The Effect and Mechanism of Adipose-Derived Stem Cells Transplantation on Expression of Neuroglobin in Rats with Cerebral Ischemia
HUANG Huan1,2*, ZHENG Mouwei1,2, MEI Ainong1,2
The objective of this research was to investigate the impact of ADSC (adipose-derived stem cell) transplantation on Ngb (neuroglobin) expression in the peri-infarct cortex of rats with cerebral ischemia, and to elu cidate the mechanisms by which ADSC facilitate the recovery of neurological function following cerebral infarc tion. MCAO (middle cerebral artery occlusion) model was established in SD (Sprague-Dawley) rats using modified Longa’s method, and the animals were randomly assigned to three groups: sham group, MCAO group, and ADSC group. At 24 hours post-model establishment, the ADSC group received intravenous injection of 50 μL ADSC sus pension (approximately 2×106 cells) via the carotid artery, whereas the MCAO group was administered an equiva lent volume of saline. Neurological function was assessed using mNSS (modified neurological severity scores) on the 1st, 3rd, and 7th days post-model establishment. Subsequently, the rats were euthanized, and their brains were harvested for analysis. Mitochondrial damage in the peri-infarct cortex was examined using transmission electron microscope, and levels of oxidative stress and energy metabolism indicators were measured using assay kits. The expression of Ngb was determined using Western blot and immunofluorescence techniques. The results indicated that ADSC transplantation significantly improved the mNSS scores of rats, mitigated mitochondrial damage in the peri-infarct cortex, and increased the levels of ATP (adenosine triphosphate), Na+-K+-ATPase, Ca2+-Mg2+-ATPase, and SOD (superoxide dismutase), while also suppressing the levels of MDA (malondialdehyde) and NO (nitric ox ide). Furthermore, ADSC transplantation notably elevated the expression of Ngb protein within the cytoplasm of neuronal cells. In summary, ADSC transplantation appears to enhance neurological function in rats post-cerebral infarction, potentially through the upregulation of Ngb expression in the peri-infarct cortex, which may protect mi tochondrial structure, ameliorate energy metabolism deficiencies, and diminish the oxidative stress response.
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