title: Potassium Aspartate Attenuates Brain Injury Induced by Controlled Cortical Impact in Rats Through Increasing Adenosine Triphosphate (ATP) Levels, Na+/K+-ATPase Activity and Reducing Brain Edema.
abstract: BACKGROUND Potassium aspartate (PA), as an electrolyte supplement, is widely used in clinical practice. In our previous study, we found PA had neuroprotective effects against apoptosis after cerebral ischemia/reperfusion in rats. In this study, we examine whether PA has protective effects on traumatic brain injury (TBI). MATERIAL AND METHODS TBI was induced by controlled cortical impact (CCI) in rats. Vehicle treatment (control) or PA treatment was administered intraperitoneally at 30 minutes after CCI. The modified neurological severity score (mNSS) and cortical lesion volume were examined. Brain edema and blood-brain barrier (BBB) integrity were measured, as well as brain ATP contents, lactic acid levels, and Na+/K+-ATPase activities. RESULTS We found that CCI induced cortical injury in rats. Acute PA treatment at the dose of 62.5 mg/kg and 125 mg/kg significantly improved neurological deficits (p<0.05 and p<0.001, respectively) and decreased the cortical lesion volume (p<0.05 and p<0.001, respectively) compared with vehicle-only treatment. PA treatment at the dose of 125 mg/kg attenuated brain edema and ameliorated BBB integrity. In addition, PA treatment significantly reduced the loss of ATP (p<0.01), reduced lactic acid levels (p<0.001), and increased the activity of Na+/K+-ATPase (p<0.01). CONCLUSIONS Our results indicate PA has neuroprotective effects on TBI through increasing ATP levels, Na+/K+-ATPase activity, and reducing brain edema. It provides experimental evidence for the clinical application of PA.
authors.affiliation: Department of Pharmacology, Beijing Neurosurgical Institute, Beijing Tiantan Hospital, Capital Medical University, Beijing Key Laboratory of Central Nervous System Injury, China National Clinical Research Center for Neurological Diseases, Beijing, China (mainland).
authors.forename: Yi
authors.initials: Y
authors.lastname: Gu
authors.affiliation: Department of Pediatrics, Shanghai General Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China (mainland).
authors.forename: Jie
authors.initials: J
authors.lastname: Zhang
authors.affiliation: Department of Pharmacology, Beijing Neurosurgical Institute, Beijing Tiantan Hospital, Capital Medical University, Beijing Key Laboratory of Central Nervous System Injury, China National Clinical Research Center for Neurological Diseases, Beijing, China (mainland).
authors.forename: Yumei
authors.initials: Y
authors.lastname: Zhao
authors.affiliation: Department of Pathology, Beijing Neurosurgical Institute, Beijing Tiantan Hospital, Capital Medical University, Beijing Key Laboratory of Central Nervous System Injury, China National Clinical Research Center for Neurological Diseases, Beijing, China (mainland).
authors.forename: Yujin
authors.initials: Y
authors.lastname: Su
authors.affiliation: Department of Pharmacology, Beijing Neurosurgical Institute, Beijing Tiantan Hospital, Capital Medical University, Beijing Key Laboratory of Central Nervous System Injury, China National Clinical Research Center for Neurological Diseases, Beijing, China (mainland).
authors.forename: Yazhuo
authors.initials: Y
authors.lastname: Zhang
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism*; D000818:Animals; D001224:Aspartic Acid / Q000494:pharmacology*; D001812:Blood-Brain Barrier / Q000187:drug effects; D000070642:Brain Injuries, Traumatic / Q000188:drug therapy* / Q000378:metabolism*; D004195:Disease Models, Animal; D008297:Male; D018696:Neuroprotective Agents / Q000494:pharmacology; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D018696:Neuroprotective Agents; D001224:Aspartic Acid; D000255:Adenosine Triphosphate