. Because LPS-induced response involves macrophages activation, the protective effect of oral methylprednisolone was also evaluated. RESULTS: An inhalation of 50 microg LPS induced a significant ( P < .001) rise in CC16 after 6 hours (from 7.24 [+/-0.68] microg/L to 10.69 [+/-0.99] microg/L) that normalized at 24 hours (6.65 [+/-0.33] microg/L). The CC16 response was dose-related, with the no-response threshold 0.5 microg LPS. A 6-day treatment with 20 mg/d methylprednisolone inhibited significantly ( P < .001) the CC16 response to 50 microg LPS. CONCLUSION: Exposure to LPS by inhalation in healthy subjects induces an intravascular leakage of CC16 that can be blocked by corticosteroids. These observations further validate plasma CC16 as a noninvasive test of the alveolocapillary barrier permeability.     

Restoration of the normal Clara cell phenotype after chronic allergic inflammation

Bronchiolar Clara cells play a critical role in lung homoeostasis. The main goal of this study was to evaluate the effects of chronic allergy on these cells and the efficacy of budesonide (BUD) and montelukast (MK) in restoring their typical phenotypes after ovalbumin‐induced chronic allergy in mice. Chronic allergy induced extensive bronchiolar Alcian blue‐periodic acid‐Schiff (AB/PAS)‐positive metaplasia. In addition, cells accumulated numerous big electron‐lucent granules negative for Clara cell main secretory protein (CC16), and consequently, CC16 was significantly reduced in bronchoalveolar lavage. A concomitant reduction in SP‐D and CYP2E1 content was observed. The phenotypic changes induced by allergy were pharmacologically reversed by both treatments; MK was more efficient than BUD in doing so. MK decreased AB/PAS reactivity to control levels whereas they remained persistently elevated after BUD. Moreover, most non‐ciliated cells recovered their normal morphology after MK, whereas for BUD normal cells coexisted with ‘transitional’ cells that contained remnant mucous granules and stained strongly for CC16 and SP‐D. Glucocorticoids were also less able to reduce inflammatory infiltration and maintained higher percentage of neutrophils, which may have contributed to prolonged mucin expression. These results show that chronic allergy‐induced mucous metaplasia of Clara cells affects their defensive mechanisms. However, anti‐inflammatory treatments were able to re‐establish the normal phenotype of Clara cell, with MK being more efficient at restoring a normal profile than BUD. This study highlights the role of epithelial cells in lung injuries and their contribution to anti‐inflammatory therapies.     

冬虫夏草对慢性阻塞性肺疾病大鼠树突状细胞功能的影响

目的: 研究冬虫夏草对慢性阻塞性肺疾病(COPD)大鼠树突状细胞(DCs)功能的影响及其分子机制。方法: 将大鼠随机分为COPD模型组、冬虫夏草治疗组和正常对照组,观察各组大鼠气道病理改变,分离培养鼠DCs,ELISA法检测DCs培养上清液和DCs-T细胞共培养上清液中细胞因子含量。结果: 与正常对照组相比,COPD模型组和冬虫夏草治疗组的平均肺泡计数减少(P＜0.05),冬虫夏草治疗组高于COPD模型组,但差异无统计学意义(P>0.05)。冬虫夏草治疗组DCs-T细胞共培养后上清液中IFN-γ水平高于COPD模型组和正常对照组(P<0.05),IL-5水平各组无显著差异(P>0.05)。冬虫夏草治疗组DCs上清液中TNF-α和IL-12 p70水平高于COPD模型组和正常对照组(P<0.05)。结论: 冬虫夏草可促使COPD大鼠DCs产生Th1型细胞因子,机制可能与DCs产生的IL-12 p70促进T细胞产生IFN-γ有关。     

无创正压通气对AECOPD并发呼吸衰竭患者血清KL-6、CC16及和肽素水平的影响

目的 研究无创正压通气对AECOPD并发呼吸衰竭患者血清KL-6、CC16及和肽素水平的影响,为临床治疗AECOPD提供指导.方法 将2015年10月至2016年10月期间在我院治疗的96例AECOPD并发呼吸衰竭患者按随机数字表法将患者分为对照组和观察组,各48例.两组患者均事先进行祛痰、抗感染等常规治疗方案.观察组患者使用呼吸机利用无创正压通气方式在优先保证患者舒适的状态下进行治疗,对照组患者则进行鼻导管通气治疗,记录患者治疗前后血气参数,及比较两组患者治疗前后KL-6、CC16及和肽素水平.结果 两组患者治疗后观察组临床治疗有效率为87.5%,对照组为62.5%,观察组临床疗效明显优于对照组(P<0.05);治疗前两组患者呼吸频率、血气参数、KL-6、CC15及和肽素水平等差异无统计学意义(P>0.05);经NIPPV治疗24h后两组患者的呼吸频率、血气参数等有明显改善,差异具有统计学意义(P<0.05),但观察组参数明显优于对照组(P<0.05);经治疗后患者的KL-6、CC16及和肽素水平有明显下降(P<0.05),观察组患者的下降程度更为显著(P<0.05),差异具有统计学意义.结论 采用无创正压通气治疗AECOPD并发呼吸衰竭患者,可明显降低血清KL-6、CC16及和肽素水平,缓解肺部损伤,明显改善患者病情,值得在临床推广和应用.     

