title: [Effects of acupuncture on PI3K/Akt/mTOR signaling pathway in rats with premature ovarian failure].
abstract: OBJECTIVE
  To explore the effects of acupuncture and medication on PI3K/Akt/mTOR signaling pathway in rats with premature ovarian failure.
  
  
  METHODS
  Ten of fifty SPF-grade female SD rats were randomly selected into a normal group, and the remaining 40 rats were treated with intraperitoneal injection of cyclophospha mide (30 mg/kg) for consecutive 5 days to establish rat model of premature ovarian failure. Thirty five successful rat models were randomly divided into a model group (9 cases), a medication group (9 cases), an acupuncture group A (9 cases) and an acupuncture group B (8 cases). The rats in the model group and normal group did not receive any treatment. The rats in the medication group were treated with intragastric administration of diethylstil bestrol, once a day. The rats in the acupuncture group A and acupuncture group B were respectively treated with acupuncture at different acupoints, twice a day. All the treatment was given for 4 weeks. After the treatment, enzyme-linked immunosorbent assay (ELISA) was applied to test the levels of estradiol (E2), progesterone (P), follicle stimulating hormone (FSH) and luteotropic hormone (LH). The ovarian tissue sample was processed with hematoxylin eosin (HE) staining as well as RNA and protein extraction to test the mRNA expression of estrogen receptor alpha (ERalpha), estrogen receptor beta (ERP), phosphatidylinositol 3-kinase/serine/threonine kinase (PI3K), protein kinase B (Akt) and mammalian target of rapamycin (mTOR).
  
  
  RESULTS
  High-dose short-term in- tervention of cyclophosphamide could establish rat model of premature ovarian failure with a successful rate of 87.5%. Compared with the normal group, the vaginal smear in the model group was featured with signs of estro gen deficiency, early-follicle reduction, structural damage to the follicle, and reducing number of mature follicles; the level of E2 was significantly reduced (P<0.05), levels of P, FSH and ILH were increased (all P<0.05), and mRNA expression of estrogen-related ERP3, PI3K, Akt and mTOR were all reduced (all P<0.05). Compared with the model group, the number of mature follicle was increased in the medication group and acupuncture groups, the levels of E2 was obviously increased (all P<0.05). level of FSH was reduced (all P<0.05), and mRNA expression of PI3K, Akt and mTOR all showed an increasing trend (all P<0.05). The differences of each index result between acupuncture groups and medication group were not significant (all P>0.05).
  
  
  CONCLUSIONS
  Acupuncture has certain advantage for the treatment of premature ovarian failure, which achieves similar therapeu tic effect as estrogen; the possible mechanism may be related to up-regulation of gene and protein expression in PI3K/Akt/mTOR signaling pathway.
authors.forename: Yimin
authors.initials: Y
authors.lastname: Zhang
authors.forename: Bin
authors.initials: B
authors.lastname: Yu
authors.forename: Jia
authors.initials: J
authors.lastname: Chen
authors.forename: Zhisheng
authors.initials: Z
authors.lastname: Zhao
authors.lastname: Wang Jiali
authors.forename: Fasen
authors.initials: F
authors.lastname: Huang
authors.forename: Yuee
authors.initials: Y
authors.lastname: Lin
authors.forename: Mengwei
authors.initials: M
authors.lastname: Wang
authors.forename: Yupei
authors.initials: Y
authors.lastname: Zhang
authors.forename: Bo
authors.initials: B
authors.lastname: Wei
mesh_terms: D015669:Acupuncture Points; D015670:Acupuncture Therapy; D000818:Animals; D004958:Estradiol / Q000097:blood; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood; D006801:Humans; D051058:Oncogene Protein v-akt / Q000235:genetics / Q000378:metabolism*; D019869:Phosphatidylinositol 3-Kinases / Q000235:genetics / Q000378:metabolism; D016649:Primary Ovarian Insufficiency / Q000097:blood / Q000201:enzymology / Q000235:genetics / Q000628:therapy*; D011374:Progesterone / Q000097:blood; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction; D058570:TOR Serine-Threonine Kinases / Q000235:genetics / Q000378:metabolism*
chemical_list: D004958:Estradiol; D005640:Follicle Stimulating Hormone; D051058:Oncogene Protein v-akt; D019869:Phosphatidylinositol 3-Kinases; D011374:Progesterone; D058570:TOR Serine-Threonine Kinases; C546843:mTOR protein, mouse