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慢性阻塞性肺疾病合并肺气肿患者肺泡壁细胞凋亡与肺气肿改变有关。

Apoptosis of alveolar wall cells in chronic obstructive pulmonary disease patients with pulmonary emphysema is involved in emphysematous changes.

作者信息

Liu Hongmei, Ma Lijun, Wu Jizhen, Wang Kai, Chen Xianliang

机构信息

Division of Respiratory Diseases, Department of Internal Medicine, He'nan Provincial People's Hospital, Zhengzhou, 450003, China.

出版信息

J Huazhong Univ Sci Technolog Med Sci. 2009 Aug;29(4):466-9. doi: 10.1007/s11596-009-0415-7. Epub 2009 Aug 7.

Abstract

This study explored the role of apoptosis of alveolar wall cells of chronic obstructive pulmonary disease (COPD) patients with pulmonary emphysema in the pathogenesis of emphysema. The subjects were divided into three groups: COPD patients with pulmonary emphysema (COPD group), asymptomatic smokers and non-smokers. Lung tissues were harvested and histologically assessed. TUNEL assay was employed to determine the apoptotic cells. The expression of PCNA, Bax and SP-C in the lung alveolar wall cells were immunohistochemically determined. SP-C immunofluorescence staining was used to identify type II alveolar cells in the TUNEL-positive cells. The mean linear interval (MLI), mean alveoli number (MAN) and mean alveoli area (MAA) in COPD group were significantly different as compared with those in asymptomatic smokers and non-smokers, respectively (P<0.01). The proliferation index (PI), apoptosis index (AI) and the percentage of Bax-positive cells in COPD group were significantly greater than those of asymptomatic smokers and non-smokers (P<0.01). However, the percentage of SP-C-positive cells was significantly lower in COPD group than in asymptomatic smokers and non-smokers (P<0.01). Most of the TUNEL-positive cells expressed SP-C. In COPD group, the apoptosis of alveolar wall cells, especially apoptosis of type-II cells, may take part in the pathogenesis of emphysema. Up-regulation of Bax expression may be responsible for the apoptosis of alveolar wall cells in the COPD patients with pulmonary emphysema.

摘要

本研究探讨慢性阻塞性肺疾病(COPD)合并肺气肿患者肺泡壁细胞凋亡在肺气肿发病机制中的作用。将研究对象分为三组:COPD合并肺气肿患者(COPD组)、无症状吸烟者和非吸烟者。采集肺组织并进行组织学评估。采用TUNEL法检测凋亡细胞。免疫组化法检测肺泡壁细胞中PCNA、Bax和SP-C的表达。利用SP-C免疫荧光染色在TUNEL阳性细胞中鉴定Ⅱ型肺泡细胞。COPD组的平均线性截距(MLI)、平均肺泡数(MAN)和平均肺泡面积(MAA)与无症状吸烟者和非吸烟者相比,差异均有统计学意义(P<0.01)。COPD组的增殖指数(PI)、凋亡指数(AI)和Bax阳性细胞百分比均显著高于无症状吸烟者和非吸烟者(P<0.01)。然而,COPD组SP-C阳性细胞百分比显著低于无症状吸烟者和非吸烟者(P<0.01)。大多数TUNEL阳性细胞表达SP-C。在COPD组中,肺泡壁细胞凋亡,尤其是Ⅱ型细胞凋亡,可能参与了肺气肿的发病机制。Bax表达上调可能是COPD合并肺气肿患者肺泡壁细胞凋亡的原因。

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