目的探讨慢性阻塞性肺疾病(COPD)合并阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者血浆内皮素-1(ET-1)、一氧化氮(NO)与肺动脉高压的关系。方法选择COPD患者53例,其中合并肺动脉高压患者18例;OSAHS患者50例,其中合并肺动脉高压患者14例...目的探讨慢性阻塞性肺疾病(COPD)合并阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者血浆内皮素-1(ET-1)、一氧化氮(NO)与肺动脉高压的关系。方法选择COPD患者53例,其中合并肺动脉高压患者18例;OSAHS患者50例,其中合并肺动脉高压患者14例和重叠综合征(COPD合并OSAHS,即OS)患者25例,其中合并肺动脉高压患者12例,应用超声心动图评估肺动脉压,放射免疫法测定血浆ET-1水平,硝酸酶还原法测定NO水平,比较3组患者睡眠呼吸暂停严重程度及睡眠时缺氧程度。结果 3组患者睡眠呼吸暂停低通气指数(apneahypopnea index,AHI)、血氧饱和度(SaO2)<90%时间占总睡眠时间百分比(cumulative percentage of sleep time withSaO2below90%,TSaO2<90%)、最低血氧饱和度(MinSaO2)比较,差异均有统计学意义(P<0.01),OS组与COPD组、OSAHS组相比夜间MinSaO2降低(P<0.05)、TSaO2<90%增加,差异均有统计学意义(P<0.05);AHI升高亦有统计学意义(P<0.05)。3组合并肺动脉高压患者NO和ET-1水平比较,差异均有统计学意义(P<0.01)。OS合并肺动脉高压患者较未合并肺动脉高压患者ET-1水平升高,NO水平降低,差异均有统计学意义(P<0.05)。结论 OS患者较单纯的COPD和单纯OSAHS患者夜间缺氧更明显,更易形成肺动脉高压。血浆NO降低、ET-1升高与肺动脉压升高有一定关系。展开更多
Objective To evaluate the antagonistic effects of N-acetylcysteine(NAC)on mitogen-activated protein kinases(MAPK)pathway activation,oxidative stress and inflammatory responses in rats with lung injury induced by fine ...Objective To evaluate the antagonistic effects of N-acetylcysteine(NAC)on mitogen-activated protein kinases(MAPK)pathway activation,oxidative stress and inflammatory responses in rats with lung injury induced by fine particulate matter(PM2.5).Methods Forty eight male Wistar rats were randomly divided into six groups:blank control group(C1),water drip control group(C2),PM2.5 exposed group(P),low-dose NAC treated and PM2.5 exposed group(L),middle-dose NAC treated and PM2.5 exposed group(M),and high-dose NAC treated and PM2.5 exposed group(H).PM2.5 suspension(7.5 mg/kg)was administered tracheally once a week for four times.NAC of 125 mg/kg,250 mg/kg and 500 mg/kg was delivered intragastrically to L,M and H group respectively by gavage(10 ml/kg)for six days before PM2.5 exposure.The histopathological changes and human mucin 5 subtype AC(MUC5AC)content in lung tissue of rats were evaluated.We investigated IL-6 in serum and bronchoalveolar lavage fluid(BALF)by Enzyme-linked immunosorbent assay(ELISA),MUC5AC in lung tissue homogenate by ELISA,glutathione peroxidase(GSH-PX)in serum and BALF by spectrophotometry,and the expression of p-ERK1/2,p-JNK1/2 and p-p38 proteins by Western blot.All the measurements were analyzed and compared statistically.Results Lung tissue of rats exposed to PM2.5 showed histological destruction and increased mucus secretion of bronchial epithelial cells.Rats receiving NAC treatment showed less histological destruction and mucus secretion.Of P,L,M and H group,MUC5AC in lung tissue,IL-6 in serum and BALF were higher than controls(C1 and C2)(all P<0.05),with the highest levels found in the P group and a decreasing trend with increase of NAC dose.The activity of GSH-PX in serum and BALF of PM2.5 exposed rats(P,L,M and H)was lower than that of controls(all P<0.05),with higher activities found in NAC treated rats(L,M,and H),and an increasing trend with increase of NAC dose.The expressions of p-ERK1/2,p-JNK1/2 and p-p38 proteins in PM2.5 exposed lung tissue(P,L,M and H)was higher than controls(all P<0.05),with decreased levels and dose dependent downregulation found in NAC treated rats.Conclusion NAC can antagonize major MAPK pathway activation,lung oxidative stress and inflammatory injury induced by PM2.5 in rats.展开更多