Clara cell secretory protein (CC16): characteristics and perspectives as lung peripheral biomarker

Clara cell protein (CC16) is a 15.8-kDa homodimeric protein secreted in large amounts in airways by the non-ciliated bronchiolar Clara cells. This protein increasingly appears to protect the respiratory tract against oxidative stress and inflammation. In vitro, CC16 has been shown to modulate the production and/or the activity of various mediators of the inflammatory response including PLA2, interferon-gamma and tumour necrosis factor-alpha. CC16 has also been found to inhibit fibroblast migration or to bind various endogenous or exogenous substances such as polychlorobiphenyls (PCBs). This protective role is confirmed by studies on transgenic mice, showing that CC16 deficiency is associated with an increased susceptibility of the lung to viral infections and oxidative stress. In humans, a polymorphism of the CC16 gene, localized to a region linked to airway diseases, has recently been discovered in association with an increased risk of developing childhood asthma. Finally, CC16 also presents a major interest as a peripheral marker for assessing the integrity of the lung epithelium. The determination of CC16 in serum is a new non-invasive test to detect Clara cell damage or an increased epithelial permeability in various acute and chronic lung disorders.     

Inverse relation between nasal fluid Clara Cell Protein 16 levels and symptoms and signs of rhinitis in allergen-challenged patients with intermittent allergic rhinitis

BACKGROUND: Decreased levels of the anti-inflammatory Clara Cell Protein 16 (CC16) are found in intermittent allergic rhinitis (IAR) and asthma. In asthma this decrease has been associated with hyperreactivity and the A38G single nucleotide polymorphism (SNP). The aim of this study was to examine if IAR is associated with signs and symptoms of rhinitis and the A38G SNP. METHODS: Nasal fluid CC16 was analyzed in 20 patients with IAR before allergen challenge and 1 and 6 h after challenge, and from 28 healthy controls. The A38G SNP was analyzed in 80 patients with IAR and 106 controls. Nasal biopsies were obtained from three subjects in each group for immunohistochemical analysis of CC16. RESULTS: In the allergen-challenged patients symptoms and rhinoscopic signs of rhinitis increased after 1 h and normalized after 6 h. In contrast, nasal fluid CC16 decreased 1 h after allergen challenge and returned to baseline after 6 h. Nasal fluid CC16 levels did not differ from controls before and 6 h after challenge. Immunohistochemical investigation showed intense CC16 staining in the nasal epithelium of both patients before season and healthy controls, but weak staining in symptomatic patients during season. No significant association between the A38G SNP and IAR was found. CONCLUSION: There was an inverse relation between nasal fluid CC16 levels and symptoms and signs of rhinitis in allergen-challenged patients with IAR. However, there was no association between IAR and the A38G SNP.     

Low levels of CC16 in nasal fluid of children with birch pollen-induced rhinitis

BACKGROUND: Clara cell protein 16 (CC16; secretoglobin 1A1) is an anti-inflammatory protein mainly expressed in the epithelial cells in the airways. OBJECTIVE: To compare the levels of CC16 in nasal lavage (NAL) from children with intermittent allergic rhinitis and healthy controls and to study the effect of a local steroid. METHODS: Thirty schoolchildren with birch pollen allergy and 30 healthy controls from the same schools were included in the study. The NAL fluid was collected before the season, during the birch pollen season and, for the patients, after 1 week of treatment with a local steroid. Symptom scores were obtained on every occasion. CC16 and eosinophil cationic protein (ECP) were analyzed with enzyme-linked immunosorbent assay. RESULTS: The nasal fluid levels of CC16 were significantly lower in patients than in controls, before and during pollen season. Before the season, the median CC16 concentrations were 9.1 (range 1.1-117) microg/l in patients and 25.7 (6.1-110.2) microg/l in controls. During the season, the median CC16 concentrations in nasal fluid were 12.9 (2.3-89.7) microg/l in the allergic children and 22.0 (9.5-90.1) microg/l in the healthy controls (P = 0.0005). Symptom scores, nasal fluid eosinophils and ECP were higher in patients during the season. Treatment with a local steroid did not change the CC16 levels. CONCLUSIONS: Nasal fluid CC16 levels were lower in children with birch pollen-induced allergic rhinitis than in healthy controls both before and during the pollen season. We speculate that reduction in anti-inflammatory activity by CC16 may contribute to the pathogenesis of allergic rhinitis.     

生长激素对急性肺损伤大鼠CC16表达的调控

目的：研究生长激素（GH）对内毒素血症所致急性肺损伤（ALI）的影响及机制.方法：112只雄性SD大鼠内毒素致急性肺损伤后随机均分为ALI组和GH组.分别用Western blot法、免疫荧光法和半定量RT-PCR法测定大鼠肺组织中CC16蛋白含量、核因子NF-κB的表达与活化、CC16 mRNA的表达水平,并分析CC16与肺损伤程度及NF-κB等炎性因子之间的关系.结果：内毒素致伤后6小时内ALI组大鼠CC16 mRNA表达水平及CC16蛋白含量均进行性下降,6小时后逐渐恢复.致伤后GH组大鼠肺组织CC16 mRNA水平和CC16蛋白水平均较ALI组同时相点下降更明显.NF-κB表达、活化的变化趋势与CC16的变化趋势相反.相关性分析显示,CC16与肺损伤程度及NF-κB等炎性因子显著相关.结论：CC16表达变化在内毒素血症致急性肺损伤的发病中有重要作用,生长激素可通过下调肺源性抗炎因子CC16的表达而加剧内毒素血症所致的急性肺损伤.