We have located links that may give you full text access.
[Protective effects of metallothionein induced by dexamethasone against ischemia/reperfusion injury of myocardium of isolated rat heart].
OBJECTIVE: To investigate the protective effects of metallothionein (MT) induced by dexamethasone (DEX) against ischemia/reperfusion (I/R) injury of myocardium of isolated rat heart.
METHODS: Thirty-two Sprague-Dawley (SD) rats were divided randomly into the DEX and control groups. In the former group, the rats were pretreated with DEX, and in latter group distilled water was given before their hearts were isolated for Langendorff perfusion and I/R. MT was assessed by Western blotting. The left ventricular developed pressure (LVDP), maximal change rate of intraventricular pressure rise/down (+/-dp/dt max), coronary artery flow (CF) and reperfusion arrhythmias were observed dynamically before ischemia and during 60-minute reperfusion following 30-minute ischemia, The hearts were perfused with triphenyltetrazolium (TTC) after 60-minute reperfusion. The myocardial infarct size was measured with Adobe Photoshop. The levels of MB isoenzyme of creatine kinase (CK-MB), malonaldehyde (MDA), total superoxide dismutase (T-SOD), CuZn-SOD, catalase (CAT), glutathione peroxidase (GSH-Px) and the activities of Na+-K+-ATPase, Ca2+-Mg2+-ATPase were detected.
RESULTS: Compared with control group, the expression of MT was significantly increased (3.085+/-1.065 vs. 1.028+/-0.016, P<0.05), the LVDP, +/-dp/dt max and CF were greatly improved (all P<0.05), the accumulated point of ventricular arrhythmia and the infarct size were significantly reduced in DEX group [(2.00+/-1.41) scores vs. (6.63+/-4.24) scores and (28.38+/-11.22)% vs. (47.39+/-8.30)%, respectively, both P<0.01]. The level of CK-MB was significantly lowered in the DEX group compared with control group [(8.69+/-4.16)U/g vs. (18.15+/-5.59) U/g, P<0.01], and myocardium MDA content was decreased (P<0.05). Moreover, the levels of T-SOD, CuZn-SOD, CAT, GSH-Px, and the activities of Na+-K+-ATPase and Ca2+-Mg2+-ATPase were significantly increased (P<0.05 or/and P<0.01) in DEX group.
CONCLUSION: DEX induces upregulation of MT, which attenuates I/R injury in rat heart.
METHODS: Thirty-two Sprague-Dawley (SD) rats were divided randomly into the DEX and control groups. In the former group, the rats were pretreated with DEX, and in latter group distilled water was given before their hearts were isolated for Langendorff perfusion and I/R. MT was assessed by Western blotting. The left ventricular developed pressure (LVDP), maximal change rate of intraventricular pressure rise/down (+/-dp/dt max), coronary artery flow (CF) and reperfusion arrhythmias were observed dynamically before ischemia and during 60-minute reperfusion following 30-minute ischemia, The hearts were perfused with triphenyltetrazolium (TTC) after 60-minute reperfusion. The myocardial infarct size was measured with Adobe Photoshop. The levels of MB isoenzyme of creatine kinase (CK-MB), malonaldehyde (MDA), total superoxide dismutase (T-SOD), CuZn-SOD, catalase (CAT), glutathione peroxidase (GSH-Px) and the activities of Na+-K+-ATPase, Ca2+-Mg2+-ATPase were detected.
RESULTS: Compared with control group, the expression of MT was significantly increased (3.085+/-1.065 vs. 1.028+/-0.016, P<0.05), the LVDP, +/-dp/dt max and CF were greatly improved (all P<0.05), the accumulated point of ventricular arrhythmia and the infarct size were significantly reduced in DEX group [(2.00+/-1.41) scores vs. (6.63+/-4.24) scores and (28.38+/-11.22)% vs. (47.39+/-8.30)%, respectively, both P<0.01]. The level of CK-MB was significantly lowered in the DEX group compared with control group [(8.69+/-4.16)U/g vs. (18.15+/-5.59) U/g, P<0.01], and myocardium MDA content was decreased (P<0.05). Moreover, the levels of T-SOD, CuZn-SOD, CAT, GSH-Px, and the activities of Na+-K+-ATPase and Ca2+-Mg2+-ATPase were significantly increased (P<0.05 or/and P<0.01) in DEX group.
CONCLUSION: DEX induces upregulation of MT, which attenuates I/R injury in rat heart.
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