We have located links that may give you full text access.
English Abstract
Journal Article
[The cardioprotective effects of ischemic postconditioning on myocardial interstitium following ischemic/reperfusion in rats].
Chinese Journal of Applied Physiology 2014 September
OBJECTIVE: To investigate the effects of ischemic postconditioning (IPTC) on the changes of matrix metalloproteinases-2 (MMP-2) and tissue inhibitor of metalloproteinase-2 (TIMP-2) protein and mRNA levels in rat heart subjected to ischemia/reperfusion, and explore the mechanism by which IPTC protects myocardial interstitium following ischemic/reperfusion (I/R).
METHODS: Twenty four healthy male SD rats were randomly divided into 3 groups (n = 8): sham control (SC) group, I/R group and IPTC group. The parameters of left ventricular function including left ventricular systolic pressure (LVSP) and its derivate (±dp/dt) were measured; the amount of myocardial collagen contents was determined by hydroxyproline quantification; the plasma activity of creatine kinase (CK) and lactate dehydrogenase (LDH) was detected; the protien levels of MMP-2 and TIMP-2 was measured by Western blot and the mRNA levels of MMP-2 and TIMP-2 was detected by real-time PCR.
RESULTS: The myocardial collagen contents, left ventricular function and the protein and mRNA levels of TIMP-2 were significantly decreased in I/R group compared with those of SC group, wherease the activities of CK and LDH in the plasma and the protein and mRNA levels of MMP-2 were significantly enhanced in I/R group when compared to SC group. Compared with I/R group, the myocardial collagen contents, left ventricular function and the protein and mRNA levels of TIMP-2 were increased in IPTC group, the activities of CK and LDH in the plasma and the protein and mRNA level of MMP-2 were decreased in IPTC group.
CONCLUSION: These findings indicate that IPTC has protective effects on myocardial interstitial after the myocardial ischemia/reperfusion injury, and IPTC may exert its cardioprotectve effect via inhibiting MMP-2 and enhancing TIMP-2 expression in cardiac muscle.
METHODS: Twenty four healthy male SD rats were randomly divided into 3 groups (n = 8): sham control (SC) group, I/R group and IPTC group. The parameters of left ventricular function including left ventricular systolic pressure (LVSP) and its derivate (±dp/dt) were measured; the amount of myocardial collagen contents was determined by hydroxyproline quantification; the plasma activity of creatine kinase (CK) and lactate dehydrogenase (LDH) was detected; the protien levels of MMP-2 and TIMP-2 was measured by Western blot and the mRNA levels of MMP-2 and TIMP-2 was detected by real-time PCR.
RESULTS: The myocardial collagen contents, left ventricular function and the protein and mRNA levels of TIMP-2 were significantly decreased in I/R group compared with those of SC group, wherease the activities of CK and LDH in the plasma and the protein and mRNA levels of MMP-2 were significantly enhanced in I/R group when compared to SC group. Compared with I/R group, the myocardial collagen contents, left ventricular function and the protein and mRNA levels of TIMP-2 were increased in IPTC group, the activities of CK and LDH in the plasma and the protein and mRNA level of MMP-2 were decreased in IPTC group.
CONCLUSION: These findings indicate that IPTC has protective effects on myocardial interstitial after the myocardial ischemia/reperfusion injury, and IPTC may exert its cardioprotectve effect via inhibiting MMP-2 and enhancing TIMP-2 expression in cardiac muscle.
Full text links
Related Resources
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app