CAJ | 학술논문

探讨了粉防己碱（Tet）抑制培养的大鼠主动脉平滑肌细胞（AVSMC）增殖的作用，MTT法分析细胞增殖，［3H］TdR参入法分析细胞DNA合成. 结果显示：①肾血管性高血压〔RH，二肾一夹（2K1C）术后18周〕大鼠AVSMC超微结构呈典型的合成细胞特征; ②RH大鼠AVSMC具有更活跃的增殖倾向,血管紧张素Ⅱ(AngⅡ)和去甲肾上腺素(NE)刺激下指数增长期细胞数和在NE刺激下的AVSMC生长率均明显增高；③Tet（50 mg*kg-1*d-1，po，2K1C术后9周始，连续9周）治疗组的AVSMC对NE和AngⅡ诱导的细胞增殖反应性和生长率较RH组明显降低；④对RH组和伪手术组大鼠的AVSMC， Tet（0.1～10 μmol*L-1）体外给药可浓度依赖性地抑制NE或AngⅡ诱导的增殖和［3H］TdR参入.研究表明，RH大鼠AVSMC对NE和AngⅡ促增殖作用敏感性及反应性增高；Tet可降低其对NE和AngⅡ的反应性，抑制AVSMC增殖和DNA合成.
탐토료분방기감（Tet）억제배양적대서주동맥평활기세포（AVSMC）증식적작용，MTT법분석세포증식，［3H］TdR삼입법분석세포DNA합성. 결과현시：①신혈관성고혈압〔RH，이신일협（2K1C）술후18주〕대서AVSMC초미결구정전형적합성세포특정; ②RH대서AVSMC구유경활약적증식경향,혈관긴장소Ⅱ(AngⅡ)화거갑신상선소(NE)자격하지수증장기세포수화재NE자격하적AVSMC생장솔균명현증고；③Tet（50 mg*kg-1*d-1，po，2K1C술후9주시，련속9주）치료조적AVSMC대NE화AngⅡ유도적세포증식반응성화생장솔교RH조명현강저；④대RH조화위수술조대서적AVSMC， Tet（0.1～10 μmol*L-1）체외급약가농도의뢰성지억제NE혹AngⅡ유도적증식화［3H］TdR삼입.연구표명，RH대서AVSMC대NE화AngⅡ촉증식작용민감성급반응성증고；Tet가강저기대NE화AngⅡ적반응성，억제AVSMC증식화DNA합성.
To analyse the effect of tetrandrine(Tet) on proliferation of aortic vascular smooth muscle cells ( AVSMC), AVSMC were isolated and cultured from sham-operated rats(Sham), renovascular hypertensive rats〔RHR, 18 weeks after two kidney one clip(2K1C) operation〕, and Tet (50 mg*kg-1*d-1 po for 9 weeks from week 9 after 2K1C operation)treated RHR. The proliferation of AVSMC was detected by MTT method, and the DNA synthesis was evaluated by ［3H］-thymidine incorporation. The results showed that ①The ultrastructure of aorta suggested that AVSMC in RHR had transferred from contractile phenotype to synthetic phenotype; ②Compared to Sham, AVSMC from RHR showed a higher proliferative property with a higher cell number and an increased growth rate stimulated by norepinephrine(NE) or angiotensinⅡ(AngⅡ); ③Compared to untreated RHR, AVSMC from Tet treated RHR showed a reduced reactivity to NE- or AngⅡ-stimulated proliferation and growth rate; ④Tet(0.1－10 μmol*L-1) treated in vitro induced a concentration-dependent depression in ［3H］ thymidine-incorporation stimulated by NE or AngⅡ in AVSMC from either RHR or Sham. This study provides an evidence of increased reactivity to NE or AngⅡ in AVSMC of RHR. Tet inhibits the proliferation and DNA synthesis in AVSMC, depresses the susceptibility of AVSMC to AngⅡ and NE, both contribute to the regression effect on hypertensive vascular remodeling.