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高血压对靶器官细胞凋亡影响的实验研究(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
1999年第3期
页码:
179-181
栏目:
博士之窗
出版日期:
1999-05-01

文章信息/Info

Title:
Experimental study of hypertension on apoptosis in the target organ
作者:
高　天1X　郑道声2XX
上海第二医科大学附属仁济医院　1老年科　2心内科　上海 200001
Author(s):
Gao Tian;  Zheng Daosheng
Renji Hospital, Shanghai Second Medical University, Shanghai, 200001
关键词:
高血压　肥大;  左室　细胞凋亡　大鼠　基因
Keywords:
hypertension 　hypertrophy;  left ventricle 　cells;  smooth muscle 　apoptosis 　rat gene
分类号:
-
DOI:
-
文献标识码:
-
摘要:
本研究采用自发性高血压大鼠(SHR)、服用依那普利的SHR大鼠(SHR-d)及正常血压大鼠(WKY)三组作对照研究,应用原位标记检测技术观察高血压左室肥厚及心脏左室逆转后心肌平滑肌细胞凋亡现象。并检测凋亡相关基因bcl-2, c-myc的表达。结果显示: SHR-d左室肥厚逆转,其左室壁细胞凋亡数比SHR组明显增多(P<0.01)。SHR组左心室肥厚, 其左室壁细胞凋亡数则比WKY,即无高血压及左室肥厚组明显增多(P<0.01)。各组bcl-2, c-myc 均有表达, 依据辉度检测表达强度, 则bcl-2表达的强度为SHR明显高于SHR-d及WKY(P<0.01);SHR-d和WKY辉度接近(P>0.05); c-myc表达的强度为SHR-d>SHR>WKY,各组比较,差别有非常显著意义(P<0.01)或显著意义(P<0.05)。
Abstract:
Three groups of rats were used for our controlled study: ①spontaneously hypertensive rats(SHR),②SHR which were given enalapril(SHR-d)and③Normotensive rate(Wistar-Kyoto rat, WKY).By means of in-situ detection,apoptosis in cardiac smooth muscles was examined in hypertensive left ventricular hypertrophy after the reversions of the hypertrophy.The expression of gene bcl-2 and c-myc,which are closely related to apotosis were also scrutinized.The result showed the left ventricular hypertrophy of the SHR-d group was reversed,with the number of apoptic cells on the ventricular wall increasing more markedly P<0.01)than that of the SHR group.The SHR group suffered left ventricular hypertrophy and its number of apoptic cells on the ventricular wall also increased more drastically(P<0.01)than that of the WKY group.Each group had its expressions of bcl-2 and -c-myc.According to laser densitometry,the expression of bcl-2 was significantly higher in the SHR group(P<0.01)than in the SHR-d and WKY groups which shared similar densities(P>0.05).The expression of c-myc was arranged as SHR-d>SHR>WKY.When the groups were compared, the differences might be very significant (P<0.01)or significant(P<0.05).

参考文献/References

［1］Vaux DL,Strasser A.The molecular biology of apoptosis.Proc Natl Acad Sci USA,1996;93:2239.

［2］Bennett MR, Evan GI,Newby AC,et al.Deregulated expression of the c-myc oncogene abolishes inhibition of proliferation of rat vascular smooth muscle cells by serum reduction,interferon-γ,heparin,and cyclic nucleotide analogues and induces apoptosis.Circulation Research,1994;74(3):525.

［3］Dariusz L,Yejun Z,Mikko L,et al.Apoptosis of vascular smooth muscle cells.Am J Pathol,1994;145 (6):1265.

［4］Pia S,Pollack MD.Proto-oncogenes and the cardiovascular system.CHEST,1995;107(3):826.

［5］Oscar H,Bing L.Hypothesis:apoptosis may be a mechanism for the transition to heart failure with chronic pressure overload.J Mol Cell Cardiol,1994;26:943.

［6］Pavel H,Lucie R,Than-Vinh D,et al.Apoptosis in target organ of hypertension. Hypertension,1995;26(4):642.

［7］Javier D,Angel P,Marta H,et al.Is the regulation of apoptosis altered in smooth muscle cells of adult spontaneously hypertensive rats? Hypertension,1997;29(3):776.

［8］Pavel H.Proliferation and apoptosis of vascular smooth muscle in hypertension.Curr Opin Nephrol Hypertens,1995;4:1.

［9］Adams MA,Alexander B,Korner PI.Enalapril can prevent vascular amplifier development in spontaneously hypertensive rats. Hypertension,1990;16(3):252.

［10］Yael G,Yoav S,Shmuel A,et al.Identification of programmed cell death in situ via specific labeling of nuclear DNA fragmentation.J Cell Bio,1992;119(3):493.

备注/Memo

备注/Memo:
收稿1998-08-20　修回1999-04-26)ⅹ博士生，ⅹⅹ导师
更新日期/Last Update: 1999-05-01