Quercetin improves hypoxia-ischemia induced cognitive deficits via promoting remyelination in neonatal rat.
Myelination failure is associated with perinatal cerebral hypoxia-ischemia (PHI) induced brain injury in premature infants. How to efficiently promote remyelination is crucial for improving cognitive deficits caused by brain injury. Here, we demonstrated that quercetin (Que), a kind of flavonoids, significantly improved cognitive deficits and the behavior of PHI-rat in Morris water maze and open field tasks. After administration of Que to PHI-rat, the number of neogenetic Olig2⁺ oligodendrocyte progenitor cells (OPCs) was evidently increased in the subventricular zone. Additionally, in corpus callosum (CC), the expression of MBP (myelin basic protein) was increased, and the myelin sheaths reached normal level at 30 days with more compact while less damaged myelin sheaths and more mature oligodendrocytes (OLs) repopulating the CC compared with PHI groups. In a word, our findings indicated that Que could remarkably improve both cognition performance and myelination in the context of PHI-induced brain injury by promoting the proliferation of OPCs and strengthening survival of OLs in vivo.
Department of Neurobiology, Xuzhou Medical College, Xuzhou 221009, Jiangsu, PR China.
Xuebin
X
Qu
Department of Neurobiology, Xuzhou Medical College, Xuzhou 221009, Jiangsu, PR China.
Dashi
D
Qi
Department of Neurobiology, Xuzhou Medical College, Xuzhou 221009, Jiangsu, PR China.
Fuxing
F
Dong
Department of Neurobiology, Xuzhou Medical College, Xuzhou 221009, Jiangsu, PR China.
Bei
B
Wang
Department of Neurobiology, Xuzhou Medical College, Xuzhou 221009, Jiangsu, PR China.
Rui
R
Guo
Department of Neurobiology, Xuzhou Medical College, Xuzhou 221009, Jiangsu, PR China.
Mengjiao
M
Luo
Department of Neurobiology, Xuzhou Medical College, Xuzhou 221009, Jiangsu, PR China. Electronic address: wenxi_yao@163.com.
Ruiqin
R
Yao
D000818:Animals; D000831:Animals, Newborn; D051792:Basic Helix-Loop-Helix Proteins / Q000378:metabolism; D049109:Cell Proliferation / Q000187:drug effects; D003072:Cognition Disorders / Q000188:drug therapy / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D003337:Corpus Callosum / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D005106:Exploratory Behavior / Q000187:drug effects / Q000502:physiology; D015870:Gene Expression / Q000187:drug effects; D006624:Hippocampus / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D020925:Hypoxia-Ischemia, Brain / Q000150:complications / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology*; D008124:Locomotion / Q000187:drug effects / Q000502:physiology; D018782:Maze Learning / Q000187:drug effects; D004676:Myelin Basic Protein / Q000378:metabolism; D009186:Myelin Sheath / Q000187:drug effects* / Q000473:pathology / Q000502:physiology*; D009419:Nerve Tissue Proteins / Q000378:metabolism; D058953:Neural Stem Cells / Q000187:drug effects / Q000473:pathology / Q000502:physiology; D018696:Neuroprotective Agents / Q000494:pharmacology*; D000076104:Oligodendrocyte Transcription Factor 2; D009836:Oligodendroglia / Q000187:drug effects / Q000473:pathology / Q000502:physiology; D011794:Quercetin / Q000494:pharmacology*; D051381:Rats
D051792:Basic Helix-Loop-Helix Proteins; D004676:Myelin Basic Protein; D009419:Nerve Tissue Proteins; D018696:Neuroprotective Agents; D000076104:Oligodendrocyte Transcription Factor 2; D011794:Quercetin; C436006:Mbp protein, rat; C522729:Olig2 protein, rat
Cognitive deficit; Oligodendrocyte; Oligodendrocyte progenitor cell; Perinatal cerebral hypoxia-ischemia