LncRNA PVT1通过靶向miR-145-5p促进H<sub>2</sub>O<sub>2</sub>诱导的心肌细胞H9C2凋亡及氧化应激

doi:10.3877/cma.j.issn.2095-1221.2025.06.004

目的

探究LncRNA浆细胞瘤变异易位1 （PVT1）与miR-145-5p的靶向关系，及其对H₂O₂诱导的心肌细胞H9C2凋亡和氧化应激的影响。

方法

收集急性心肌梗死（AMI）患者（AMI组）和健康体检者（对照组）血清样本，RT-qPCR检测PVT1和miR-145-5p表达水平。培养心肌细胞H9C2，分为：NC组、H₂O₂组、H₂O₂+si-NC组、H₂O₂+si-PVT1组、H₂O₂+si-PVT1+anti-miR-NC组、H₂O₂+si-PVT1+anti-miR-145-5p组。RT-qPCR检测各组H9C2中PVT1和miR-145-5p表达水平；CCK-8、免疫荧光检测H9C2细胞的增殖情况；流式细胞术、AO/EB染色和Caspase-3活性检测H9C2细胞的凋亡情况；DCFH-DA探针法和试剂盒检测H9C2细胞的氧化应激情况；双荧光素酶活性和RIP实验检测H9C2细胞中PVT1和miR-145-5p靶向关系。多组间比较采用单因素方差分析，组间两两比较采用SNK-q检验。利用Pearson相关分析检验变量间相关性。

结果

与对照组比较，AMI组患者中PVT1表达上调（1.80 ± 0.58比1.08 ± 0.34，P < 0.05），miR-145-5p表达下调（0.52 ± 0.16比1.02 ± 0.32，P < 0.05）；并且二者表达呈负相关（r = -0.612，P < 0.05）。PVT1主要定位于细胞质，与NC组比较，H₂O₂处理可上调PVT1表达（2.35 ± 0.49比1.01 ± 0.08，P < 0.05），并促进细胞凋亡，表现为流式凋亡率[（32.16 ± 5.06）%比（5.16 ± 0.45）%，P < 0.05]、AO/EB凋亡率[（40.24 ± 6.16）%比（6.49 ± 0.97）%，P < 0.05]、Caspase-3活性[（70.54 ± 9.16）比（15.98 ± 1.69） U/mL，P < 0.05]的升高，同时氧化应激水平也明显增强，如ROS荧光强度（423.87 ± 45.16比98.33 ± 11.36，P < 0.05）、LDH活性[（375.69 ± 30.16）比（132.56 ± 18.63）U/L，P < 0.05]和MDA含量[（16.98 ± 2.36）比（3.69 ± 0.51） nmol/mL，P < 0.05]均增加。相反，H₂O₂处理抑制miR-145-5p表达（0.25 ± 0.04比1.04 ± 0.06，P < 0.05）和细胞增殖指标能力，具体表现为OD值（0.34 ± 0.06比0.83 ± 0.09，P < 0.05）和Ki67阳性率[（21.09 ± 4.03）%比（68.96 ± 8.65）%，P < 0.05]的下调；敲低PVT1 （H₂O₂+si-PVT1组）可逆转H₂O₂诱导的上述效应（P均< 0.05）；而抑制miR-145-5p （H₂O₂+si-PVT1+anti-miR-145-5p组）则能部分抵消敲低PVT1带来的保护作用，即重新加剧细胞凋亡和氧化应激，并抑制增殖（P均< 0.05）。双荧光素酶和RIP实验证实PVT1可靶向结合miR-145-5p （P < 0.05）。

结论

PVT1通过靶向负调控miR-145-5p，促进H₂O₂诱导的心肌细胞H9C2凋亡和氧化应激。

关键词: LncRNA PVT1, miR-145-5p, H₂O₂, 心肌细胞, 凋亡, 氧化应激

Objective

To investigate the targeting relationship between LncRNA Plasmacytoma Variant Translocation 1 (PVT1) and miR-145-5p, and its effects on H₂O₂-induced apoptosis and oxidative stress in H9C2 cardiomyocytes.

Methods

Serum samples were collected from patients with acute myocardial infarction (AMI) (AMI group) and healthy individuals (control group). RT-qPCR were used to detect the expression levels of PVT1 and miR-145-5p. H9C2 cardiomyocytes were cultured and divided into NC group, H₂O₂ group, H₂O₂+si-NC group, H₂O₂+si-PVT1 group, H₂O₂+si-PVT1+anti-miR-NC group, and H₂O₂+si-PVT1+anti-miR-145-5p group. RT-qPCR was used to detect the expression levels of PVT1 and miR-145-5p in H9C2 of each group. CCK-8 and immunofluorescence were used to detect the proliferation ability of H9C2 cells in each group. Flow cytometry, AO/EB staining, and Caspase-3 activity were used to assess apoptosis of H9C2 cells in each group. The DCFH-DA probe method and reagent kit were used to measure the oxidative stress of H9C2 cells in each group. In addition, dual luciferase activity and RIP assay were used to detect the targeting relationship between PVT1 and miR-145-5p in H9C2 cells. One-way analysis of variance was used for comparisons among multiple groups, and SNK-q test was used for pairwise comparisons between groups. Pearson correlation analysis was used to examine the correlations between variables.

