The effect of chronic intermittent hypoxia on atherosclerosis in rat offspring

• Published in: International journal of cardiology Vol. 335; pp. 98 - 103
• Main Authors: Wang, Ziyan, Zeng, Yiming, Lin, Huihuang
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 15.07.2021
• Subjects: Animals; Atherosclerosis; Atherosclerosis - etiology; Chronic intermittent hypoxia; Female; Hypoxia - complications; Inflammation; Offspring; p38 Mitogen-Activated Protein Kinases; Pregnancy; Prenatal Exposure Delayed Effects; Rats; Sleep apnea; Transcription Factor RelA; Tunica Intima; Offspring; Inflammation; Sleep apnea; Chronic intermittent hypoxia; Atherosclerosis
• ISSN: 0167-5273; 1874-1754
• DOI: 10.1016/j.ijcard.2021.04.065

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. 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. 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). 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. •CIH caused tunica intima thickening in offspring.•CIH caused development of pre-atherosclerotic lesions.•CIH increases levels of p-p38MAPK and NF-κB p65.