摘要
目的探讨肿瘤坏死因子-α(TNF-α)对精氨酸加压素(AVP)诱导下大鼠心肌成纤维细胞(CFs)诱导型一氧化氮合酶(iNOS)-一氧化氮(NO)系统活性的影响。方法胰酶消化法分离培养Sprague-Dawley仔鼠CFs,应用硝酸还原酶法、分光光度法和逆转录-聚合酶链式反应(RT-PCR)测定不同浓度TNF-α与AVP联合作用下CFs的NO含量、NOS活性和iNOSmRNA表达。结果AVP诱导CFsiNOSmRNA表达上调,NOS活性提高,NO合成增加。一定浓度下TNF-α可与AVP联合作用,剂量依赖性地增加AVP对CFsiNOS-NO系统活性的提高作用。但当TNF-α浓度过高时,CFs的iNOS-NO系统活性不继续升高,反而有所下降。结论TNF-α可与AVP联合提高CFs的iNOS-NO系统活性,NO合成增加可拮抗TNF-α和AVP的促心脏重构作用。
AIM: To explore the effects of tumor necrosis factor-α (TNF-α) on inducible nitric oxide synthase (iNOS)-nitric oxide (NO) system activity in arginine vasopressin (AVP)-induced rat cardiac fibroblasts (CFs). METHODS: CFs were isolated by trypsin digestion method. Nitrate reductase method, spectrophotometry and reverse transcription-polymerase chain reaction (RT-PCR) were used to detect NO contents, NOS activity and iNOS mRNA expression, respectively. RESULTS: AVP significantly increased iNOS mRNA expression, NOS activity and NO contents in CFs. Combined with AVP, TNF-α enhanced the effects of AVP on iNOS-NO system activity in a concentration-dependent manner. However, if the concentration of TNF-α was too high, the iNOS-NO system activity did not increase accordingly, but slightly decreased instead. CONCLUSION: TNF-α stimulates iNOS-NO system activity in coordination with AVP in CFs. The enhancement of NO contents inhibits ventricular remodeling induced by AVP and TNF-α. [
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2005年第1期81-84,共4页
Chinese Journal of Pathophysiology
