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目的研究烟雾暴露大鼠在体应用结缔组织生长因子(CTGF)反义寡核苷酸(ASON)对肺血管重塑的影响,探讨 CTGF 在烟雾暴露致肺血管重塑中的作用。方法 35只大鼠按随机数字表法分为正常对照组(A 组)、烟雾暴露1个月组(B 组)、烟雾暴露+大剂量 CTGF ASON 1个月组(C组)、烟雾暴露+小剂量 CTGF ASON 1个月组(D 组)、烟雾暴露2个月组(E 组)、烟雾暴露+大剂量CTGF ASON 2个月组(F 组)、烟雾暴露+小剂量 CTGF ASON 2个月组(G 组),每组5只。用苏木精-伊红(HE)染色观察肺血管重塑;用免疫组化法观察 CTGF 在肺动脉中的表达;用逆转录-聚合酶链反应(RT-PCR)检测肺动脉 CTGF mRNA 表达。采用 SPSS 12.0软件,数据以±s表示,组间差异显著性检验采用方差分析,两两比较采用 q 检验,相关分析采用直线回归法,P<0.05为差异有统计学意义。结果 (1)A 组肺动脉管壁面积/管总面积(WA%)为(28.6±1.2)%、B 组为(42.5±2.3)%、C组为(33.7±1.8)%、D 组为(42.1±2.4)%、E 组为(49.6±2.1)%、F 组为(34.3±1.9)%、G 组为(38.4±2.0)%。C 组与 B 组比较差异有统计学意义(q=5.09,P<0.01),F、G 组与 E 组比较差异均有统计学意义(q 值分别为8.15、3.75,P 均<0.05);(2)A 组肺动脉平滑肌 CTGF 蛋白表达吸光度(A)值为0.098±0.015、B 组为0.159±0.023、C 组为0.118±0.017、D 组为0.153±0.022、E 组为0.406±0.036、F 组为0.109±0.012、G 组为0.146±0.024。C 组与 B 组比较差异有统计学意义(q=3.26,P<0.05),F、G 组与 E 组比较差异均有统计学意义(q 值分别为67.08、18.09,P 均<0.01);(3)A 组肺动脉 CTGF mRNA 表达为0.051±0.010、B 组为0.823±0.096、C 组为0.216±0.056、D 组为0.810±0.085、E 组为2.452±0.267、F 组为0.207±0.062、G 组为0.509±0.067。C 组与 B 组比较差异有统计学意义(q=53.50,P<0.01),F、G 组与 E 组比较差异均有统计学意义(q 值分别为132.22、93.70,P 均<0.01)。结论应用 CTGF ASON 可显著降低烟雾暴露诱导的大鼠肺血管重塑,CTGF 可能在肺动脉高压的发生、发展中起重要作用。
Objective To investigate the effect of CTGF antisense oligonucleotide (ASON) on pulmonary vascular remodeling in smog-exposed rats and to explore the role of CTGF in pulmonary vascular remodeling induced by smoke exposure. Methods 35 rats were randomly divided into normal control group (group A), smoke exposure for 1 month (group B), smoke exposure + high dose CTGF ASON for 1 month (group C), smoke exposure + Low dose CTGF ASON 1 month group (group D), smoke exposure 2 month group (group E), smoke exposure + high dose CTGF ASON 2 month group (group F), smoke exposure + low dose CTGF ASON 2 months Group (G group), each group of five. Pulmonary vascular remodeling was observed by hematoxylin-eosin (HE) staining. The expression of CTGF in pulmonary arteries was observed by immunohistochemistry. The expression of CTGF mRNA in pulmonary arteries was detected by reverse transcription-polymerase chain reaction (RT-PCR). Using SPSS 12.0 software, the data to ± s said significant differences between groups using analysis of variance, comparison of two by q test, correlation analysis using linear regression, P <0.05 was considered statistically significant. Results (1) The pulmonary wall area / total vessel area (WA%) in group A was (28.6 ± 1.2)%, in group B was (42.5 ± 2.3)%, in group C was (33.7 ± 1.8)%, in group D 42.1 ± 2.4)% in group E, (49.6 ± 2.1)% in group E, (34.3 ± 1.9)% in group F and (38.4 ± 2.0)% in group G, respectively. There was significant difference between group C and group B (q = 5.09, P <0.01). There was significant difference between group F and group G and group E (q = 8.15 and 3.75, P <0.05 respectively). (2) The expression of CTGF protein in group A was 0.098 ± 0.015, in group B was 0.159 ± 0.023, in group C was 0.118 ± 0.017, in group D was 0.153 ± 0.022, in group E was 0.406 ± 0.036, and in group F Was 0.109 ± 0.012, G group was 0.146 ± 0.024. There was significant difference between group C and group B (q = 3.26, P <0.05). There was significant difference between group F and group G and group E (q = 67.08 and 18.09, P <0.01 respectively). (3) The expression of CTGF mRNA in group A was 0.051 ± 0.010, group B was 0.823 ± 0.096, group C was 0.216 ± 0.056, group D was 0.810 ± 0.085, group E was 2.452 ± 0.267, group F was 0.207 ± 0.062, G Group was 0.509 ± 0.067. The difference between group C and group B was statistically significant (q = 53.50, P <0.01). There was significant difference between group F and group G and group E (q = 132.22, 93.70, P <0.01 respectively). Conclusions Application of CTGF ASON can significantly reduce pulmonary vascular remodeling induced by smoke exposure. CTGF may play an important role in the occurrence and development of pulmonary hypertension.