人诱导多能干细胞来源外泌体对肾缺血再灌注损伤保护作用研究

doi:10.3877/cma.j.issn.1674-3903.2025.06.006

目的

探讨人诱导多能干细胞(hiPSCs)来源外泌体(Exo)对肾缺血再灌注损伤(IRI)的影响。

方法

培养hiPSCs，收集上清液超速离心提取外泌体，蛋白质印迹法(WB)检测外泌体特异性标志物(CD9、CD63和CD81)以及阴性指标Calnexin蛋白表达，通过透射电镜观察其形态、纳米粒径分析检测粒径大小，对外泌体进行鉴定。将SD大鼠随机分为假手术组、IRI组、IhiPSCs组和IhiPSCs-Exo组，每组各6只。IRI后48 h行血清肌酐(Scr)、血尿素氮(BUN)测定及肾组织切片HE染色，并进行改良Paller肾小管损伤评分。实时荧光定量聚合酶链反应测定IL-1β、TNF-α、SOD2和Nrf-2表达，免疫组化测定CD163、CD168、α-SMA、COL-1和FN-1表达，WB测定p-MEK1/2、p-ERK1/2、Caspase-3、Bcl-2和Bax表达。以人肾小管上皮细胞(HK-2细胞)为基础设立缺氧/复氧(H/R)组和H/R＋hiPSCs-Exo组，CCK-8测定增殖差异，Annexin V-FITC/PI测定凋亡差异，WB测定Caspase-3、Bcl-2和Bax的表达。组间比较采用单因素方差分析，进一步两两比较采用Tukey HSD检验。P<0.05为差异具有统计学意义。

结果

外泌体具有双层膜结构，呈典型杯状形态，平均粒径为(88.0±0.6)nm，表达标志蛋白CD9、CD63和CD81。体内实验结果显示，与IRI组比较，IhiPSCs组和ihiPSCs-Exo组Scr、BUN和改良Paller肾小管损伤评分降低，IL-1β、TNF-α水平下降，SOD2、Nrf-2水平升高；免疫组化染色显示，与IRI组比较，IhiPSCs组和IhiPSCs-Exo组CD68、α-SMA、COL-1和FN-1表达量均降低，CD163表达量升高，P-MEK1/2、P-ERK1/2、Caspase-3和Bax蛋白相对表达量均降低，Bcl-2相对表达量升高(P均<0.05)。体外实验显示，与H/R组比较，H/R＋hiPSCs-Exo组HK-2细胞增殖能力提高，凋亡细胞和坏死细胞减少，Caspase-3、Bax蛋白表达量下降，Bcl-2表达量升高。

结论

hiPSCs来源外泌体可通过抑制氧化应激、炎症因子表达和凋亡等多种途径，发挥对肾IRI的保护作用，通过抑制MEK/ERK途径改善肾IRI。

关键词: 人诱导多能干细胞, 外泌体, 大鼠, 肾缺血再灌注损伤, 保护作用

Objective

To investigate the effects of exosomes (Exo) derived from human induced pluripotent stem cells (hiPSCs) on renal ischemia-reperfusion injury (IRI).

Methods

HiPSCs were cultured, and Exo were isolated from the supernatant by ultracentrifugation. The isolated Exo were characterized by detecting the specific markers CD9, CD63, CD81 and the negative marker Calnexin via Western blot (WB), observing their morphology by transmission electron microscopy, and analyzing particle size via nanoparticle tracking analysis. SD rats were randomly assigned to four groups (n=6 per group): sham-operated group, IRI group, IhiPSCs group, and IhiPSCs-Exo group. At 48 hours post-intervention, serum creatinine (Scr) and blood urea nitrogen (BUN) levels were measured, and renal pathological sections were stained with hematoxylin and eosin for evaluation using a modified Paller tubular injury score. The mRNA expression levels of IL-1β, TNF-α, SOD-2, and Nrf-2 were determined by quantitative real-time polymerase chain reaction. The protein expression of CD163, CD68, α-SMA, COL-1, and FN-1 was assessed by immunohistochemistry. WB was performed to determine the protein expression levels of p-MEK1/2, p-ERK1/2, Caspase-3, Bcl-2, and Bax. Using human renal tubular epithelial cells (HK-2 cells), a hypoxia/reoxygenation (H/R) model was established, including H/R group and H/R + hiPSCs-Exo group. Cell proliferation was measured by CCK-8 assay, apoptosis was detected by Annexin V-FITC/PI staining, and the expression of Caspase-3, Bcl-2, and Bax was analyzed by WB. One-way analysis of variance was used for comparisons between groups, and further pairwise comparisons were conducted using the Tukey HSD test, with a P value <0.05 considered statistically significant.

