title: Levothyroxine replacement therapy with vitamin E supplementation prevents the oxidative stress and apoptosis in hippocampus of hypothyroid rats.
abstract: OBJECTIVE
  To examine the effect of levothyroxine (L-T4), vitamin E or both on oxidative stress status and hippocampal apoptosis in a propylthiouracil (PTU)-induced hypothyroid rat model.
  
  
  METHODS
  Sprague-Dawley rats were randomly divided into five groups: Control, PTU+PTU+L-T4+PTU+Vit E, PTU+Vit E+L-T4. In each group we assessed levels of serum triiodothyronine (T3), tetraiodothyronine (T4), thyroid stimulating hormone (TSH), hippocampus cellular apoptosis index (AI), hippocampus nicotinamide adenine denucleotide hydrogen (NADPH)oxidase and superoxide dismutase (SOD).
  
  
  RESULTS
  1) Compared with the control group, NADPH oxidase levels were significantly increased, and SOD levels were significantly reduced in the PTU groups (p<0.05). 2) Compared to the PTU group, SOD levels were significantly increased in the PTU+Vit E and PTU+L-T4+Vit E group (p<0.05). NADPH oxidase levels were significantly decreased in the PTU+L-T4, PTU+Vit E and PTU+ L-T4+Vit E group (p<0.05). 3) Compared with the control group, hippocampus AI increased significantly in the PTU group (p<0.05). Compared with the PTU group, hippocampus AI was significantly reduced in the PTU+L-T4 group and PTU+L-T4+Vit E group (p<0.05). 4) Hippocampus AI was positively correlated with NADPH oxidase expression levels in hippocampus tissue (r=0.644, p<0.01).
  
  
  CONCLUSIONS
  Levothyroxine replacement therapy combined with vitamin E reduces hippocampus AI by improving oxidative stress. This study suggested that the mechanisms of hippocampus tissue injury in a hypothyroid rat model is related to hippocampus apoptosis from increased oxidative stress.
authors.affiliation: Department of Endocrinology, The Second Affiliated Hospital of Anhui Medical University, Hefei, China.
authors.forename: Yanyun
authors.initials: Y
authors.lastname: Guo
authors.affiliation: Department of Endocrinology, The 82nd Hospital of the People's Liberation Army, HuaiAn, China.
authors.forename: Si Yuan
authors.initials: SY
authors.lastname: Wan
authors.affiliation: Department of Endocrinology, The Second Affiliated Hospital of Anhui Medical University, Hefei, China.
authors.forename: Xing
authors.initials: X
authors.lastname: Zhong
authors.affiliation: Department of Physiology, Institute of Basic Medical Sciences of Anhui Medical University, Hefei, China.
authors.forename: Ming Kui
authors.initials: MK
authors.lastname: Zhong
authors.affiliation: Department of Endocrinology, The Second Affiliated Hospital of Anhui Medical University, Hefei, China.
authors.forename: Tian Rong
authors.initials: TR
authors.lastname: Pan
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects* / Q000502:physiology; D019587:Dietary Supplements; D004195:Disease Models, Animal; D004359:Drug Therapy, Combination; D006624:Hippocampus / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D020249:Hormone Replacement Therapy; D007037:Hypothyroidism / Q000188:drug therapy*; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects* / Q000502:physiology; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D013974:Thyroxine / Q000008:administration & dosage / Q000494:pharmacology*; D014810:Vitamin E / Q000008:administration & dosage / Q000494:pharmacology*
chemical_list: D014810:Vitamin E; D013974:Thyroxine