CAJ | 학술논문

目的：探讨牵张激活离子通道（SACs）在自发性高血压大鼠（SHR）体内高敏C反应蛋白（hsCRP）表达机制中的作用。方法用SACs抑制剂链霉素分别干预高血压形成早期的SHR和尚未发生高血压的SHR的主动脉平滑肌血管环。酶联免疫吸附法测定血清hsCRP水平，反转录聚合酶链反应和免疫组织化学染色检测主动脉平滑肌细胞CRP的表达情况。结果5周龄后，SHR的收缩压、血清hsCRP浓度和主动脉平滑肌CRP的表达量均进行性增高，而链霉素在无降血压作用的前提下能显著抑制CRP的表达、降低血清hsCRP的浓度。机械牵拉还未形成高血压的SHR的主动脉平滑肌可导致其CRP的迅速表达，而链霉素预处理后能显著抑制机械张力所诱导的CRP的表达。结论链霉素抑制SACs是抑制SHR的hsCRP表达的主要机制。
목적：탐토견장격활리자통도（SACs）재자발성고혈압대서（SHR）체내고민C반응단백（hsCRP）표체궤제중적작용。방법용SACs억제제련매소분별간예고혈압형성조기적SHR화상미발생고혈압적SHR적주동맥평활기혈관배。매련면역흡부법측정혈청hsCRP수평，반전록취합매련반응화면역조직화학염색검측주동맥평활기세포CRP적표체정황。결과5주령후，SHR적수축압、혈청hsCRP농도화주동맥평활기CRP적표체량균진행성증고，이련매소재무강혈압작용적전제하능현저억제CRP적표체、강저혈청hsCRP적농도。궤계견랍환미형성고혈압적SHR적주동맥평활기가도치기CRP적신속표체，이련매소예처리후능현저억제궤계장력소유도적CRP적표체。결론련매소억제SACs시억제SHR적hsCRP표체적주요궤제。
Objective To investigate the role of stretch-activated ion channels (SACs) on the mechanisms of hsCRP expression in spontaneously hypertensive rats (SHR).Methods SACs inhibitor streptomycin was used respectively to intervene in SHR during the early stage of hypertension and in vascular rings of aortic smooth muscle of SHR without the development of hypertension. Serum hsCRP levels were determined by ELISA. CRP expression levels in aortic smooth muscle cells were detected by RT-PCR and immunohistochemical staining. Results After 5 weeks, the levels of systolic pressure, serum hsCRP and aortic CRP expression of SHR raised increasingly, while streptomycin, without the effect of decreasing hypertension, could significantly inhibit the CRP expression and decrease the serum hsCRP concentration. Mechanical stretching caused the rapid expression of CRP in the aortic smooth muscle of SHR without the development of hypertension, while the intervention of streptomycin could significantly inhibit the CRP expression induced by mechanical strain.Conclusion The inhibition of streptomycin in SACs is the main mechanism of inhibiting hsCRP expression of SHR.