Results

The isolated Exo exhibited a typical cup-shaped morphology with a double-membrane structure, an average particle size of (88.0±0.6) nm, and expressed the specific marker proteins CD9, CD63, and CD81. In vivo experiments showed that compared with the IRI group, the IhiPSCs group and IhiPSCs-Exo group exhibited significantly lower levels of Scr, BUN, and modified Paller tubular injury scores (all P<0.05). Furthermore, these groups showed decreased mRNA levels of IL-1β and TNF-α, increased mRNA levels of SOD-2 and Nrf-2, reduced protein expression of CD68, α-SMA, COL-1, and FN-1 by immunohistochemistry, and elevated protein expression of CD163 (all P<0.05). WB analysis revealed that compared with the IRI group, the relative protein expression levels of p-MEK1/2, p-ERK1/2, Caspase-3, and Bax were decreased, while the expression of Bcl-2 was increased in the IhiPSCs group and IhiPSCs-Exo group (all P<0.05). In vitro experiments demonstrated that compared with the H/R group, the hiPSCs-Exo group showed enhanced HK-2 cell proliferation, reduced numbers of apoptotic and necrotic cells, decreased protein expression of Caspase-3 and Bax, and increased expression of Bcl-2.

Conclusions

Exo derived from hiPSCs exert a protective effect against renal IRI through multiple pathways, including the suppression of oxidative stress, inflammatory factor expression, and apoptosis. This protective effect is associated with the inhibition of the MEK/ERK signaling pathway.

Key words: Human induced pluripotent stem cells, Exosomes, Mouse, Renal ischemia-reperfusion injury, Protective effects

图1 人诱导多能干细胞来源外泌体的鉴定注：a．透射电镜下外泌体形态；b．外泌体粒径区间检测；c．蛋白质印迹法检测外泌体标志物；hiPSCs.人诱导多能干细胞；hiPSCs-Exo.人诱导多能干细胞来源外泌体；GAPDH.甘油醛-3-磷酸脱氢酶

表1 假手术组、IRI组、IhiPSCs组和IhiPSCs-Exo组大鼠肾IRI后48 h血清肌酐、血尿素氮水平和改良Paller肾小管损伤评分(

±s)

组别	数量(只)	血清肌酐(μmol/L)	血尿素氮(mmol/L)	改良Paller肾小管损伤评分(分)
假手术组	6	83.4±22.6	8.31±0.63	1.32±0.39
IRI组	6	462.0±33.2^a	40.28±1.34^a	15.04±1.47^a
IhiPSCs组	6	176.7±19.8^ab	22.51±2.78^ab	7.49±1.13^ab
IhiPSCs-Exo组	6	221.6±29.3^abc	29.36±3.73^abc	9.23±0.96^abc

表1 假手术组、IRI组、IhiPSCs组和IhiPSCs-Exo组大鼠肾IRI后48 h血清肌酐、血尿素氮水平和改良Paller肾小管损伤评分(

±s)

组别	数量(只)	血清肌酐(μmol/L)	血尿素氮(mmol/L)	改良Paller肾小管损伤评分(分)
假手术组	6	83.4±22.6	8.31±0.63	1.32±0.39
IRI组	6	462.0±33.2^a	40.28±1.34^a	15.04±1.47^a
IhiPSCs组	6	176.7±19.8^ab	22.51±2.78^ab	7.49±1.13^ab
IhiPSCs-Exo组	6	221.6±29.3^abc	29.36±3.73^abc	9.23±0.96^abc

图2 IRI后48 h各组大鼠肾脏病理学改变(HE ×200)注：a、b、c、d分别为假手术组、IRI组、IhiPSCs组和IhiPSCs-Exo组；IRI.缺血再灌注损伤；hiPSCs.人诱导多能干细胞；hiPSCs-Exo.人诱导多能干细胞来源外泌体

表2 假手术组、IRI组和IhiPSCs-Exo组大鼠肾IRI后48 h各标志物阳性细胞面积比(%，

±s)