Results

Compared to the control group, the expression level of PVT1 was significantly up regulated (1.80 ± 0.58 vs 1.08 ± 0.34, P < 0.05) in AMI patients, while the expression level of miR-145-5p was significantly downregulated (0.52 ± 0.16 vs 1.02 ± 0.32, P < 0.05), and the expression of PVT1 and miR-145-5p were negatively correlated (r = -0.612, P < 0.05). PVT1 is primarily localized in the cytoplasm. Compared to the NC group, H₂O₂ treatment could significantly up-regulated the expression of PVT1 (2.35 ± 0.49 vs 1.01 ± 0.08, P < 0.05), cell apoptosis rate[ (32.16 ± 5.06) %vs (5.16 ± 0.45) %, P < 0.05], AO/EB apoptosis rate[ (40.24 ± 6.16) %vs (6.49 ± 0.97) %, P < 0.05], Caspase-3 activity [ (70.54 ± 9.16) vs (15.98 ± 1.69) U/mL, P < 0.05]and enhance the oxidative stress levels, including a significant increase in ROS fluorescence intensity (423.87 ± 45.16 vs 98.33 ± 11.36, P < 0.05), LDH activity[ (375.69 ± 30.16) vs (132.56 ± 18.63) U/L, P < 0.05], and MDAcontent [ (16.98 ± 2.36) vs (3.69 ± 0.51) nmol/mL, P < 0.05]. Conversely, H₂O₂ treatment significantly inhibited miR-145-5p expression (0.25 ± 0.04 vs 1.04 ± 0.06, P < 0.05) and cell proliferation capacity, specifically manifested as decreased OD value (0.34 ± 0.06 vs 0.83 ± 0.09, P < 0.05) and Ki67 positive rate [ (21.09 ± 4.03) % vs (68.96 ± 8.65) %, P < 0.05]. Knocking down PVT1 (H₂O₂+si-PVT1 group) reversed the effects induced by H₂O₂ (all P < 0.05). In contrast, inhibiting miR-145-5p (H₂O₂+si-PVT1+anti-miR-145-5p group) partially counteracted the protective effect conferred by PVT1 knockdown, thereby re-aggravating apoptosis and oxidative stress, and suppressing proliferation (all P < 0.05). Dual-luciferase and RIP assays confirmed that PVT1 can directly target and bind to miR-145-5p (P < 0.05) .

Conclusion

PVT1 promotes H₂O₂-induced apoptosis and oxidative stress in H9C2 cardiomyocytes by targeting and negatively regulating miR-145-5p.

Key words: LncRNA PVT1, miR-145-5p, H₂O₂, Cardiomyocytes, Apoptosis, Oxidative stress

表1 引物序列信息

基因	序列（5'→3'）	预期扩增产物长度（bp）
PVT1	上游TGGAATGTAAGACCCCGACTCT	154
	下游GATGGCTGTATGTGCCAAGGT
β-actin	上游CTGGGACGACATGGAGAAAA	146
	下游AAGGAAGGCTGGAAGAGTGC
miR-145-5p	上游GTCCAGTTTTCCCAGGAATC	96
	下游GATTCCTGGGAAAACTGGAC
U6	上游GCTTCGGCAGCACATATACTAAAAT	83
	下游CGCTTCACGAATTTGCGTGTCAT
GAPDH	上游GGCATCGTGGAGGGACTTATG	186
	下游GCCAGTGAGCTTCCCGTTGAG

表1 引物序列信息

基因	序列（5'→3'）	预期扩增产物长度（bp）
PVT1	上游TGGAATGTAAGACCCCGACTCT	154
	下游GATGGCTGTATGTGCCAAGGT
β-actin	上游CTGGGACGACATGGAGAAAA	146
	下游AAGGAAGGCTGGAAGAGTGC
miR-145-5p	上游GTCCAGTTTTCCCAGGAATC	96
	下游GATTCCTGGGAAAACTGGAC
U6	上游GCTTCGGCAGCACATATACTAAAAT	83
	下游CGCTTCACGAATTTGCGTGTCAT
GAPDH	上游GGCATCGTGGAGGGACTTATG	186
	下游GCCAGTGAGCTTCCCGTTGAG

