title: [Prenatal exposure to lipolysaccharide result in expression changes of myocardial renin angiotensin system in offspring rats].
abstract: OBJECTIVE
  To explore expression changes of myocardial renin angiotensin system induced by prenatal exposure to lipopolysaccharide in offspring rats.
  
  
  METHODS
  Twelve pregnant SD rats were randomly divided into three groups: LPS model group: intraperitoneal injection of LPS (0.79 mg/kg) at 8, 10, 12 days of pregnancy; control group: intraperitoneal injection of sterile saline (0.5 ml) at 8, 10, 12 days of pregnancy; LPS + PDTC group: intraperitoneal injection of LPS (0.79 mg/kg) at 8, 10, 12 days of pregnancy plus daily intraperitoneal injection of NF-κB inhibitor -pyrrolidine dithiocarbamate (PDTC, 100 mg/kg) on day 8 to 14 pregnancy day. Protein expression of AngiotensinII(AngII) in heart was detected by immunohistochemistry; myocardial ACE,ACE2 mRNA expression was detected by real-time PCR; protein expression of ACE and ACE2 in heart was detected by Western blot in offspring rats of various groups.
  
  
  RESULTS
  Compared with control group (0.07 ± 0.02,0.11 ± 0.01), AngII protein levels (0.14 ± 0.04) were significantly increased at 6 weeks (P < 0.01) and 16 weeks (0.17 ± 0.04, P < 0.05) in offspring rats of LPS model group, which could be significantly attenuated by PDTC intervention (0.10 ± 0.01,0.13 ± 0.03, respectively, all P < 0.05).Similarly, myocardial ACE mRNA expression in 16 weeks offspring rats of LPS model group was significantly upregulated compared with control group (1.10 ± 0.26 vs.0.72 ± 0.22, P < 0.05), which was significantly attenuated by PDTC intervention (0.67 ± 0.01, P < 0.01 vs.LPS group). Myocardial protein expression ACE2 in 16 weeks offspring rats of LPS model group was significantly downregulated compared to control group, which was slightly upregulated by PDTC intervention (P > 0.05).
  
  
  CONCLUSIONS
  Pregnancy exposure to lipopolysaccharide increases myocardial ACE and AngII expression while reduces myocardial ACE2 expression in offspring rats, which might be one of the pathomechanisms of offspring hypertension.
authors.affiliation: Department of Pharmaceutics, Pharmaceutical College, Institute of Materia Medica, Third Military Medical University, Chongqing 400038, China.
authors.forename: Yujie
authors.initials: Y
authors.lastname: Tang
authors.affiliation: Department of Pharmaceutics, Pharmaceutical College, Institute of Materia Medica, Third Military Medical University, Chongqing 400038, China.
authors.forename: Jianzhi
authors.initials: J
authors.lastname: Zhou
authors.affiliation: Department of Pharmaceutics, Pharmaceutical College, Institute of Materia Medica, Third Military Medical University, Chongqing 400038, China. Email: lpsh008@aliyun.com.
authors.forename: Xiaohui
authors.initials: X
authors.lastname: Li
mesh_terms: D000804:Angiotensin II / Q000378:metabolism; D000085962:Angiotensin-Converting Enzyme 2; D000818:Animals; D005260:Female; D008070:Lipopolysaccharides / Q000633:toxicity*; D009206:Myocardium / Q000378:metabolism*; D007703:Peptidyl-Dipeptidase A / Q000378:metabolism; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D012084:Renin-Angiotensin System
chemical_list: D008070:Lipopolysaccharides; D000804:Angiotensin II; D007703:Peptidyl-Dipeptidase A; C000705329:Ace2 protein, rat; D000085962:Angiotensin-Converting Enzyme 2