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The effect of chronic intermittent hypoxia on atherosclerosis in rat offspring
Ziyan Wang1, Yiming Zeng1, Huihuang Lin1
1Department of Pulmonary and Critical Care Medicine, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian, China.
Insights
Offspring exposed to chronic intermittent hypoxia (CIH) in utero developed arterial wall thickening. Subsequent CIH exposure exacerbated these pre-atherosclerotic lesions, indicating long-term cardiovascular risks.
Area of Science:
- Cardiovascular Biology
- Developmental Biology
- Inflammation Research
Background:
- Chronic intermittent hypoxia (CIH) during pregnancy may impact offspring cardiovascular health.
- Understanding the long-term effects of prenatal CIH exposure is crucial for cardiovascular disease prevention.
Purpose of the Study:
- To investigate if rat offspring exposed to CIH in utero develop systemic inflammation and arterial injury.
- To evaluate the susceptibility of these offspring to CIH-mediated arterial damage.
Main Methods:
- Established a CIH rat model to study prenatal and postnatal exposure effects.
- Measured inflammatory markers (p38MAPK, NF-κB p65, CRP, TNFα, IL-8) and assessed arterial pathology in offspring.
Main Results:
- Intrauterine CIH significantly upregulated p-P38MAPK and NF-κB p65, key inflammatory markers.
- Prenatal CIH exposure led to increased arterial tunica intima thickness in offspring.
- Combined prenatal and postnatal CIH exposure synergistically worsened arterial wall thickening.
Conclusions:
- Prenatal CIH exposure induces arterial wall thickening and pre-atherosclerotic lesions in offspring via NF-κB p65 and p-p38 MAPK pathways.
- Postnatal CIH re-exposure exacerbates these lesions, highlighting sustained cardiovascular vulnerability.
Background:
To determine whether rat offspring born under conditions of chronic intermittent hypoxia (CIH) would develop systemic inflammation and be susceptible to CIH-mediated injury on artery.
Methods:
CIH rat model was established. The expression levels of p38MAPK, NF-κB p65, CRP, TNFα, and IL-8 were measured. The arterial pathology of offspring whose mothers were exposed to CIH during pregnancy was evaluated.
Results:
The levels of p-P38MAPK and NF-κB p65 were significantly up-regulated following induction of intra-uterine CIH Induction of intra- and extra-uterine CIH had an interaction regarding the expression profiles of these markers (P < 0.01, P < 0.01, P < 0.01, P < 0.01, P = 0.020, respectively). Pathologic analysis of the arteries confirmed that intra-uterine CIH increased the tunica intima thickness (P < 0.01), but had no effect on the tunica media (P = 0.974). Furthermore, induction of intra- and extra-uterine CIH had a synergistic interaction on tunica intima thickness (P = 0.004).
Conclusions:
Intra-uterine CIH caused tunica intima thickening and development of pre-atherosclerotic lesions in offspring via NF-κB p65 and p-p38 MAPK. Furthermore, the expression of NF-κB p65 and p-p38 MAPK and the extent of pre-atherosclerotic lesions were either exacerbated or alleviated in offspring when re-exposed to CIH later.
