title: Polydatin--a new mitochondria protector for acute severe hemorrhagic shock treatment.
abstract: OBJECTIVE
  The aim of the study was find out whether neuronal mitochondrial injury does take place in severe shock and to explore effective therapy for severe shock.
  
  
  METHODS
  Rats were divided in the following group: sham, shock + normal saline (NS), shock + cyclosporine A (CsA), shock + resveratrol (Res) and shock + polydatin (PD). Rats were subjected to shock for 2 h, followed by administration of NS, CsA, Res and PD, and infusion of shed blood. Morphology, metabolism and function of mitochondria were measured.
  
  
  RESULTS
  Increased lipid peroxides (LPO) levels, lysosomal injury and mitochondrial permeability transition pore opening took place in neurons, resulting in swollen mitochondria with poorly defined cristae, decreased mitochondrial membrane potential (ΔΨ) and reduced ATP content in shock + NS group, indicating mitochondrial dysfunction. Mitochondrial protectors, such as CsA, Res and PD, partially inhibited these alterations, especially following PD protection, ATP level increased from 44.14 ± 13.81% in shock + NS group to 89.57 ± 9.21% and the survival time was prolonged from 6.3 ± 5.9 h in the shock + NS group to 31.6 ± 13.7 h in shock + PD group.
  
  
  CONCLUSIONS
  The study shows that neuronal mitochondrial injury is involved in the genesis of severe shock and PD may be the best choice for protection of neuron against mitochondrial injury in severe shock.
authors.affiliation: Southern Medical University, Department of Pathophysiology, Guangdong Key Laboratory of Shock and Microcirculation Research, Guangzhou, PR China.
authors.forename: Xingmin
authors.initials: X
authors.lastname: Wang
authors.forename: Rui
authors.initials: R
authors.lastname: Song
authors.forename: Yunyan
authors.initials: Y
authors.lastname: Chen
authors.forename: Ming
authors.initials: M
authors.lastname: Zhao
authors.forename: Ke-seng
authors.initials: KS
authors.lastname: Zhao
mesh_terms: D000208:Acute Disease; D000818:Animals; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004365:Drugs, Chinese Herbal; D005960:Glucosides / Q000008:administration & dosage / Q000737:chemistry / Q000627:therapeutic use*; D015227:Lipid Peroxidation / Q000187:drug effects; D008054:Lipid Peroxides / Q000378:metabolism; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism / Q000648:ultrastructure; D033681:Mitochondrial Membrane Transport Proteins / Q000378:metabolism; D000083162:Mitochondrial Permeability Transition Pore; D009474:Neurons / Q000187:drug effects* / Q000378:metabolism / Q000648:ultrastructure; D010296:Parietal Lobe / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D020011:Protective Agents / Q000008:administration & dosage / Q000737:chemistry / Q000627:therapeutic use*; D051381:Rats; D017208:Rats, Wistar; D012720:Severity of Illness Index; D012771:Shock, Hemorrhagic / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D013267:Stilbenes / Q000008:administration & dosage / Q000737:chemistry / Q000627:therapeutic use*; D016019:Survival Analysis
chemical_list: D004365:Drugs, Chinese Herbal; D005960:Glucosides; D008054:Lipid Peroxides; D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore; D020011:Protective Agents; D013267:Stilbenes; C058229:polydatin