RESUMO
OBJECTIVE To investigate the effect of sodium ferulate (SF) on lipopolysaccharide (LPS)-induced preterm delivery and intra-uterine fetal death (IUFD). METHODS Pregnant Kunming mice were subcutaneously pretreated with SF (25 or 50 mg · kg-1) from gestational day (GD) 10 to GD 15 and with the single injection of LPS (150μg·kg-1, ip) on GD15.5. The incidence of preterm delivery and IUFD was observed. HE staining was used for uterine and placental histological evaluation. The levels of thiobarbituric acid reactive substances (TBARS) and reduced glutathione (GSH) as well as the activities of glutathione S-transferase (GST) and glutathione peroxidase (GSH-Px) were detected in the maternal liver, placenta, and fetal liver using commercial kits. Interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) levels in amniotic fluid were evaluated by enzyme linked immunosorbent assay. RESULTS For LPS group, the incidence of preterm was 47.8%, delivery time was (17.5 ± 1.3) d, and the pups′survival rate was only 42.6%. Compared with LPS-treated group, SF 50 mg · kg-1 group showed a lower incidence of preterm (14.3%, P<0.01), longer gestational days (18.4 ± 0.5, P<0.05), and a higher pups′survival rate (75.6%, P<0.01). SF 50 mg · kg-1 restored the LPS-induced GSH both in the maternal and fatal liver (a tendency without statistical significance), GST activity〔(163±82) kU·g-1 protein vs (95±90) kU·g-1 protein, P<0.01)〕in the placenta, TBARS content〔(2.5±0.4)μmol·g-1 protein vs (3.1±0.6)μmol·g-1 protein, P<0.01〕in the fetal liver, and TNF-αlevel〔(11±8) ng·L-1 vs (20±8) ng·L-1, P<0.01〕in the amniotic fluid. SF also attenuated LPS-induced placental congestion and neutrophil infiltra?tion in the uterus. CONCLUSION SF may protect against LPS-induced preterm delivery and IUFD, and anti-oxidation as well as anti-inflammation may contribute to these effects.
RESUMO
OBJECTIVE To investigate the transgenerational effects of a hypothala mic-pituitary-ad-renal (HPA)axis -associated neuroendocrine metabolic progra mming alteration fro m F1 to adult second generation (F2)with prenatal ethanol ingestion.METHODS Pregnant Wistar rats were ad ministered with ethanol (4 mg·kg -1·d -1 )fro m gestational day 1 1 until delivery.F1 rats were fed a high-fat diet fro m postnatal week 4 (PW4)and were cross-mated in PW 16 -20.F2 rats were fed a standard diet fro m PW4 and rectal te mperature was measured in PW20,oral glucose tolerance test (OGTT)was con-ducted in PW21 ,blood sa mples and hypothala mus were collected in PW24 to investigate seru m lipids and HPA axis activity.RESULTS Co mparing to the F2 control group ,rectal te mperature in F2 ethanol group were higher (P<0.01 ),sugar tolerance in F2 male group was i mpaired (P<0.05),seru m corti-costerone and hypothala mus arginine vasopressin (AVP) mRNA were increased (P <0.05);seru m insulin were decreased (P<0.05)and male rats showed i mpaired glucose tolerance (P<0.05);seru m high-density lipoproteincholesterol (HDL-C)decrease (P <0.05)and total cholesterol (TCH)/HDL-C and low density lipoproteincholesterol (LDL-C)/HDL-C ratios were markedly increased (P <0.05,P <0.01 ).CONCLUSION Prenatal ethanol exposure induced metabolic syndro me has transgenerational effects,which may originate fro m the intrauterine progra mming of altered HPA axis-associated neuroen-docrine metabolis m.