Effects of propofol on LC3II and mTOR/p-mTOR expression during ischemia-reperfusion myocardium injury in rats with type 2 diabetes mellitus.

Abstract:

:To investigate the effects of propofol on myocardial ischemia reperfusion in rats with type 2 diabetes, male adult rats were divided into five groups: Sham-operation (CC), ischemia-reperfusion (CI), low-dose propofol (LP), moderate-dose propofol (MP) and high-dose propofol (HP). The LP, MP and HP groups were administered with 6, 12 and 24 mg/kg/h propofol, respectively, prior to occlusion. Heart rate (HR), left ventricular systolic pressure (LVSP) and the rate (dp/dt max) of left ventricular pressure rise in early systole (±dp/dt max) were recorded. The role of autophagy was also studied by measuring the levels of superoxide dismutase (SOD), malondialdehyde (MDA), autophagy marker protein LC3II, mammalian target of rapamycin (mTOR)/phosphorylate (p)-mTOR and cardiac troponin T (cTnT). The myocardial morphological features were assessed using light and electron microscopy. The present results demonstrated that the HR, LVSP, +dp/dt and -dp/dt levels in the propofol groups (LP, MP and HP) were significantly increased (P<0.05) when compared with the CI group. The myocardial cells in the MP group showed mild edematous changes and partially dissolved mitochondrial cristae and membrane rupture. SOD, cTnT and MDA levels were significantly decreased (P<0.05), mTOR expression decreased significantly (P<0.05) and p-mTOR expression increased significantly in the MP group (P<0.05). The present study demonstrated the protective effects of propofol in T2DM rats exhibiting MIRI, with an optimal protective effect at an infusion rate of 12 mg/kg/h. Additionally, the results revealed that propofol led to significant reductions in LC3II and mTOR serum levels and the inhibition of autophagy in myocardial cells.

journal_name

Exp Ther Med

authors

Wang Y,Zhang K,Qi X,Yang G,Wang H,Zhang Z,Yang B

doi

10.3892/etm.2020.8499

subject

Has Abstract

pub_date

2020-04-01 00:00:00

pages

2441-2448

issue

4

eissn

1792-0981

issn

1792-1015

pii

ETM-0-0-8499

journal_volume

19

pub_type

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