Expression of KLF4 in diabetic mouse myocardium and the interventional effect of Tongxinluo capsule on diabetic cardiomyopathy
10.3969/j.issn.1001-1978.2015.06.027
- VernacularTitle:KLF4在糖尿病小鼠心肌组织的表达及通心络胶囊干预作用研究
- Author:
Zhe ZHANG
;
Chao WANG
- Publication Type:Journal Article
- Keywords:
Tongxinluo capsule;
diabetic cardiomyop-athy;
Krüppel-like factor 4;
blood sugar;
blood lipids;
NF-κB;
inflammation;
signal pathway
- From:
Chinese Pharmacological Bulletin
2015;(6):876-881
- CountryChina
- Language:Chinese
-
Abstract:
Aim To observe the expressions of KLF4 in the myocardium of diabetic mice and their changes under Tongxinluo capsule intervention. Methods For-ty KK/Upj-Ay mice were randomly divided into diabet-ic model group(n=10)and diabetic model with Tongx-inluo(TXL low,middle,high) groups(n =10,respec-tively). C57BL/6 mice were selected as control group ( n=10 ) . At the end of the 3 th month the mice were sacrificed and were weighed. The fasting blood-glucose (FBG),glycosylated hemoglobin(HbA1c),triglyceride ( TG) ,total cholesterol ( TC ) and insulin ( FINS ) were measured to calculate HOMA-IR. Radioimmunoassay was used to measure serum TNF-αand IL-6 . The path-ological changes in the myocardium of mice were ob-served by HE staining. KLF4 mRNA was examined by Real-time PCR, while KLF4 and NF-κB protein were measured by Western blot. Results Compared to the control group,FBG,HbA1c,TG,TC,FINS,HOMA-IR,
TNF-α and IL-6 in model group were markedly in-creased;the expressions of myocardial KLF4 were markedly decreased and the expression of nuclear NF-κB protein were markedly increased ( P < 0. 01 ) . Tongxinluo capsule could significantly reduce myocar-dial pathological damage, FINS, TG, TC, TNF-α, IL-6 level and the expression of nuclear NF-κB protein and up-regulate the expression of KLF4 ( P <0. 05 ) , but had no effect on FBG and HbA1c(P>0. 05). Conclu-sions KLF4 may be involved in the development of myocardial injury during diabetes. Tongxinluo capsule can ameliorate the myocardial damage and improve the function of diabetic myocardium by up-regulating the expression of KLF4 and inhibiting the activation of NF-κB inflammatory signal pathway.
