摘要
探讨气道平滑肌细胞（ＡＳＭＣ）自分泌的内皮素（ＥＴ）是否介导了吸烟对ＡＳＭＣ的作用。方法在体外培养的家兔ＡＳＭＣ上加入香烟烟雾提取物（ＣＩＳＥ）测定细胞存活率，乳酸脱氢酶（ＬＤＨ）水平，并用Ｈ－ＴｄＲ掺入法及放射免疫方法观察ＣＳＥ对ＡＳＭＣ的增殖作用，及对ＥＴ－１释放的影响。用３Ｈ－ＴｄＲ掺入实验，观察低浓度（５％）ＣＳＥ对ＡＳＭＣ增殖的影响及与ＥＴ的关系。结果１０％和３０％ＣＳＥ对ＡＳＭＣ呈现明显毒性作用，表现为细胞存活率降低，脂质过氧化终产物丙二醛（ＭＤＡ）含量增加和细胞ＬＤＨ漏出随时间进行性增加。５％ＣＳＥ呈时间依赖地刺激ＡＳＭＣ释放ＥＴ－１并促进ＡＳＭＣ（３Ｈ－ＴｄＲ）掺入（较对照组增加５９．９％，Ｐ＜０．０１）。内皮素Ａ受体（ＥＴＡ受体）拮抗剂ＪＫＣ－３０１呈浓度依赖地抑制５％ＣＳＥ促ＡＳＭＣ增殖作用。
Objective To investigate whether the effect of smoking on airway smooth muscle cells(ASMC)ismediated by the autocrine action of endothelin 1(ET 1).Methods Abbit ASMC was cultured exposed to cigarette smoke extract(CSE),we examined the mitogenic effect of CSE on ASMC in vitro and whether the ET Areceptor antagonist JKC 301can inhibit this effect.Results The exposure of ASMC to 10% and 30% CSE resulted in obvious cytotoxity.The viability of ASMC was decreased,the lipid peroxides(MDA)formation was increased,and the release of lactate dehydrogenase(LDH)in to supernatant was enhanced.5% CSE signifficantly enhanced the cultured ASMC thymidine( 3H-TdR)incorporation by59.9%( P <0.01)over control.The ASMC proliferative response to 5% CSE was dose dependently inhibited by JKC 301.Moreover,5% CSE evoked time dependent release of endogenous ET 1from ASMC.Conclusion These data demonstrate that 5% CSE mediates ASMC proliferation via release and autocrine mitogenic action of ET 1.
出处
《中华医学杂志》
CAS
CSCD
北大核心
1997年第3期201-204,共4页
National Medical Journal of China