文摘目的探讨慢性阻塞性肺疾病(COPD)合并阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者血浆内皮素-1(ET-1)、一氧化氮(NO)与肺动脉高压的关系。方法选择COPD患者53例,其中合并肺动脉高压患者18例;OSAHS患者50例,其中合并肺动脉高压患者14例和重叠综合征(COPD合并OSAHS,即OS)患者25例,其中合并肺动脉高压患者12例,应用超声心动图评估肺动脉压,放射免疫法测定血浆ET-1水平,硝酸酶还原法测定NO水平,比较3组患者睡眠呼吸暂停严重程度及睡眠时缺氧程度。结果 3组患者睡眠呼吸暂停低通气指数(apneahypopnea index,AHI)、血氧饱和度(SaO2)<90%时间占总睡眠时间百分比(cumulative percentage of sleep time withSaO2below90%,TSaO2<90%)、最低血氧饱和度(MinSaO2)比较,差异均有统计学意义(P<0.01),OS组与COPD组、OSAHS组相比夜间MinSaO2降低(P<0.05)、TSaO2<90%增加,差异均有统计学意义(P<0.05);AHI升高亦有统计学意义(P<0.05)。3组合并肺动脉高压患者NO和ET-1水平比较,差异均有统计学意义(P<0.01)。OS合并肺动脉高压患者较未合并肺动脉高压患者ET-1水平升高,NO水平降低,差异均有统计学意义(P<0.05)。结论 OS患者较单纯的COPD和单纯OSAHS患者夜间缺氧更明显,更易形成肺动脉高压。血浆NO降低、ET-1升高与肺动脉压升高有一定关系。
文摘Objective To evaluate the antagonistic effects of N-acetylcysteine(NAC)on mitogen-activated protein kinases(MAPK)pathway activation,oxidative stress and inflammatory responses in rats with lung injury induced by fine particulate matter(PM2.5).Methods Forty eight male Wistar rats were randomly divided into six groups:blank control group(C1),water drip control group(C2),PM2.5 exposed group(P),low-dose NAC treated and PM2.5 exposed group(L),middle-dose NAC treated and PM2.5 exposed group(M),and high-dose NAC treated and PM2.5 exposed group(H).PM2.5 suspension(7.5 mg/kg)was administered tracheally once a week for four times.NAC of 125 mg/kg,250 mg/kg and 500 mg/kg was delivered intragastrically to L,M and H group respectively by gavage(10 ml/kg)for six days before PM2.5 exposure.The histopathological changes and human mucin 5 subtype AC(MUC5AC)content in lung tissue of rats were evaluated.We investigated IL-6 in serum and bronchoalveolar lavage fluid(BALF)by Enzyme-linked immunosorbent assay(ELISA),MUC5AC in lung tissue homogenate by ELISA,glutathione peroxidase(GSH-PX)in serum and BALF by spectrophotometry,and the expression of p-ERK1/2,p-JNK1/2 and p-p38 proteins by Western blot.All the measurements were analyzed and compared statistically.Results Lung tissue of rats exposed to PM2.5 showed histological destruction and increased mucus secretion of bronchial epithelial cells.Rats receiving NAC treatment showed less histological destruction and mucus secretion.Of P,L,M and H group,MUC5AC in lung tissue,IL-6 in serum and BALF were higher than controls(C1 and C2)(all P<0.05),with the highest levels found in the P group and a decreasing trend with increase of NAC dose.The activity of GSH-PX in serum and BALF of PM2.5 exposed rats(P,L,M and H)was lower than that of controls(all P<0.05),with higher activities found in NAC treated rats(L,M,and H),and an increasing trend with increase of NAC dose.The expressions of p-ERK1/2,p-JNK1/2 and p-p38 proteins in PM2.5 exposed lung tissue(P,L,M and H)was higher than controls(all P<0.05),with decreased levels and dose dependent downregulation found in NAC treated rats.Conclusion NAC can antagonize major MAPK pathway activation,lung oxidative stress and inflammatory injury induced by PM2.5 in rats.
