PMID- 37403489
OWN - NLM
STAT- MEDLINE
DCOM- 20230921
LR  - 20231012
IS  - 2472-1727 (Electronic)
VI  - 115
IP  - 15
DP  - 2023 Sep 1
TI  - Prenatal immobility stress: Relationship with oxidative stress, inflammation, 
      apoptosis, and intrauterine growth restriction in rats.
PG  - 1398-1410
LID - 10.1002/bdr2.2205 [doi]
AB  - BACKGROUND: Prenatal stress is a significant risk factor affecting pregnant women 
      and fetal health. In the present study, we aimed to investigate the effect of 
      immobility stress at different periods of pregnancy on oxidative stress, 
      inflammation, placental apoptosis and intrauterine growth retardation in rats. 
      METHODS: Fifty adult virgin female Wistar albino rats were used. Pregnant rats 
      were exposed to 6 h/day immobilization stress in a wire cage at different stages 
      of pregnancy. Groups I and II (Day 1-10 stress group) were sacrificed on the 10th 
      day of pregnancy, and Group III, Group IV (10-19th-day stress group), and Group V 
      (1-19th-day stress group) were sacrificed on the 19th day of pregnancy. 
      Inflammatory cytokines, including interleukin-6 (IL-6) and interleukin-10 
      (IL-10), serum corticotropin-releasing hormone (CRH), and corticosterone levels 
      were measured by enzyme-linked immunosorbent assay. Malondialdehyde (MDA), 
      superoxide dismutase (SOD), and catalase (CAT) levels in the placenta were 
      spectrophotometrically measured. Histopathological analyses of the placenta were 
      evaluated by hematoxylin and eosin staining. Tumor necrosis factor-alpha (TNF-alpha) 
      and caspase-3 immunoreactivity in placenta tissues were determined by the 
      indirect immunohistochemical method. Placental apoptosis was determined by the 
      TUNEL staining method. RESULTS: We found that the immobility stress during 
      pregnancy significantly increased serum corticosterone levels. Our results showed 
      that the immobility stress diminished the number and weight of fetuses in rats 
      compared to the non-stress group. The immobility stress caused significant 
      histopathological changes in the connection zone and labyrinth zone and increased 
      placental TNF-alpha and caspase-3 immunoreactivity and placental apoptosis. In 
      addition, immobility stress significantly increased the levels of 
      pro-inflammatory IL-6 and MDA and caused a significant decrease in the levels of 
      antioxidant enzymes such as SOD, CAT, and anti-inflammatory IL-10. CONCLUSIONS: 
      Our data suggest that immobility stress causes intrauterine growth retardation by 
      activating the hypothalamic-pituitary-adrenal axis and deteriorating placental 
      histomorphology and deregulating inflammatory and oxidative processes.
CI  - (c) 2023 Wiley Periodicals LLC.
FAU - Kaya, Sinem Albayrak
AU  - Kaya SA
AD  - Department of Midwifery, Biruni University, Faculty of Health Sciences, Istanbul, 
      Turkiye.
FAU - Okuyan, Hamza Malik
AU  - Okuyan HM
AD  - Department of Physiotherapy and Rehabilitation-Faculty of Health Sciences, 
      Biomedical Technologies Application and Research Center, Sakarya University of 
      Applied Sciences, Sakarya, Turkiye.
FAU - Erboga, Zeynep Fidanol
AU  - Erboga ZF
AD  - Department of Histology and Embriology, Tekirdag Namik Kemal University, Faculty 
      of Medicine, Tekirdag, Turkiye.
FAU - Guzel, Savas
AU  - Guzel S
AD  - Department of Medical Biochemistry, Faculty of Medicine, Tekirdag Namik Kemal 
      University, Tekirdag, Turkiye.
FAU - Yilmaz, Ahsen
AU  - Yilmaz A
AD  - Department of Medical Biochemistry, Cerrahpasa Faculty of Medicine, Istanbul 
      University-Cerrahpasa Istanbul, Istanbul, Turkiye.
FAU - Karaboga, Ihsan
AU  - Karaboga I
AD  - Department of Histology and Embryology, Faculty of Medicine, Kirklareli 
      University, Kirklareli, Turkiye.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20230705
PL  - United States
TA  - Birth Defects Res
JT  - Birth defects research
JID - 101701004
RN  - 130068-27-8 (Interleukin-10)
RN  - EC 3.4.22.- (Caspase 3)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (Interleukin-6)
RN  - W980KJ009P (Corticosterone)
RN  - EC 1.15.1.1 (Superoxide Dismutase)
SB  - IM
MH  - Humans
MH  - Rats
MH  - Female
MH  - Pregnancy
MH  - Animals
MH  - *Fetal Growth Retardation
MH  - *Placenta/metabolism
MH  - Interleukin-10/metabolism/pharmacology
MH  - Caspase 3/metabolism/pharmacology
MH  - Rats, Wistar
MH  - Tumor Necrosis Factor-alpha/metabolism/pharmacology
MH  - Interleukin-6/pharmacology
MH  - Corticosterone/metabolism/pharmacology
MH  - Hypothalamo-Hypophyseal System/metabolism
MH  - Pituitary-Adrenal System/metabolism
MH  - Oxidative Stress
MH  - Inflammation/complications/metabolism/pathology
MH  - Apoptosis
MH  - Superoxide Dismutase/metabolism
OTO - NOTNLM
OT  - immobility stress
OT  - inflammation
OT  - intrauterine growth retardation
OT  - oxidative stress
OT  - placental apoptosis
EDAT- 2023/07/05 06:42
MHDA- 2023/09/21 06:42
CRDT- 2023/07/05 03:13
PHST- 2023/04/14 00:00 [revised]
PHST- 2022/03/23 00:00 [received]
PHST- 2023/05/10 00:00 [accepted]
PHST- 2023/09/21 06:42 [medline]
PHST- 2023/07/05 06:42 [pubmed]
PHST- 2023/07/05 03:13 [entrez]
AID - 10.1002/bdr2.2205 [doi]
PST - ppublish
SO  - Birth Defects Res. 2023 Sep 1;115(15):1398-1410. doi: 10.1002/bdr2.2205. Epub 
      2023 Jul 5.