图1 Pearson法分析AMI患者PVT1与miR-145-5p相关性注：PVT1为浆细胞瘤变异易位1；AMI为急性心肌梗死

图2 PVT1的亚细胞定位分析结果注：PVT1为浆细胞瘤变异易位1

表2 H9C2细胞中PVT1、miR-145-5p表达水平比较（

± s，n = 3）

分组	PVT1	miR-145-5p
NC组	1.01 ± 0.08	1.04 ± 0.06
H₂O₂组	5.35 ± 0.49^a	0.25 ± 0.04^a
H₂O₂+si-NC组	5.51 ± 0.56	0.23 ± 0.03
H₂O₂+si-PVT1组	1.59 ± 0.14^b	0.65 ± 0.09^b
H₂O₂+si-PVT1+anti-miR-NC组	1.67 ± 0.21	0.70 ± 0.10
H₂O₂+si-PVT1+anti-miR-145-5p组	1.78 ± 0.13	0.44 ± 0.08^c
F值	23.465	56.127
P值	< 0.001	< 0.001

表2 H9C2细胞中PVT1、miR-145-5p表达水平比较（

± s，n = 3）

分组	PVT1	miR-145-5p
NC组	1.01 ± 0.08	1.04 ± 0.06
H₂O₂组	5.35 ± 0.49^a	0.25 ± 0.04^a
H₂O₂+si-NC组	5.51 ± 0.56	0.23 ± 0.03
H₂O₂+si-PVT1组	1.59 ± 0.14^b	0.65 ± 0.09^b
H₂O₂+si-PVT1+anti-miR-NC组	1.67 ± 0.21	0.70 ± 0.10
H₂O₂+si-PVT1+anti-miR-145-5p组	1.78 ± 0.13	0.44 ± 0.08^c
F值	23.465	56.127
P值	< 0.001	< 0.001

图3 荧光显微镜下观察H9C2细胞的Ki67免疫荧光染色结果（DAPI，×400）

图4 流式细胞术检测H9C2细胞的凋亡率

图5 荧光显微镜下观察H9C2细胞的AO/EB染色结果（×200）

表3 H9C2细胞的OD值、Ki67阳性率、流式凋亡率、AO/EB凋亡率和Caspase-3活性比较（

± s，n = 3）

分组	OD值	Ki67阳性率（%）	流式凋亡率（%）	AO/EB凋亡率（%）	Caspase-3活性（U/mL）
NC组	0.83 ± 0.09	68.96 ± 8.65	5.16 ± 0.45	6.49 ± 0.97	15.98 ± 1.69
H₂O₂组	0.34 ± 0.06^a	21.09 ± 4.03^a	32.16 ± 5.06^a	40.24 ± 6.16^a	70.54 ± 9.16^a
H₂O₂+si-NC组	0.38 ± 0.05	23.64 ± 5.62	34.69 ± 4.19	43.98 ± 5.87	78.62 ± 10.01
H₂O₂+si-PVT1组	0.65 ± 0.07^b	43.18 ± 5.19^b	12.69 ± 2.54^b	16.06 ± 1.65^b	28.98 ± 3.65^b
H₂O₂+si-PVT1+anti-miR-NC组	0.64 ± 0.04	45.69 ± 4.68	13.54 ± 2.36	17.15 ± 2.14	30.19 ± 3.69
H₂O₂+si-PVT1+anti-miR-145-5p组	0.44 ± 0.07^c	31.09 ± 4.19^c	25.62 ± 3.16^c	29.65 ± 3.19^c	52.64 ± 5.62^c
F值	25.528	30.071	39.000	43.450	78.080
P值	< 0.001	< 0.001	< 0.001	< 0.001	< 0.001

表3 H9C2细胞的OD值、Ki67阳性率、流式凋亡率、AO/EB凋亡率和Caspase-3活性比较（

± s，n = 3）

分组	OD值	Ki67阳性率（%）	流式凋亡率（%）	AO/EB凋亡率（%）	Caspase-3活性（U/mL）
NC组	0.83 ± 0.09	68.96 ± 8.65	5.16 ± 0.45	6.49 ± 0.97	15.98 ± 1.69
H₂O₂组	0.34 ± 0.06^a	21.09 ± 4.03^a	32.16 ± 5.06^a	40.24 ± 6.16^a	70.54 ± 9.16^a
H₂O₂+si-NC组	0.38 ± 0.05	23.64 ± 5.62	34.69 ± 4.19	43.98 ± 5.87	78.62 ± 10.01
H₂O₂+si-PVT1组	0.65 ± 0.07^b	43.18 ± 5.19^b	12.69 ± 2.54^b	16.06 ± 1.65^b	28.98 ± 3.65^b
H₂O₂+si-PVT1+anti-miR-NC组	0.64 ± 0.04	45.69 ± 4.68	13.54 ± 2.36	17.15 ± 2.14	30.19 ± 3.69
H₂O₂+si-PVT1+anti-miR-145-5p组	0.44 ± 0.07^c	31.09 ± 4.19^c	25.62 ± 3.16^c	29.65 ± 3.19^c	52.64 ± 5.62^c
F值	25.528	30.071	39.000	43.450	78.080
P值	< 0.001	< 0.001	< 0.001	< 0.001	< 0.001

