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Article: The role of heme oxygenase-1 in the protection of chronic intermittent hypoxia-induced lung injury in vivo

TitleThe role of heme oxygenase-1 in the protection of chronic intermittent hypoxia-induced lung injury in vivo
慢性间歇性低氧导致鼠肺部损伤的机制及血红素加氧酶-1的保护作用
Authors
KeywordsSleep apnea syndrome (睡眠呼吸暂停综合征)
Obstructive Pulmonary disease (阻塞性肺疾病)
Chronic obstructive (慢性阻塞性)
Inflammatory effect (炎症反应)
Cell apoptosis (细胞凋亡)
Issue Date2015
PublisherZhong Hua Yi Xue Hui Za Zhi She (中华医学会杂志社). The Journal's web site is located at http://lung.org.cn/
Citation
Chinese journal of tuberculosis and respiratory diseases, 2015, v. 38 n. 07, p. 516-519 How to Cite?
中华结核和呼吸杂志, 2015, v. 38 n. 07, p. 516-519 How to Cite?
Abstract目的 观察慢性间歇低氧(CIH)对大鼠肺脏局部炎症反应以及肺泡结构的影响,探讨药物诱导血红素加氧酶-1(HO-1)在此过程中的干预效果.方法 Sprague-Dawley雄性大鼠24只,按随机数字表法分为常氧对照组、CIH组、常氧+hemin干预组(hemin组)和CIH+hemin干预组(CIH+ hemin组),每组6只.CIH组大鼠予间歇低氧环境中(4 min10% +2 min21% 02,8 h/d,共6周),对照组大鼠置于常氧环境中.利用腹腔注射hemin(4 mg/kg)诱导HO-1表达,IN组及CIH组腹腔注射等体积生理盐水.采用western blot检测大鼠肺脏HO-1及cleaved caspase3表达水平,ELISA检测大鼠肺脏局部炎症因子中性粒细胞化学趋化因子-1(CINC-1)、IL-6、肿瘤坏死因子-α(TNF-α)和单核细胞趋化蛋白-1(MCP-1)的表达水平,使用HE染色观察大鼠肺脏病理改变.结果 为期6周的CIH可明显升高肺脏炎症因子TNF-α[(2.20 ±0.10) vs (1.80±0.08) ng/ml]、IL-6[(0.87 ±0.05) vs(0.52 ±0.05) ng/ml]、CINC-1[(66 ±6) vs (39 ±5) pg/ml]和MCP-1[(2.20土0.09)vs(1.40±0.10) ng/ml]以及cleaved caspase3表达(均P<0.05),hemin可明显抑制由于CIH诱导的肺脏炎症因子[(TNF-α:(1.60±0.20) ng/ml,IL-6:(0.60±0.07) ng/ml,CINC-1:(45±6) pg/ml,MCP-1:(1.80 ±0.10) ng/ml,均P<0.05]水平增高以及cleaved caspase3表达(P<0.01),肺脏HO-1表达明显升高.hemin可进一步增加CIH下肺脏HO-1的表达水平.CIH导致肺泡结构损伤,而hemin诱导的HO-1升高可明显抑制由于CIH诱导的肺脏病理改变.结论 CIH可导致肺脏局部炎症因子表达升高,细胞凋亡及肺泡结构破坏,药物诱导HO-1升高可抑制CIH诱导的局部炎症反应和细胞凋亡,逆转肺泡结构损伤,表明CIH对肺脏的损伤作用及HO-1的保护功能.
Persistent Identifierhttp://hdl.handle.net/10722/232029
ISSN
2015 SCImago Journal Rankings: 0.150

 

