α-SMA和PCNA在OSAS继发高血压模型大鼠血管中的表达

摘要

目的：比较α-平滑肌肌动蛋白（α-SMA）和增殖细胞核蛋白（PCNA）在阻塞性睡眠呼吸暂停综合征（OSAS）继发高血压大鼠模型腹主动脉及肾动脉中的表达情况。方法：36只SD大鼠随机分为对照组、模型组，模型组每日8 h使之处于间歇低氧环境内。全程每周监测鼠尾动脉血压，低氧时程12周时处死大鼠， ELISA法检测血清TNF-α、IL-6、IL-10及hs-CRP的水平，免疫组化法检测腹主动脉及肾动脉α-SMA和PCNA的阳性表达水平。结果：模型组大鼠血压于低氧4周时升高明显，在低氧12周时血压最高达到186 mmHg，与对照组比较，差异有统计学意义（P ＜0．01）；TNF-α、IL-6、IL-10及hs-CRP水平均高于对照组，差异具有统计学意义（P ＜0．01）；与对照组比较，腹主动脉α-SMA表达降低（P ＜0．05），PCNA表达升高（P ＜0．05）；肾动脉中α-SMA和PCNA表达升高（P ＜0．05）。结论： OSAS模型大鼠存在血压升高，α-SMA和PCNA在腹主动脉及肾动脉中的表达不同，说明OSAS继发性血压升高在不同血管中的重构表现不同，其分子机制不同。%Objective To investigate and analyze the expression of α-SMA and PCNA in abdominal aorta and renal artery in obstructive sleep apnea syndrome(OSAS)combined with hypertension rats. Methods 36 SD rats were randomly divided into normal control group and model group. The model group was subjected to intermittent hypoxia condition for 8h everyday. Rat tail artery pressure was monitored every week and all subjects were sacrificed at 12th week. The level of TNF-α, IL-6, IL-10 and hs-CRP expression in serum were measured by ELISA method. Immunohistochemical analysis was performed on α-smooth muscle actin (α-SMA) and proliferating cell nuclear antigen (PCNA). Results Compared with control group,model rats blood pressure increased significantly (P < 0.01) when exposed for 4 weeks under intermittent hypoxia condition,and reached the peak value of 186mmHg at 12 weeks. The level of TNF-α, IL-6 , IL-10 and hs-CRP in serum were higher than in control group (P < 0.01). Immunohistochemical staining showed that the expression of α-SMA in abdominal aorta decreased more significantly than control group (P < 0.05),while there was a stronger positive expression of PCNA in model group than those in control (P < 0.05). In addition,compared with control rats, model rats showed a higher expression of α-SMA and PCNA significantly in renal artery(P < 0.05). Conclusion The intermittent hypoxia condition could result in higher blood pressure,while the different expression of α-SMA and PCNA illustrate that high pressure show different reconstruction performance in different vascular,underlying different molecular mechanism.