title: The Effect of Pyrroloquinoline Quinone on Apoptosis and Autophagy in Traumatic Brain Injury.
abstract: Pyrroloquinoline quinone is an anionic, water-soluble compound with antioxidant characteristic. The role of pyrroloquinoline quinone in pharmacology and nutrition has attracted wide attention of researchers. Although a few experiments have confirmed that pyrroloquinoline quinone plays an obvious effective role in neuroprotection. There are few reports about the effect of pyrroloquinoline quinone on traumatic brain injury. Traumatic brain injury is one of the leading causes for adult disability and death. So far, there are no effective treatment methods for the injury because of its complex pathophysiology.
  
  
  
  In the present study, a model of traumatic brain injury in rat was established to study the role of pyrroloquinoline quinone in central nervous system injury.
  
  
  
  The results showed that the protein expression of cleaved-Caspase 3/Caspase 3 increased after traumatic brain injury and the expression decreased by treatment with 2mM pyrroloquinoline quinone. Terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL) staining displayed that the TUNEL positive signals were up-regulated after traumatic brain injury and were down-regulated after treatment with 2mM pyrroloquinoline quinone. The protein expression of LC3II/LC3I or lysosome-associated membrane protein 2(LAMP2) was elevated after traumatic brain injury and reduced after administration with 2mM pyrroloquinoline quinone. Transmission electron microscopy showed that the number of autophagosomes increased markedly after traumatic brain injury and decreased on administration of 2mM pyrroloquinoline quinone. Electroencephalogram indicated that pyrroloquinoline quinone improved brain electrophysiological function after traumatic brain injury. The results of CCK-8 test showed that pyrroloquinoline quinone could increase the viability of primary astrocyte treated with Glutamate. Lactate dehydrogenase (LDH) assay demonstrated that pyrroloquinoline quinone decreased LDH content in primary astrocyte exposed to Glutamate.
  
  
  
  Pyrroloquinoline quinone could play a neuroprotective role after traumatic brain injury in rat, which might be associated with inhibiting apoptosis and autophagy caused by traumatic brain injury.
authors.affiliation: The Jiangsu Key Laboratory of Neuroregeneration, Nantong University, Nantong, 226001. China.
authors.forename: Pengju
authors.initials: P
authors.lastname: Zhang
authors.affiliation: The Jiangsu Key Laboratory of Neuroregeneration, Nantong University, Nantong, 226001. China.
authors.forename: Yongqi
authors.initials: Y
authors.lastname: Ye
authors.affiliation: The Jiangsu Key Laboratory of Neuroregeneration, Nantong University, Nantong, 226001. China.
authors.forename: Yuhang
authors.initials: Y
authors.lastname: Qian
authors.affiliation: The Jiangsu Key Laboratory of Neuroregeneration, Nantong University, Nantong, 226001. China.
authors.forename: Baoxin
authors.initials: B
authors.lastname: Yin
authors.affiliation: The Jiangsu Key Laboratory of Neuroregeneration, Nantong University, Nantong, 226001. China.
authors.forename: Jianmei
authors.initials: J
authors.lastname: Zhao
authors.affiliation: The Jiangsu Key Laboratory of Neuroregeneration, Nantong University, Nantong, 226001. China.
authors.forename: Shunxin
authors.initials: S
authors.lastname: Zhu
authors.affiliation: The Jiangsu Key Laboratory of Neuroregeneration, Nantong University, Nantong, 226001. China.
authors.forename: Li
authors.initials: L
authors.lastname: Zhang
authors.affiliation: Jiangsu Key Laboratory of Neuroregeneration, Nantong University, 19 Qi-xiu Road, Nantong, Jiangsu 226001. China.
authors.forename: Meijuan
authors.initials: M
authors.lastname: Yan
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D017209:Apoptosis / Q000187:drug effects*; D001253:Astrocytes / Q000187:drug effects; D000071182:Autophagosomes / Q000187:drug effects / Q000473:pathology / Q000648:ultrastructure; D001343:Autophagy / Q000187:drug effects*; D000070642:Brain Injuries, Traumatic / Q000188:drug therapy* / Q000473:pathology* / Q000503:physiopathology; D053148:Caspase 3 / Q000378:metabolism; D002478:Cells, Cultured; D004195:Disease Models, Animal; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D018698:Glutamic Acid / Q000633:toxicity; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D052119:Lysosomal-Associated Membrane Protein 2 / Q000378:metabolism; D008297:Male; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D045542:PQQ Cofactor / Q000627:therapeutic use*; D010751:Phosphopyruvate Hydratase / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012844:Sincalide / Q000378:metabolism
chemical_list: D053148:Caspase 3; D005904:Glial Fibrillary Acidic Protein; D018698:Glutamic Acid; D007770:L-Lactate Dehydrogenase; D052119:Lysosomal-Associated Membrane Protein 2; D008869:Microtubule-Associated Proteins; D018696:Neuroprotective Agents; D045542:PQQ Cofactor; D010751:Phosphopyruvate Hydratase; D012844:Sincalide; C526109:Anxa3 protein, rat
keywords: Apoptosis; autophagy; electroencephalogram; pyrroloquinoline quinone; rat; traumatic brain injury