DC FieldValueLanguage
dc.contributor.authorHan, Q-
dc.contributor.authorLi, G-
dc.contributor.authorMak, JCW-
dc.contributor.authorZhang, Y-
dc.contributor.authorIp, MSM-
dc.contributor.authorZhang, N-
dc.creatorcsl 161130-
dc.date.accessioned2016-09-20T05:27:06Z-
dc.date.available2016-09-20T05:27:06Z-
dc.date.issued2015-
dc.identifier.citationChinese journal of tuberculosis and respiratory diseases, 2015, v. 38 n. 07, p. 516-519-
dc.identifier.citation中华结核和呼吸杂志, 2015, v. 38 n. 07, p. 516-519-
dc.identifier.issn1001-0939-
dc.identifier.urihttp://hdl.handle.net/10722/232029-
dc.description.abstract目的 观察慢性间歇低氧(CIH)对大鼠肺脏局部炎症反应以及肺泡结构的影响,探讨药物诱导血红素加氧酶-1(HO-1)在此过程中的干预效果.方法 Sprague-Dawley雄性大鼠24只,按随机数字表法分为常氧对照组、CIH组、常氧+hemin干预组(hemin组)和CIH+hemin干预组(CIH+ hemin组),每组6只.CIH组大鼠予间歇低氧环境中(4 min10% +2 min21% 02,8 h/d,共6周),对照组大鼠置于常氧环境中.利用腹腔注射hemin(4 mg/kg)诱导HO-1表达,IN组及CIH组腹腔注射等体积生理盐水.采用western blot检测大鼠肺脏HO-1及cleaved caspase3表达水平,ELISA检测大鼠肺脏局部炎症因子中性粒细胞化学趋化因子-1(CINC-1)、IL-6、肿瘤坏死因子-α(TNF-α)和单核细胞趋化蛋白-1(MCP-1)的表达水平,使用HE染色观察大鼠肺脏病理改变.结果 为期6周的CIH可明显升高肺脏炎症因子TNF-α[(2.20 ±0.10) vs (1.80±0.08) ng/ml]、IL-6[(0.87 ±0.05) vs(0.52 ±0.05) ng/ml]、CINC-1[(66 ±6) vs (39 ±5) pg/ml]和MCP-1[(2.20土0.09)vs(1.40±0.10) ng/ml]以及cleaved caspase3表达(均P<0.05),hemin可明显抑制由于CIH诱导的肺脏炎症因子[(TNF-α:(1.60±0.20) ng/ml,IL-6:(0.60±0.07) ng/ml,CINC-1:(45±6) pg/ml,MCP-1:(1.80 ±0.10) ng/ml,均P<0.05]水平增高以及cleaved caspase3表达(P<0.01),肺脏HO-1表达明显升高.hemin可进一步增加CIH下肺脏HO-1的表达水平.CIH导致肺泡结构损伤,而hemin诱导的HO-1升高可明显抑制由于CIH诱导的肺脏病理改变.结论 CIH可导致肺脏局部炎症因子表达升高,细胞凋亡及肺泡结构破坏,药物诱导HO-1升高可抑制CIH诱导的局部炎症反应和细胞凋亡,逆转肺泡结构损伤,表明CIH对肺脏的损伤作用及HO-1的保护功能.-
dc.languagechi-
dc.publisherZhong Hua Yi Xue Hui Za Zhi She (中华医学会杂志社). The Journal's web site is located at http://lung.org.cn/-
dc.relation.ispartofChinese journal of tuberculosis and respiratory diseases-
dc.relation.ispartof中华结核和呼吸杂志-
dc.subjectSleep apnea syndrome (睡眠呼吸暂停综合征)-
dc.subjectObstructive Pulmonary disease (阻塞性肺疾病)-
dc.subjectChronic obstructive (慢性阻塞性)-
dc.subjectInflammatory effect (炎症反应)-
dc.subjectCell apoptosis (细胞凋亡)-
dc.titleThe role of heme oxygenase-1 in the protection of chronic intermittent hypoxia-induced lung injury in vivo-
dc.title慢性间歇性低氧导致鼠肺部损伤的机制及血红素加氧酶-1的保护作用-
dc.typeArticle-
dc.identifier.emailMak, JCW: judithmak@hku.hk-
dc.identifier.emailZhang, Y: zyl1999@hku.hk-
dc.identifier.emailIp, MSM: msmip@hku.hk-
dc.identifier.authorityHan, Q=rp02224-
dc.identifier.authorityLi, G=rp02224-
dc.identifier.authorityMak, JCW=rp00352-
dc.identifier.authorityIp, MSM=rp00347-
dc.identifier.authorityZhang, N=rp02224-
dc.identifier.doi10.3760/cma.j.issn.1001-0939.2015.07.011-
dc.identifier.hkuros264387-
dc.identifier.volume38-
dc.identifier.issue07-
dc.identifier.spage516-
dc.identifier.epage519-
dc.publisher.placeBeijing (北京)-

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