天津医药
天津醫藥
천진의약
TIANJIN MEDICAL JOURNAL
2015年
2期
113-116
,共4页
杨晓琨%高梦丽%刘亚萌%李彩丽%曹洁%冯靖
楊曉琨%高夢麗%劉亞萌%李綵麗%曹潔%馮靖
양효곤%고몽려%류아맹%리채려%조길%풍정
缺氧%高血压,肺性%增殖细胞核抗原%肌动蛋白类%间歇低氧%肺动脉高压%RhoA/ROCK
缺氧%高血壓,肺性%增殖細胞覈抗原%肌動蛋白類%間歇低氧%肺動脈高壓%RhoA/ROCK
결양%고혈압,폐성%증식세포핵항원%기동단백류%간헐저양%폐동맥고압%RhoA/ROCK
anoxia%hypertension,pulmonary%proliferating cell nuclear antigen%actins%intermittent hypoxia%pulmonary hypertension%RhoA/ROCK
目的:探讨间歇低氧(IH)对大鼠肺组织RhoA/ROCK通路及肺血管新生肌化的影响。方法将40只Wistar雄性大鼠随机分为对照组和IH组各20只,对照组:间歇正常氧暴露(21%O2);IH组:IH暴露(5%~21%O2),持续4周。暴露结束后,2组均采用Real-time PCR和Western blot检测肺组织RhoA、ROCK mRNA和蛋白表达情况,免疫组化法测定肺组织和肺动脉的增殖细胞核抗原(PCNA)及α-平滑肌肌动蛋白(SM-α-actin)的表达情况。结果 IH组肺组织RhoA mRNA(0.463±0.067 vs 0.182±0.040)、ROCK mRNA(0.384±0.062 vs 0.192±0.052)、RhoA蛋白(0.827±0.065 vs 0.424±0.075)及ROCK蛋白(0.488±0.088 vs 0.336±0.102)表达水平均高于对照组(均P<0.05);IH组肺组织PCNA[(54.67±1.80)%vs (9.14±0.91)%]、肺动脉PCNA[(49.40±1.21)%vs (8.38±1.13)%]、肺组织SM-α-actin [(42.66±1.63)%vs (35.44±1.41)%]与肺动脉SM-α-actin[(62.62±2.53)%vs (45.54±2.58)%]表达水平均明显高于对照组(均P<0.05)。结论 RhoA/ROCK传导通路在IH所致肺动脉高压发病机制中可能起着重要作用;IH可通过促进肺动脉的新生肌化进一步促进肺动脉压力升高。
目的:探討間歇低氧(IH)對大鼠肺組織RhoA/ROCK通路及肺血管新生肌化的影響。方法將40隻Wistar雄性大鼠隨機分為對照組和IH組各20隻,對照組:間歇正常氧暴露(21%O2);IH組:IH暴露(5%~21%O2),持續4週。暴露結束後,2組均採用Real-time PCR和Western blot檢測肺組織RhoA、ROCK mRNA和蛋白錶達情況,免疫組化法測定肺組織和肺動脈的增殖細胞覈抗原(PCNA)及α-平滑肌肌動蛋白(SM-α-actin)的錶達情況。結果 IH組肺組織RhoA mRNA(0.463±0.067 vs 0.182±0.040)、ROCK mRNA(0.384±0.062 vs 0.192±0.052)、RhoA蛋白(0.827±0.065 vs 0.424±0.075)及ROCK蛋白(0.488±0.088 vs 0.336±0.102)錶達水平均高于對照組(均P<0.05);IH組肺組織PCNA[(54.67±1.80)%vs (9.14±0.91)%]、肺動脈PCNA[(49.40±1.21)%vs (8.38±1.13)%]、肺組織SM-α-actin [(42.66±1.63)%vs (35.44±1.41)%]與肺動脈SM-α-actin[(62.62±2.53)%vs (45.54±2.58)%]錶達水平均明顯高于對照組(均P<0.05)。結論 RhoA/ROCK傳導通路在IH所緻肺動脈高壓髮病機製中可能起著重要作用;IH可通過促進肺動脈的新生肌化進一步促進肺動脈壓力升高。
목적:탐토간헐저양(IH)대대서폐조직RhoA/ROCK통로급폐혈관신생기화적영향。방법장40지Wistar웅성대서수궤분위대조조화IH조각20지,대조조:간헐정상양폭로(21%O2);IH조:IH폭로(5%~21%O2),지속4주。폭로결속후,2조균채용Real-time PCR화Western blot검측폐조직RhoA、ROCK mRNA화단백표체정황,면역조화법측정폐조직화폐동맥적증식세포핵항원(PCNA)급α-평활기기동단백(SM-α-actin)적표체정황。결과 IH조폐조직RhoA mRNA(0.463±0.067 vs 0.182±0.040)、ROCK mRNA(0.384±0.062 vs 0.192±0.052)、RhoA단백(0.827±0.065 vs 0.424±0.075)급ROCK단백(0.488±0.088 vs 0.336±0.102)표체수평균고우대조조(균P<0.05);IH조폐조직PCNA[(54.67±1.80)%vs (9.14±0.91)%]、폐동맥PCNA[(49.40±1.21)%vs (8.38±1.13)%]、폐조직SM-α-actin [(42.66±1.63)%vs (35.44±1.41)%]여폐동맥SM-α-actin[(62.62±2.53)%vs (45.54±2.58)%]표체수평균명현고우대조조(균P<0.05)。결론 RhoA/ROCK전도통로재IH소치폐동맥고압발병궤제중가능기착중요작용;IH가통과촉진폐동맥적신생기화진일보촉진폐동맥압력승고。
Objective To explore the effect of intermittent hypoxia (IH) on RhoA/ROCK pathway in lung and on the muscularization in pulmonary vascular in rat model. Methods Wistar rats (n=40) were randomly divided into two groups:the normal oxygen control group (n=20) and the IH group ( n=20). For 4 weeks, rats in control group and IH group were ex?posed to intermittent normal oxygen (21%O2) or IH (5%-21%O2) respectively. Then, mRNA transcription and protein trans?lation levels of RhoA/ROCK were examined by Real-time PCR and Western blot. Expression of proliferation cell nuclear an?tigen (PCNA) andα-smooth muscle actin (SM-α-actin ) of lung and pulmonary artery were detected by immunohistochemis?try. Results RhoA mRNA transcription level(0.463 ± 0.067 vs 0.182 ± 0.040), ROCK mRNA transcription level(0.384 ± 0.062 vs 0.192 ± 0.052), RhoA protein expression level(0.827 ± 0.065 vs 0.424 ± 0.075)and ROCK protein expression level (0.488±0.088 vs 0.336±0.102)were higher in IH group than those in control group(P<0.05);Levels of PCNA in lung tissue [(54.67±1.80)%vs (9.14±0.91)%], PCNA in pulmonary artery [(49.40±1.21)%vs (8.38±1.13)%], SM-α-actin in lung tis?sue [(42.66±1.63)%vs (35.44±1.41)%] and SM-α-actin in pulmonary artery [(62.62±2.53)%vs (45.54±2.58)%] were also higher in IH group than those in control group(P<0.05). Conclusion Rho/ROCK pathway may play an important role in developing pulmonary hypertension (PH) associated with IH;and IH can promote the muscularization in pulmonary vascular to accelerate PH.