氨基胍可部分预防糖尿病大鼠肝脏丙酮酸激酶活性的降低。

Aminoguanidine partially prevents the reduction in liver pyruvate kinase activity in diabetic rats.

作者信息

Majd Alimohammad Amiri, Goodarzi Mohammad Taghi, Hassanzadeh Taghi, Tavilani Heidar, Karimi Jamshid

机构信息

Department of Biochemistry Medical School, Hamadan University of Medical Sciences, 65178 Hamadan, Iran.

Research Center for Molecular Medicine, Hamadan University of Medical Sciences, 65178 Hamadan, Iran.

出版信息

Adv Biomed Res. 2014 Dec 31;3:260. doi: 10.4103/2277-9175.148233. eCollection 2014.

DOI:10.4103/2277-9175.148233

PMID:25625099

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4298874/

Abstract

BACKGROUND

Low molecular weight aldehydes and carbonyl compounds which are derived from glucose metabolism are prevalent in diabetic plasma. These compounds react to amino groups of Lys and Arg and lead to the formation of advanced glycation end products (AGEs). This modification changes the function of the proteins. The present study aimed to survey the effect of diabetes on rat liver pyruvate kinase activity and to show the inhibitory effect of aminoguanidine (AG).

MATERIALS AND METHODS

Male Wistar rats (n = 18, 6 to 8 weeks old) were divided randomly in three groups: the first group as control; second and third groups were induced diabetes using streptozocin. Third group received AG orally for 8 weeks after diabetes induction. Liver cell homogenate was prepared from all studied groups and L-type pyruvate kinase was separated from the homogenate. Pyruvate kinase activity was determined in both liver cell homogenate and extracted L-type PK. The PK activity was compared in all samples between groups.

RESULTS

PK activity in isolated form and in liver cell homogenate was lower in diabetic rats as compared to control group. AG-treated group showed higher PK activity compared to untreated diabetic group; however, the difference was not significant. Non-significant difference in PK activity between AG-treated diabetic and non-diabetic (control) group indicated the inhibitory effect of AG in glycation of PK.

CONCLUSION

The obtained results showed PK activity decreased in diabetic rats and AG can partially prevent the reduction in PK activity.

摘要

背景

源自葡萄糖代谢的低分子量醛类和羰基化合物在糖尿病患者血浆中普遍存在。这些化合物与赖氨酸和精氨酸的氨基发生反应，导致晚期糖基化终产物（AGEs）的形成。这种修饰改变了蛋白质的功能。本研究旨在调查糖尿病对大鼠肝脏丙酮酸激酶活性的影响，并显示氨基胍（AG）的抑制作用。

材料与方法

雄性Wistar大鼠（n = 18，6至8周龄）随机分为三组：第一组为对照组；第二组和第三组用链脲佐菌素诱导糖尿病。第三组在糖尿病诱导后口服AG 8周。从所有研究组制备肝细胞匀浆，并从匀浆中分离出L型丙酮酸激酶。测定肝细胞匀浆和提取的L型丙酮酸激酶中的丙酮酸激酶活性。比较所有样本组间的丙酮酸激酶活性。