Repeated Oral Administration of Human Serum Albumin Protects from the Cerebral Ischemia in Rat Brain Following MCAO

Albumin is known to have neuroprotective effects. The protein has a long half-life circulation, and its effects can therefore persist for a long time to aid in the recovery of brain ischemia. In the present study, we investigated the neuroprotective effects of human serum albumin (HSA) on brain hemodynamics. Albumin is administrated using repeated oral gavage to the rodents. Sprague-Dawley rats underwent middle cerebral artery occlusion procedures and served as a stroke model. Afterwards, 25% human serum albumin (1.25 g/kg) or saline (5 ml/kg) was orally administrated for 2 weeks in alternating days. After 2 weeks, the rodents were assessed for levels of brain ischemia. Our testing battery consists of behavioral tests and in vivo optical imaging sessions. Modified neurological severity scores (mNSS) were obtained to assess the levels of ischemia and the effects of HSA oral administration. We found that the experimental group demonstrated larger hemodynamic responses following sensory stimulation than controls that were administered with saline. HSA administration resulted in more significant changes in cerebral blood volume following direct cortical electric stimulation. In addition, the mNSS of the treatment group was lower than the control group. In particular, brain tissue staining revealed that the infarct size was also much smaller with HSA administration. This study provides support for the efficacy of HSA, and that long-term oral administration of HSA may induce neuroprotective effects against brain ischemia.

Functional Improvement by Human Adipose Tissue Stromal Cells after Cerebral Ischemia in Rats / 대한해부학회지

Adipose tissue may represent an alternative source of cells capable of neuronal differentiation, potentially enhancing their usefulness in the treatment of neurological disease. We examined that human adipose tissue stromal cells (ATSCs) can be induced to undergo neuronal differentiation. After neuronal induction, the phenotype of hATSCs changed towards neuronal morphology and hATSCs were injected into the lateral ventricle of the rat brain. Implanted cells migrated to brain injury region which was induced by middle cerebral artery occlusion (MCAO). Intracerebral grafting of hATSCs significantly enhances sensory and motor recovery of functional deficits in MCAO rats. These data indicate that transplanted hATSCs survive, migrate and differentiate in the ischemic microenvironment and improve neurological function recovery after stroke in rats. Therefore, we anticipate that transplantation of hATSCs may provide a powerful autoplastic therapy for human neurological injury and degenerative disorders.