图6 荧光显微镜下观察DCFH-DA探针法检测的H9C2细胞的ROS荧光强度（×200）

表4 H9C2细胞的ROS荧光强度、LDH活性和MDA含量比较（

± s，n = 3）

分组	ROS荧光强度	LDH活性（U/L）	MDA含量（nmol/mL）
NC组	98.33 ± 11.36	132.56 ± 18.63	3.69 ± 0.51
H₂O₂组	423.87 ± 45.16^a	375.69 ± 30.16^a	16.98 ± 2.36^a
H₂O₂+si-NC组	439.69 ± 40.14	391.65 ± 33.65	18.36 ± 3.19
H₂O₂+si-PVT1组	178.62 ± 18.97^b	198.62 ± 18.65^b	6.54 ± 0.68^b
H₂O₂+si-PVT1+anti-miR-NC组	192.63 ± 22.36	201.36 ± 20.03	7.06 ± 0.85
H₂O₂+si-PVT1+anti-miR-145-5p组	297.65 ± 25.95^c	289.36 ± 22.19^c	10.19 ± 1.34^c
F值	65.741	54.422	33.704
P值	< 0.001	< 0.001	< 0.001

表4 H9C2细胞的ROS荧光强度、LDH活性和MDA含量比较（

± s，n = 3）

分组	ROS荧光强度	LDH活性（U/L）	MDA含量（nmol/mL）
NC组	98.33 ± 11.36	132.56 ± 18.63	3.69 ± 0.51
H₂O₂组	423.87 ± 45.16^a	375.69 ± 30.16^a	16.98 ± 2.36^a
H₂O₂+si-NC组	439.69 ± 40.14	391.65 ± 33.65	18.36 ± 3.19
H₂O₂+si-PVT1组	178.62 ± 18.97^b	198.62 ± 18.65^b	6.54 ± 0.68^b
H₂O₂+si-PVT1+anti-miR-NC组	192.63 ± 22.36	201.36 ± 20.03	7.06 ± 0.85
H₂O₂+si-PVT1+anti-miR-145-5p组	297.65 ± 25.95^c	289.36 ± 22.19^c	10.19 ± 1.34^c
F值	65.741	54.422	33.704
P值	< 0.001	< 0.001	< 0.001

图7 Starbase网站预测PVT1与miR-145-5p靶向互补位点注：PVT1为浆细胞瘤变异易位1

表5 双荧光素酶报告基因实验检测H9C2细胞的相对荧光素酶活性（

± s，n = 3）

分组	PVT1-WT	PVT1-MUT
NC mimic组	1.02 ± 0.04	0.98 ± 0.07
miR-145-5p mimic组	0.42 ± 0.06	1.03 ± 0.08
t值	14.412	0.815
P值	< 0.001	0.461

表5 双荧光素酶报告基因实验检测H9C2细胞的相对荧光素酶活性（

± s，n = 3）

分组	PVT1-WT	PVT1-MUT
NC mimic组	1.02 ± 0.04	0.98 ± 0.07
miR-145-5p mimic组	0.42 ± 0.06	1.03 ± 0.08
t值	14.412	0.815
P值	< 0.001	0.461

表6 RIP实验检测PVT1与miR-145-5p的靶向结合关系（

± s，n = 3）

分组	PVT1	miR-145-5p
IgG组	1.05 ± 0.09	1.04 ± 0.05
Ago2组	7.03 ± 0.98	8.10 ± 0.97
t值	10.525	12.590
P值	< 0.001	< 0.001

表6 RIP实验检测PVT1与miR-145-5p的靶向结合关系（

± s，n = 3）

分组	PVT1	miR-145-5p
IgG组	1.05 ± 0.09	1.04 ± 0.05
Ago2组	7.03 ± 0.98	8.10 ± 0.97
t值	10.525	12.590
P值	< 0.001	< 0.001

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LncRNA PVT1 promotes H₂O₂-induced apoptosis and oxidative stress in H9C2 cardiomyocytes by targeting miR-145-5p

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LncRNA PVT1 promotes H2O2-induced apoptosis and oxidative stress in H9C2 cardiomyocytes by targeting miR-145-5p

LncRNA PVT1 promotes H₂O₂-induced apoptosis and oxidative stress in H9C2 cardiomyocytes by targeting miR-145-5p