肺泡上皮细胞在高氧急性肺损伤中的作用研究

刘芳君,龚财惠,刘莎

doi:10.13718/j.cnki.xsxb.2018.05.016

西南师范大学学报(自然科学版)

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肺泡上皮细胞在高氧急性肺损伤中的作用研究

刘芳君,龚财惠,刘莎. 肺泡上皮细胞在高氧急性肺损伤中的作用研究[J]. 西南师范大学学报(自然科学版), 2018, 43(5): 95-100. doi: 10.13718/j.cnki.xsxb.2018.05.016

引用本文:

刘芳君,龚财惠,刘莎. 肺泡上皮细胞在高氧急性肺损伤中的作用研究[J]. 西南师范大学学报(自然科学版), 2018, 43(5): 95-100. doi: 10.13718/j.cnki.xsxb.2018.05.016

LIU Fang-jun, GONG Cai-hui, LIU Sha. On Role of Alveolar Epithelial Cells in Hyperoxic Acute Lung Injury[J]. Journal of Southwest China Normal University(Natural Science Edition), 2018, 43(5): 95-100. doi: 10.13718/j.cnki.xsxb.2018.05.016

Citation:

LIU Fang-jun, GONG Cai-hui, LIU Sha. On Role of Alveolar Epithelial Cells in Hyperoxic Acute Lung Injury[J]. Journal of Southwest China Normal University(Natural Science Edition), 2018, 43(5): 95-100. doi: 10.13718/j.cnki.xsxb.2018.05.016

肺泡上皮细胞在高氧急性肺损伤中的作用研究

刘芳君,龚财惠,刘莎

重庆医科大学附属儿童医院呼吸中心, 儿科学重庆市重点实验室, 儿童发育重大疾病国家国际科技合作基地, 儿童发育疾病研究教育部重点实验室, 重庆 400014

On Role of Alveolar Epithelial Cells in Hyperoxic Acute Lung Injury

LIU Fang-jun, GONG Cai-hui, LIU Sha

Department of Respiratory Medicine, Children's Hospital of Chongqing Medical University, Chongqing Key Laboratory of Pediatrics, China International Science and Technology Cooperation base for Child Development and Critical Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing 400014, China

摘要: 目的：观察新生小鼠肺组织甲状腺转录因子[TTF-1]及肺表面活性物质蛋白B[SP-B]的表达，探讨高氧急性肺损伤[HALI]可能存在的损伤机制.方法：新生1 d的C57BL/6小鼠30只，随机分为：高氧暴露组及空气对照组，每组15只.高浓度氧暴露72 h建立ALI小鼠模型，各组于24，48及72h随机取5只小鼠肺组织标本，测定肺湿/干重（W/D）比值、观察肺组织形态学变化并进行病理评分及肺泡计数（RAC），荧光定量PCR法及免疫荧光标记法检测各组各实验点TTF-1，SP-BmRNA及蛋白的表达情况.结果：与空气对照组比较，高氧暴露48 h时，肺组织出现肺泡间质细胞数量增多及肺水肿等HALI的表现；W/D比值及病理评分显著升高（PPP<0.05）.结论：高浓度氧暴露能导致ALI，肺泡上皮细胞的损伤在HALI发生进程中可能发挥重要作用.
- 高氧急性肺损伤 /
- 肺泡上皮细胞 /
- 甲状腺转录因子 /
- 肺表面活性物质蛋白B /
- 新生小鼠
Abstract: Observed the expressions of thyroid transcription factor-1(TTF-1)and surfactant protein B (SP-B) in the lungs of newborn mice with exposed to hyperoxia in order to explain the possible pathogenesis of hyperoxia acute lung injury(HALI). Totally 30 postnatal day 1 mice, which were randomly divided into hyperoxia exposed group and air control group(n=15)respectively. hyperoxia exposed for 72 hours induce the HALI.assessed the wet/dry weight(W/D)ratio,observed the changes of lung pathology, injury score andradical alveolar counts. The protein and mRNA expressions of thyroid transcription factor-1(TTF-1)and surfactant protein B (SP-B) were detected by immunofluorescence and real-time PCR after 24,48and72 hours, respectively. Contrasted the air control group, lung tissue gradually showed increased interstitial cell and pulmonary edema at hyperoxia exposed for 48 hours.andW/D ratio and injury scores of 48 hours(all PP<0.05). The mRNA and protein expression of TTF-1 and SP-B in lung tissue were decreased markedly at 72 hours of hyperoxia exposed group compared with the air control group. In newborn mice hyperoxia exposed can induced lung injury, and disrupts pulmonary epithelial may be plays an very important role in the development of HALI.
- Hyperoxic acute lung injury /
- alveolar epithelial cells /
- Thyroid transcription factor 1 /
- Surfactant protein B /
- Newborn mice .

