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异丙肾上腺素诱导的心肌梗死对大鼠某些糖水解酶和组织蛋白酶的影响。

Influence of isoproterenol-induced myocardial infarction on certain glycohydrolases and cathepsins in rats.

作者信息

Ravichandran L V, Puvanakrishnan R, Joseph K T

机构信息

Department of Biochemistry, Central Leather Research Institute, Madras, India.

出版信息

Biochem Med Metab Biol. 1991 Feb;45(1):6-15. doi: 10.1016/0885-4505(91)90003-4.

DOI:10.1016/0885-4505(91)90003-4
PMID:2015110
Abstract

The changes in the activities of certain lysosomal hydrolases, viz., beta-glucuronidase, beta-N-acetylglucosaminidase, beta-galactosidase, beta-glucosidase, alpha-glucosidase, alpha-galactosidase, alpha-mannosidase, cathepsin B, cathepsin D, and collagenolytic cathepsin, in serum and heart of rats subject to myocardial infarction with isoproterenol, were studied during the periods of peak infarction and recovery. The activities of all the enzymes assayed exhibited a significant increase both in serum and in heart at peak infarction stage and these levels returned to normal during the stage of recovery and repair. The infiltration of inflammatory cells at the infarct regions and the altered lysosomal fragility are probably responsible for the increased activity of the enzymes studied. This may also bring about the catabolism of connective tissue constituents as reported in literature.

摘要

研究了异丙肾上腺素致大鼠心肌梗死时,在梗死高峰期和恢复期血清及心脏中某些溶酶体水解酶(即β-葡萄糖醛酸酶、β-N-乙酰氨基葡萄糖苷酶、β-半乳糖苷酶、β-葡萄糖苷酶、α-葡萄糖苷酶、α-半乳糖苷酶、α-甘露糖苷酶、组织蛋白酶B、组织蛋白酶D和胶原分解组织蛋白酶)活性的变化。在梗死高峰期,所有检测酶的活性在血清和心脏中均显著增加,在恢复和修复阶段这些水平恢复正常。梗死区域炎症细胞的浸润以及溶酶体脆性的改变可能是所研究酶活性增加的原因。这也可能如文献报道的那样导致结缔组织成分的分解代谢。

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