Key result
Phosphocreatine reduces myocardial ultrastructural damage and injury biomarkers following spinal cord injury in rats.
Why the study?
The cardioprotective effects of phosphocreatine on myocardial ultrastructure and calcium-sensing receptor expression following high-level spinal cord injury were unclear.
p-value: p=<0.05
Phosphocreatine exhibits cardioprotective effects in a rat model of acute high-level spinal cord injury by preserving myocardial ultrastructure and reducing myocardial injury markers.
Hypothesis-generating for phosphocreatine after spinal cord injury; clinical trials needed before human translation.
Phosphocreatine (PCr) mobilizes high-energy phosphates in cardiac muscles, which is potentially useful as a cardioprotective agent in patients with spinal cord injury (SCI). The cardioprotective effects of PCr on myocardial cell ultrastructure and calcium-sensing receptor (CaSR) expression following high-level spinal cord injury (SCI) were investigated. Healthy adult male Sprague-Dawley (SD) rats (n=54) weighing 250-300 g were subjected to C7 SCI injury by Allen's method with or without treatment by abdominal injection of PCr (200 mg/kg) at 6, 12, 24 or 48 h (SCI + treatment and SCI-only groups, respectively; 6 rats/group/time point). Right apical tissues were sampled 2 h following each time interval. Surgeries without SCI were performed in 6 control rats (sham operation group). Cardiac troponin I (cTnI), serum creatine kinase (CK) and creatine kinase (CK-MB) levels were assessed automatically. Myocardial morphology was examined by transmission electron microscopy (TEM). Quantitative real‑time polymerase chain reaction (qRT-PCR) and western blot analysis were used to determine myocardial tissue calcium-sensing receptor (CaSR) mRNA and protein expression, respectively. Normal myocardial ultrastructure was observed in the sham operation group, while SCI-only groups exhibited progressive and extensive damage to myofibrils, sarcomere structure, mitochondrial membranes and vacuole structures, occasionally accompanied by punctured cell membranes, nuclear chromatin condensation and cavitation. SCI + treatment groups, however, exhibited significantly relieved ultrastructural abnormalities and reduced the levels of CaSR, cTnI, CK and CK-MB mRNA and protein expression at all time intervals (P<0.05). In the SCI rat model, PCr exhibited cardioprotection by relieving myocardial ultrastructural abnormalities and preserving the normal metabolic energy balance, including calcium regulation.
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Chen et al. (2014) studied Spinal cord injury (n=54). Phosphocreatine vs. Normal saline was evaluated on Myocardial ultrastructural abnormalities and levels of CaSR, cTnI, CK, and CK-MB (p=<0.05). Phosphocreatine treatment significantly relieved myocardial ultrastructural abnormalities and reduced the levels of CaSR, cTnI, CK, and CK-MB at all time intervals following spinal cord injury in rats.
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