[1]	KALLET R H,MATTHAY M A.Hyperoxic Acute Lung Injury[J].Respir Care,2013,58(1):123-141.
[2]	CROSBY L M,WATERS C M.Epithelial Repair Mechanisms in the Lung[J].Am J Physiol Lung Cell Mol Physiol,2010,298(6):L715-L731.
[3]	刘芳君, 刘莎, 符州, 等. 氧体积分数对新生鼠肺组织损伤的影响[J]. 西南师范大学学报(自然科学版), 2016, 41(5):190-193.
[4]	BHANDARI V,CHOO-WING R,HOMER RJ,et al.Increased Hyperoxia-Induced Mortality and Acute Lung Injury in IL-13 Null Mice[J].J Immunol,2007,178(8):4993-5000.
[5]	DOS SANTOS C C.Hyperoxic Acute Lung Injury and Ventilator-Induced/Associated Lung Injury:New Insights into Intracellular Signaling Pathways[J].Crit Care,2007,11(2):126.
[6]	YEE M,VITIELLO P F,ROPER J M,et al.Type Ⅱ Epithelial Cells are Critical Target for Hyperoxia-Mediated Impairment of Postnatal Lung Development[J].Am J Physiol Lung Cell Mol Physiol,2006,291(5):L1101-L1111.
[7]	DAS A,ACHARYA S,GOTTIPATI K R,et al.Thyroid Transcription Factor-1(TTF-1) Gene:Identification of ZBP-89,Sp1,and TTF-1 Sites in the Promoter and Regulation by TNF-alpha in Lung Epithelial Cells[J].Am J Physiol Lung Cell Mol Physiol,2011,301(4):L427-L440.
[8]	刘芳君, 邓春, 郭春宝, 等. 高氧及TGF-β1对肺泡Ⅱ型细胞上皮间质转化的影响[J]. 细胞与分子免疫学杂志, 2012, 28(5):474-477.

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肺泡上皮细胞在高氧急性肺损伤中的作用研究

刘芳君,龚财惠,刘莎

重庆医科大学附属儿童医院呼吸中心, 儿科学重庆市重点实验室, 儿童发育重大疾病国家国际科技合作基地, 儿童发育疾病研究教育部重点实验室, 重庆 400014

收稿日期: 2016-03-02

关键词:

摘要: 目的：观察新生小鼠肺组织甲状腺转录因子[TTF-1]及肺表面活性物质蛋白B[SP-B]的表达，探讨高氧急性肺损伤[HALI]可能存在的损伤机制.方法：新生1 d的C57BL/6小鼠30只，随机分为：高氧暴露组及空气对照组，每组15只.高浓度氧暴露72 h建立ALI小鼠模型，各组于24，48及72h随机取5只小鼠肺组织标本，测定肺湿/干重（W/D）比值、观察肺组织形态学变化并进行病理评分及肺泡计数（RAC），荧光定量PCR法及免疫荧光标记法检测各组各实验点TTF-1，SP-BmRNA及蛋白的表达情况.结果：与空气对照组比较，高氧暴露48 h时，肺组织出现肺泡间质细胞数量增多及肺水肿等HALI的表现；W/D比值及病理评分显著升高（PPP<0.05）.结论：高浓度氧暴露能导致ALI，肺泡上皮细胞的损伤在HALI发生进程中可能发挥重要作用.

English Abstract

On Role of Alveolar Epithelial Cells in Hyperoxic Acute Lung Injury

重庆医科大学附属儿童医院呼吸中心, 儿科学重庆市重点实验室, 儿童发育重大疾病国家国际科技合作基地, 儿童发育疾病研究教育部重点实验室, 重庆 400014

Received Date: 2016-03-02

Keywords:

Abstract: Observed the expressions of thyroid transcription factor-1(TTF-1)and surfactant protein B (SP-B) in the lungs of newborn mice with exposed to hyperoxia in order to explain the possible pathogenesis of hyperoxia acute lung injury(HALI). Totally 30 postnatal day 1 mice, which were randomly divided into hyperoxia exposed group and air control group(n=15)respectively. hyperoxia exposed for 72 hours induce the HALI.assessed the wet/dry weight(W/D)ratio,observed the changes of lung pathology, injury score andradical alveolar counts. The protein and mRNA expressions of thyroid transcription factor-1(TTF-1)and surfactant protein B (SP-B) were detected by immunofluorescence and real-time PCR after 24,48and72 hours, respectively. Contrasted the air control group, lung tissue gradually showed increased interstitial cell and pulmonary edema at hyperoxia exposed for 48 hours.andW/D ratio and injury scores of 48 hours(all PP<0.05). The mRNA and protein expression of TTF-1 and SP-B in lung tissue were decreased markedly at 72 hours of hyperoxia exposed group compared with the air control group. In newborn mice hyperoxia exposed can induced lung injury, and disrupts pulmonary epithelial may be plays an very important role in the development of HALI.