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目的:探讨STAT1(signaltransducerandactivatoroftranscription1)反义寡核苷酸(ASON)对博莱霉素(BLM)致肺纤维化1周大鼠肺泡巨噬细胞(AM)分泌TNF-α、IL-8和NO的影响。方法:取Wistar大鼠5只,向气管内灌注BLM复制肺纤维化模型后7d处死动物,通过支气管肺泡灌洗获取AM,并分为STAT1ASON组、STAT1正义寡核苷酸(SON)组、地塞米松(dexamethasone,DEX)组和空白对照组。分别用ASON、SON和DEX干预AM(空白对照组只加培养基),然后检测AM分泌TNF-α、IL-8和NO的能力。结果:用STAT1ASON处理AM后的培养上清中,TNF-α、IL-8和NO的含量减少,与空白对照组、SON组及DEX组相比较差异显著(P<0.05);DEX组AM的培养上清中,TNF-α、IL-8和NO的含量明显低于空白对照组和SON组(P<0.05);而空白对照组和SON组培养上清中,TNF-α、IL-8和NO的含量却无统计学意义(P>0.05)。结论:STAT1ASON和DEX能使AM分泌TNF-α、IL-8和NO的能力下降,且STAT1ASON的作用强于DEX。STAT1可作为肺纤维化治疗的靶目标。
Objective: To investigate the effect of STAT1 antisense oligonucleotide (ASON) on the secretion of TNF-α, IL-8 and NO by alveolar macrophages (AMs) from 1-week lung fibrosis induced by bleomycin (BLM) influences. Methods: Five Wistar rats were sacrificed and animals were sacrificed 7 days after intratracheal instillation of BLM to induce pulmonary fibrosis. AM was obtained by bronchoalveolar lavage and divided into STAT1ASON group and STAT1 sense oligonucleotide group Dexamethasone (DEX) group and blank control group. AM was administered with ASON, SON and DEX, respectively. The blank control group was supplemented with only medium, and then AM was tested for its ability to secrete TNF-α, IL-8 and NO. Results: The contents of TNF-α, IL-8 and NO in the supernatant of STAT1ASON-treated mice decreased significantly compared with the blank control group, SON group and DEX group (P <0.05) The contents of TNF-α, IL-8 and NO in the culture supernatant were significantly lower than those in the blank control group and the SON group (P <0.05) And NO content was not statistically significant (P> 0.05). Conclusion: STAT1ASON and DEX can decrease the ability of AM to secrete TNF-α, IL-8 and NO, and the effect of STAT1ASON is stronger than that of DEX. STAT1 can be used as a target for the treatment of pulmonary fibrosis.