Effects and underlying mechanism of exosomes of adipose-derived mesenchymal stem cells on acute lung injury of septic mice
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摘要:
目的 探讨人脂肪间充质干细胞（ADSC）外泌体对脓毒症小鼠急性肺损伤的影响及其机制。 方法 本研究为实验研究。选取第4~5代ADSC,采用差速超高速离心法分离并提取其上清液中的外泌体,对外泌体鉴定后使用。取24只成年雄性BALB/c小鼠,按照随机数字表法（分组方法下同）分成正常对照组、单纯盲肠结扎穿孔（CLP）组和CLP+ADSC外泌体组并进行相应处理,每组8只。伤后24 h,采用苏木精-伊红染色观测小鼠肺组织形态,采用原位末端转移酶标记法检测肺组织细胞凋亡情况,采用酶联免疫吸附测定法检测小鼠血清中肿瘤坏死因子α（TNF-α）和白细胞介素1β（IL-1β）水平,使用相关试剂盒检测肺组织中丙二醛和超氧化物歧化酶（SOD）的含量,采用免疫荧光法检测小鼠肺组织细胞中CD86、CD206的表达。取小鼠巨噬细胞RAW246.7,分为空白对照组、单纯LPS组和LPS+ADSC外泌体组并进行相应处理。培养12 h 后,采用相关试剂盒检测细胞中ATP含量、线粒体活性氧的阳性细胞百分比、线粒体膜电位情况,采用实时荧光定量反转录PCR法检测细胞中M1极化标志因子诱导型一氧化氮合酶（iNOS）、M2极化标志因子精氨酸酶-1（Arg1）以及炎症因子TNF-α和IL-1β的mRNA表达量。以上实验除mRNA表达量的检测样本数为3以外,其余各指标的检测样本均为4。 结果 伤后24 h,正常对照组小鼠肺组织结构清晰完整,无炎症细胞浸润；单纯CLP组较正常对照组小鼠的肺组织水肿明显,炎症细胞浸润现象明显,凋亡、坏死细胞明显增多；CLP+ADSC外泌体组较单纯CLP组小鼠肺组织水肿症状明显减轻,炎症细胞浸润明显减少,细胞凋亡、坏死情况明显改善。伤后24 h,与正常对照组比较,单纯CLP组小鼠血清中TNF-α和IL-1β含量均明显增加（t值分别为50.82、30.81,P<0.05）；与单纯CLP组比较,CLP+ADSC外泌体组小鼠血清中的TNF-α和IL-1β含量均明显降低（t值分别为16.36、19.25,P<0.05）。伤后24 h,与正常对照组比较,单纯CLP组小鼠肺组织中丙二醛含量明显升高（t=9.89,P<0.05）,SOD含量明显降低（t=5.01,P<0.05）；与单纯CLP组比较,CLP+外泌体组小鼠肺组织中丙二醛含量明显降低（t=4.38,P<0.05）,SOD含量明显升高（t=2.97,P<0.05）。伤后24 h,与正常对照组相比,单纯CLP组小鼠的肺组织中CD86阳性细胞明显增多,CD206阳性细胞明显减少；与单纯CLP组相比,CLP+ADSC外泌体组小鼠肺组织中CD86阳性细胞明显减少,CD206阳性细胞明显增多。培养12 h后,与空白对照组比较,单纯LPS组RAW246.7细胞中ATP含量明显降低（t=6.28,P<0.05）；与单纯LPS组比较,LPS+ADSC外泌体组RAW246.7细胞中ATP含量明显升高（t=4.01,P<0.05）。培养12 h后,与空白对照组的22%±4%比较,单纯LPS组RAW246.7细胞中线粒体活性氧的阳性细胞百分比40%±6%明显增加（t=5.04,P<0.05）；与单纯LPS组比较,LPS+ADSC外泌体组RAW246.7细胞中线粒体活性氧的阳性细胞百分比30%±5%明显降低（t=2.65,P<0.05）。培养12 h后,与空白对照组相比,单纯LPS组RAW246.7细胞TNF-α、IL-1β和iNOS的mRNA表达均显著增加（t值分别为16.51、31.04、7.70,P<0.05）,Arg1的mRNA表达量降低但差异无统计学意义（P>0.05）；与单纯LPS组比较,LPS+ADSC外泌体组RAW246.7细胞中TNF-α、IL-1β和iNOS的mRNA表达量均明显降低（t值分别为11.38、22.58、5.28,P<0.05）,Arg1的mRNA表达量明显升高（t=7.66,P<0.05）。 结论 人ADSC来源外泌体可能通过改善LPS诱导的RAW246.7细胞线粒体功能障碍,抑制巨噬细胞向M1极化,降低炎症反应,从而发挥改善脓毒症小鼠肺损伤作用。 Abstract:Objective To explore effects and underlying mechanism of exosomes of adipose-derived mesenchymal stem cells (ADSC) on acute lung injury of septic mice. Methods The study was an experimental study. ADSC of passages 4-5 were selected, and exosomes in their supernatant were isolated and extracted by differential ultracentrifugation. Exosomes were then used after identification. Twenty-four adult male BALB/c mice were selected and divided into control group, simple cecal ligation and puncture (CLP) group, and CLP+ADSC-exosome group according to the random number table method (the grouping method was the