TSLP在吸烟相关慢性阻塞性肺疾病患者中表达的意义

Significance of TSLP expression in patients with smoking-related chronic obstructive pulmonary disease

目的观察炎性蛋白胸腺基质淋巴细胞生成素(TSLP)在COPD患者气道中的表达情况,结合核增殖抗原Ki-67及胶原蛋白等指标,探讨TSLP在COPD患者肺组织细胞增生及胶原蛋白沉积等纤维化改变中的相关意义。方法收集10例COPD患者手术获得的肺组织病理标本,包括吸烟COPD患者1例、非吸烟COPD患者1例、吸烟肺功能正常患者3例、非吸烟肺功能正常患者5例。采用免疫组织化学染色法分析吸烟相关COPD患者肺组织TSLP、Ki-67的表达分布,苏木素-伊红染色、Masson三色染色显示肺组织胶原蛋白等结构,分析TSLP与气道病理改变的关系。结果与非吸烟肺功能正常者比较,吸烟肺功能正常者存在呼吸性末端细支气管断裂及伴行血管平滑肌增厚、胶原蛋白沉积等改变;非吸烟COPD患者肺泡腔扩大、撕裂断开,伴行小血管动脉管腔饱胀,被牵扯变形;吸烟COPD患者增厚的呼吸性气道上皮被撕裂,存在团状聚集断裂等结构形态的变化。吸烟肺功能正常者的TSLP总光密度、胶原蛋白总光密度、Ki-67均比其他3组升高(P<0.008或0.01)。吸烟COPD者的TSLP总光密度、胶原蛋白总光密度、Ki-67阳性细胞数均比非吸烟COPD者升高(P<0.008或0.01),其TSLP总光密度高于非吸烟肺功能正常者、胶原蛋白总光密度低于非吸烟肺功能正常者(P均<0.008或0.01)。非吸烟COPD者胶原蛋白总光密度低于非吸烟肺功能正常者(P<0.01)。人肺组织中TSLP的总光密度与胶原蛋白总光密度(rs=0.547,P<0.01)及Ki-67阳性细胞数(rs=0.808,P<0.01)呈正相关,胶原蛋白光密度与Ki-67阳性细胞数也呈正相关(rs=0.620,P<0.01)。结论 TSLP可能与吸烟相关COPD发病中的肺组织细胞增生及胶原蛋白沉积有关,在吸烟相关COPD肺组织细胞增生及纤维化改变中有一定临床意义,这为COPD的临床分型及个体化治疗提供了新的靶点。

Objective To investigate the effect and mechanism of nanoscale hydroxyapatite （nHAP）upon the growth of ovarian cancer cell line SKOV3. Metliods The ovarian cancer cell tured. The 30%-, 50%- and 70%-inhibitory concentrations （IC3., IC5.and IC7.） of nHAP upon the ovariancancer cell line SKOV3 were calculated, and the dose-effect and time-effect curves were delineated. The SK-OV3 cells treated with IC5.of nHAP and those untreated with nHAP were prepared for transmission electron mi-croscopic observation ad flow cytometry detection. Results After nHAP treatment for 48 h , different concen-trations of nHAP could inhibit the growth of ovarian cancer SKOV3 cells. The IC3., IC5.cancer SKOV3 cells were calculated as 9. 46,28. 83 and 60. 80 mg/L,respectively. During the 48-different concentrations of nHAP treatment , the inhibitory rate was elevated over time and remained slow andstable after 48 h. Morphological observation and quantitative analysis demonstrated that 48-h treatment withIC50 of nHAP could induce the apoptosis of ovarian cancer SKOV3 cells with a apop12.53）%, significantly higher compared with （ （0. 88 ± 5. 48 ） % in the ccrntrol group （ P 〈 0. 05 ）. Compared with the control group, the percentage of SKOV3 cells at G0/G1 phase was significantly higher, whereas the proportion of SKOV3 cells at S phase was considerably lower after treatment with IC5.of nHAP （ both P 〈 0. 05）. Conclusions nHAP exerts significant effect upon suppressing the growth of ovarian cancer cell line SKOV3. The underlying mechanism is probably that nHAP afects the ovarian cancer SKOV3 cells during phase and induces the apoptosis of cancer cells.