组别	数量(只)	CD163	CD68	α-SMA	COL-1	FN-1
假手术组	6	9.68±0.97	0.46±0.19	0.96±0.27	0.45±0.16	0.50±0.28
IRI组	6	0.94±0.15^a	15.23±1.32^a	11.60±0.50^a	9.07±0.42^a	28.26±1.21^a
IhiPSCs-Exo组	6	4.07±0.71^ab	7.50±0.68^ab	6.08±0.31^ab	4.82±0.25^ab	13.90±0.93^ab

表2 假手术组、IRI组和IhiPSCs-Exo组大鼠肾IRI后48 h各标志物阳性细胞面积比(%，

±s)

组别	数量(只)	CD163	CD68	α-SMA	COL-1	FN-1
假手术组	6	9.68±0.97	0.46±0.19	0.96±0.27	0.45±0.16	0.50±0.28
IRI组	6	0.94±0.15^a	15.23±1.32^a	11.60±0.50^a	9.07±0.42^a	28.26±1.21^a
IhiPSCs-Exo组	6	4.07±0.71^ab	7.50±0.68^ab	6.08±0.31^ab	4.82±0.25^ab	13.90±0.93^ab

图3 IRI后48 h蛋白质印迹法检测各组大鼠肾脏凋亡蛋白表达水平注：IRI.缺血再灌注损伤；hiPSCs.人诱导多能干细胞；hiPSCs-Exo.人诱导多能干细胞来源外泌体；p-ERK.磷酸化细胞外信号调节激酶；p-MEK.人磷酸化MEK激酶；Caspase-3.胱天蛋白酶3; GAPDH.甘油醛-3-磷酸脱氢酶

表3 假手术组、IRI组、IhiPSCs组和IhiPSCs-Exo组大鼠肾IRI后48 h肾脏炎症因子表达水平(%，

±s)

组别	数量(只)	TNF-α	IL-1β	SOD-2	Nrf2
假手术组	6	2.38±0.33	1.95±0.45	14.79±0.57	17.51±0.52
IRI组	6	18.72±0.42^a	19.43±0.38^a	3.06±0.64^a	4.63±0.36^a
IhiPSCs组	6	11.26±0.82^ab	12.65±0.63^ab	8.71±0.71^ab	7.91±0.39^ab
IhiPSCs-Exo组	6	13.89±0.99^abc	14.07±0.39^abc	7.35±0.32^abc	6.80±0.50^abc

表3 假手术组、IRI组、IhiPSCs组和IhiPSCs-Exo组大鼠肾IRI后48 h肾脏炎症因子表达水平(%，

±s)

组别	数量(只)	TNF-α	IL-1β	SOD-2	Nrf2
假手术组	6	2.38±0.33	1.95±0.45	14.79±0.57	17.51±0.52
IRI组	6	18.72±0.42^a	19.43±0.38^a	3.06±0.64^a	4.63±0.36^a
IhiPSCs组	6	11.26±0.82^ab	12.65±0.63^ab	8.71±0.71^ab	7.91±0.39^ab
IhiPSCs-Exo组	6	13.89±0.99^abc	14.07±0.39^abc	7.35±0.32^abc	6.80±0.50^abc

图4 CCK-8实验检测hiPSCs-Exo处理后HK-2细胞增殖情况注：H/R.缺氧/复氧；hiPSCs-Exo.人诱导多能干细胞来源外泌体

图5 Annexin V-FITC/PI染色检测HK-2细胞凋亡情况注：H/R.缺氧/复氧；hiPSCs-Exo.人诱导多能干细胞来源外泌体

图6 IRI后48 h蛋白质印迹法检测凋亡蛋白表达水平差异注：IRI.缺血再灌注损伤；H/R.缺氧/复氧；hiPSCs-Exo.人诱导多能干细胞来源外泌体；p-ERK.磷酸化细胞外信号调节激酶；p-MEK.人磷酸化MEK激酶；Caspase-3.胱天蛋白酶3; GAPDH.甘油醛-3-磷酸脱氢酶

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Protective effects of exosomes derived from human induced pluripotent stem cells on renal ischemia-reperfusion injury

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Protective effects of exosomes derived from human induced pluripotent stem cells on renal ischemia-reperfusion injury