same as below), with 8 mice in each group, which were treated accordingly. At 24 hours after injury, hematoxylin-eosin staining was used to observe the morphology of lung tissues, the in-situ end-labeling method was used to detect the apoptosis of lung tissue cells, the enzyme-linked immunosorbent assay was used to detect the levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in the serum of mice, relevant kits were used to detect the contents of malondialdehyde and superoxide dismutase (SOD) in lung tissues, and immunofluorescence method was used to detect the expressions of CD86 and CD206 in lung tissue cells of mice. Mouse macrophage RAW246.7 was taken and divided into control group, simple LPS group, and LPS+ADSC-exosome group, which were treated accordingly. Twelve hours later, the ATP content, the percentage of mitochondrial ROS positive cells, as well as mitochondrial membrane potential in cells were detected by related detection kits. The real-time fluorescence quantitative reverse-ranscription PCR method was used to detect the mRNA expression levels of M1 polarization marker factor inducible nitric oxide synthase (iNOS), M2 polarization marker factor arginase-1 (Arg1), and inflammatory factors TNF-α and IL-1β in cells. Three samples were used for mRNA expression detection, and four samples were used for the detection of other indicators. Results At 24 hours after injury, the lung tissue structure of mice in control group was clear and intact without inflammatory cell infiltration. Compared with that in control group, the lung tissue edema as well as the inflammatory cell infiltration of mice was much more obvious in simple CLP group. However, compared with that in simple CLP group, the lung tissue edema in CLP+ADSC-exosome group mice was significantly alleviated, the inflammatory cell infiltration was significantly reduced, and the cell apoptosis and necrosis were significantly improved. Twenty-four hours after injury, compared with that in control group, the contents of TNF-α and IL-1β in the serum of mice in simple CLP group were significantly increased (with t values of 50.82 and 30.81, respectively, P<0.05); compared with that in simple CLP group, the contents of TNF-α and IL-1β in the serum of mice in CLP+ADSC-exosome group were significantly decreased (with t values of 16.36 and 19.25, respectively, P<0.05). Compared with that in control group, the content of malondialdehyde in the lung tissue of mice in simple CLP group was significantly increased (t=9.89, P<0.05), and the content of SOD was significantly decreased (t=5.01, P<0.05); compared with that in simple CLP group, the content of malondialdehyde in the lung tissue of mice in CLP+ADSC-exosome group was significantly decreased (t=4.38, P<0.05), and the content of SOD was significantly increased (t=2.97, P<0.05). Twenty-four hours after injury, compared with that in control group, the number of CD86 positive cells in the lung tissue of mice in simple CLP group was significantly increased, and the number of CD206 positive cells was significantly decreased; compared with that in simple CLP group, the number of CD86 positive cells in the lung tissue of mice in CLP+ADSC-exosome group was significantly decreased, and the number of CD206 positive cells was significantly increased. After 12 hours of culture, compared with that in control group, the ATP content of RAW246.7 cells in simple LPS group was significantly decreased (t=6.28, P<0.05); compared with that in simple LPS group, the ATP content of RAW246.7 cells in LPS+ADSC-exosome group was significantly increased (t=4.01, P<0.05). After 12 hours of culture, compared with 22%±4% in blank control group, 40%±6% of positive cells of mitochondrial reactive oxygen species in RAW246.7 cells in simple LPS group was significantly increased (t=5.04, P<0.05); Compared with that in LPS group, 30%±5% of positive cells of mitochondrial reactive oxygen species in RAW246.7 cells in LPS+ADSC-exosome group was significantly decreased (t=2.65, P<0.05). After 12 hours of culture, compared with that in control group, the mRNA expressions of TNF-α, IL-1β, and iNOS in RAW246.7 cells in simple LPS group were significantly increased (with t values of 16.51, 31.04, and 7.70, respectively, P<0.05), and the decrease in the mRNA expression of Arg1 was not statistically significant (P>0.05); compared with that in simple LPS group, the mRNA expressions of TNF-α, IL-1β, and iNOS in RAW246.7 cells in LPS+ADSC-exosome group were significantly decreased (with t values of 11.38, 22.58, and 5.28, respectively, P<0.05), and the mRNA expression of Arg1 was significantly increased (t=7.66, P<0.05). Conclusions Human ADSC-exosomes may play a role in improving lung injury in septic mice by improving LPS-induced mitochondrial dysfunction in RAW246.7 cells, inhibiting macrophage polarization to M1, and reducing the inflammatory response. -
Key words:
- Sepsis /
- Acute lung injury /
- Mesenchymal stem cells /
- Exosomes /
- Macrophages /
- Mitochondrial dysfunction
