Existence of multiple organ aging in animal model of emphysema induced by cigarette smoke extract.

Existence of multiple organ aging in animal model of emphysema induced by cigarette smoke extract.
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香烟烟雾提取物致肺气肿动物模型中多器官衰老的存在

DOI:
10.18332/tid/143853
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发表时间:
2022
影响因子:
3.7
通讯作者:
Long Y
Long Y
中科院分区:
医学4区
文献类型:
--
作者:
Liang G;He Z;Chen Y;Zhang H;Peng H;Zong D;Long Y

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通常认为COPD或至少肺气肿代表部分由香烟烟雾组分的氧化损伤诱导的加速肺老化。然而,COPD或肺气肿患者的其他器官是否存在任何老化迹象的问题仍不清楚。本研究旨在探讨香烟烟雾提取物(CSE)诱导的肺气肿动物模型是否存在多器官衰老,并探讨其可能的机制。CSE诱导肺气肿动物模型。用苏木精-伊红(H&E)染色后,测量肺、心、肝、肾和脾组织的组织形态学变化。采用酶联免疫吸附法(ELISA)测定血清干细胞因子(SCF)、细胞周期蛋白D1(CyclinD 1)和超氧化物歧化酶(SOD)水平。分别采用Western blotting和定量逆转录聚合酶链反应(qRT-PCR)检测肺、心、肝、肾和脾组织中p16(INK 4a)、Sca-1和eNOS蛋白和mRNA的表达。应用地西他滨(Dec)观察其是否能改变CSE引起的改变。肺组织的组织形态学改变明显,而其他器官的结构和组织形态学正常。CSE组血清SCF、CyclinD 1和SOD浓度均低于对照组。CSE组肺、心、肝、肾和脾组织中p16(INK 4a)蛋白和mRNA的表达水平高于对照组,而Sca-1和eNOS蛋白和mRNA的表达水平低于对照组。Dec可部分减轻CSE所致的损伤,且减轻程度因器官而异。CSE所致肺气肿动物模型除肺组织老化外,心、肝、肾、脾等组织也在老化过程中,但肺对CSE的敏感性和亲和力高于其他器官。CSE所致肺气肿动物模型也可能存在多器官衰老。DEC可部分减轻CSE所致的多器官衰老。
It is commonly considered that COPD or at least emphysema represents accelerated lung aging induced in part by oxidative damage from cigarette smoke components. However, the issue if there are any aging signs in other organs in patients with COPD or emphysema remains unclear. The aim of this study is to explore whether there is multiple organ aging in the animal model of emphysema induced by cigarette smoke extract (CSE), and to ascertain the possible mechanisms, if any. The animal model of emphysema was induced by CSE. Histomorphological changes in lung, heart, liver, kidney and spleen tissues were measured after staining with hematoxylin and eosin (H&E). The concentrations of stem cell factor (SCF), CyclinD1 and superoxide dismutase (SOD) in serum were determined by ELISA kit. The expressions of p16 (INK4a), Sca-1, eNOS proteins and mRNA in lung, heart, liver, kidney and spleen tissues were detected by Western blotting and quantitative reverse transcriptase polymerase chain reaction (qRT-PCR), respectively. Decitabine (Dec) was applied to examine whether it could alter the changes caused by CSE. The histomorphology of lung tissue was significantly changed, while other organs exhibited normal structure and histomorphology. The concentrations of SCF, CyclinD1 and SOD in serum were lower in the CSE group than in the control group. The expression levels of p16(INK4a) protein and mRNA in lung, heart, liver, kidney and spleen tissues were higher in the CSE group than in the control group, while the expression levels of Sca-1 and eNOS proteins and mRNA were lower in the CSE group than in the control group, in the tissues described above. Dec could partly alleviate the damages caused by CSE and the degree of alleviation resulted by Dec varied from organ to organ. In addition to the aging of the lung tissue in the emphysema animal model induced by CSE, the tissues of the heart, liver, kidney and spleen were also in the progress of aging, but the sensibility and affinity of lung to CSE were higher than those of the other organs. Multiple organ aging may also exist in the animal model of emphysema induced by CSE. DEC can partly alleviate the multiple organ aging caused by CSE.
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影响因子: 20.1
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