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参考文献
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图 1 人脂肪间充质干细胞（ADSC）外泌体的鉴定。1A.可见清晰的囊泡呈茶托状结构 透射电子显微镜×40 000；1B.纳米颗粒跟踪分析仪检测显示粒径为60~150 nm
注：图1B为横坐标经过lg处理的数据形成的描记图
图 2 3组小鼠伤后24 h肺组织损伤情况和肺组织细胞的凋亡情况。2A、2B、2C.分别为正常对照组、单纯CLP组、CLP+ADSC外泌体组小鼠肺组织损伤情况,图2B较图2A中的肺组织水肿情况明显,炎症细胞数明显增多,图2C较图2B肺组织水肿明显改善,炎症细胞数明显减少 苏木精-伊红×100；2D、2E、2F.分别为正常对照组、单纯CLP组、CLP+ADSC外泌体组小鼠肺组织的细胞凋亡情况,图2E较图2D中的凋亡、坏死细胞数明显增加,图2F较图2E凋亡、坏死细胞数明显减少 异硫氰酸荧光素-4',6-二脒基-2-苯基吲哚×100
注：盲肠结扎穿孔（CLP）+脂肪间充质干细胞（ADSC）外泌体组和单纯CLP组小鼠均进行组名相应的处理,正常对照组小鼠仅注射磷酸盐缓冲液；凋亡细胞阳性染色为绿色
图 3 3组小鼠伤后24 h肺组织中巨噬细胞表型分布情况。3A、3B、3C.分别为正常对照组、单纯CLP组、CLP+ADSC外泌体组CD86（M1型巨噬细胞标志物）阳性细胞分别情况,图3B较图3A中的M1型巨噬细胞数明显增加,图3C较图3B中的M1型巨噬细胞数明显减少；3D、3E、3F.分别为正常对照组、单纯CLP组、CLP+ADSC外泌体组CD206（M2型巨噬细胞标志物）阳性细胞分别情况,图3E较图3D中的M2型巨噬细胞数明显增加,图3C较图3B中的M2型巨噬细胞数明显减少
注：盲肠结扎穿孔（CLP）+脂肪间充质干细胞（ADSC）外泌体组和单纯CLP组小鼠均进行组名相应的处理,正常对照组小鼠仅注射磷酸盐缓冲液；细胞阳性染色均为棕色
图 4 共培养12 h后RAW264.7细胞吞噬人脂肪间充质干细胞（ADSC）外泌体的情况 PKH26-4',6-二脒基-2-苯基吲哚×200。5A、5B、5C.分别为细胞中的外泌体染色、细胞核染色及复合染色情况,可见人ADSC外泌体成功被RAW264.7细胞吞噬
注：人ADSC外泌体阳性染色为红色,细胞核阳性为蓝色
图 5 培养12 h后3组RAW264.7细胞中线粒体膜电位情况。5A、5B、5C、5D.分别为空白对照组细胞呈蓝色荧光、绿色荧光、红色荧光及复合显色情况；5E、5F、5G、5H.分别为单纯LPS组细胞呈蓝色荧光、绿色荧光、红色荧光及复合显色情况；5I、5J、5K、5L.分别为LPS+ADSC外泌体组细胞呈蓝色荧光、绿色荧光、红色荧光及复合显色情况,图5F较图5B中的线粒体膜电位下降明显,图5J中的线粒体膜电位介于图5B与图5F之间,图5K中的正常线粒体荧光强度介于图5C与图5G之间,
注：对LPS+ADSC外泌体组和单纯LPS组细胞进行组名相应的处理,对空白对照组细胞进行常规培养；细胞核阳性染色为蓝色,受损或膜电位下降的线粒体阳性染色为绿色,正常线粒体的阳性染色为红色
Table 1. 实时荧光定量反转录PCR法检测RAW264.7细胞的各引物序列及产物大小
基因名称 引物序列（5'→3'） 产物大小（bp） IL-1β 上游：TCCAGGATGAGGACATGAGCAC 105 下游：GAACGTCACACACCAGCAGGTTA iNOS 上游：ACTACTGCTGGTGGTGACAA 106 下游：GAAGGTGTGGTTGAGTTCTCTAAG TNF-α 上游：ACTCCAGGCGGTGCCTATGT 160 下游：GTGAGGGTCTGGGCCATAGAA ARG1 上游：ACATTGGCTTGCGAGACGTA 109 下游：ATCACCTTGCCAATCCCCAG GAPDH 上游：TGTGTCCGTCGTGGATCTGA 150 下游：TTGCTGTTGAAGTCGCAGGAG 注：IL为白细胞介素,iNOS为诱导型一氧化氮合酶,TNF为肿瘤坏死因子,Arg1为精氨酸酶-1,GAPDH为甘油醛-3-磷酸脱氢酶 
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Table 2. 培养12 h后3组RAW264.7细胞M1/M2极化标志因子及炎症因子的mRNA表达量比较（
组别 样本数 TNF-α IL-1β Arg1 iNOS 空白对照组 3 1.01±0.17 1.00±0.09 1.00±0.05 1.00±0.04 单纯LPS 3 85.60±8.87 1648.67±91.95 0.84±0.10 2.46±0.33 LPS+外泌体 3 23.03±3.47 382.33±31.26 1.35±0.07 1.44±0.07 F 190.96 709.92 36.50 44.67 P <0.001 <0.001 <0.001 <0.001 t1 16.51 31.04 2.40 7.70 P1 <0.001 <0.001 0.077 <0.001 t2 11.38 22.58 7.66 5.28 P2 <0.001 <0.001 0.002 0.006 注：对LPS+ADSC外泌体组和单纯LPS组细胞进行组名相应的处理,对空白对照组细胞进行常规培养；LPS为肉毒素/脂多糖,IL为白细胞介素,iNOS为诱导型一氧化氮合酶,TNF为肿瘤坏死因子,Arg1为精氨酸酶-1；F值、P值为组间总体比较所得,t1值、P1值为空白对照组与单纯LPS组各指标比较所得,t2值、P2值为单纯LPS组与LPS+外泌体组各指标比较所得
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