Neuroglobin protects offspring rats from neuronal damage induced by sevoflurane exposure to pregnant rats by inhibiting endogenous apoptosis. Issue 76 (August 2019)

• Record Type: Journal Article
• Authors: Zhang, Yongfang; Yang, Fan; Gao, Yan; Shan, Yangyang; Dong, Yunxia; Liu, Hongtao
• Is Part Of: International journal of developmental neuroscience. Issue 76(2019:Aug.)
• Page Start: 17
• Page End: 24
• Publication Date: 2019-08
• Subjects: Neuroglobin -- Sevoflurane -- Endogenous apoptosis -- Hemin -- Neuroprotection; Developmental neurobiology -- Periodicals; Neurology -- Periodicals; Neurologie du développement -- Périodiques; Developmental neurobiology; Periodicals; 612.8
• DOI: 10.1016/j.ijdevneu.2019.06.001
• Languages: English
• ISSNs: 0736-5748

Abstract

Highlights: Maternal sevoflurane exposure in pregnancy affected Ngb expression in neonatal rats. Hemin inhibited the decline of Ngb caused by sevoflurane in offspring rats. Ngb over expression inhibited the endogenous apoptosis induced by sevoflurane. Elevated Ngb increased Hif-1α expression. Ngb over expression improved the long-term learning and memory of offspring rats. Abstract: As a general anesthesia drug, sevoflurane has been found to be potentially neurotoxic to the developing brain. Neuroglobin (Ngb) is a novel oxygen-carrying globulin that has been demonstrated to have neuroprotective effects in a variety of central nervous system disorders. However, it is unclear whether Ngb has a protective effect on nerve damage caused by sevoflurane. Therefore, this study was designed to investigate the effect and related mechanisms of Ngb on neural injury induced by sevoflurane. Pregnant rats on gestational day 20 (G20) were exposed to 3.5% sevoflurane for two hours, which led to an increase of Ngb on the 0-1st day after birth and decreased significantly on the 3rd day, while Cytochrome c increased from the 1 st day until the 7th day of offspring rats. Meanwhile, sevoflurane reduced Bcl-2 and Hif-1αand increased Bax and cleaved-caspase 3 in the third day after birth. Hemin inhibits endogenous apoptosis by increasing Ngb and Hif-1α. And increased Ngb improved the damage of long-term learning and memory induced by sevoflurane and increased the number of neurons in the hippocampus. We concluded that Ngb can improve the neuronal injury induced by sevoflurane exposure by inhibiting apoptosis and increasing the number of neurons. And this protective effect of Ngb may be related to Hif-1α signaling pathway. This finding may provide a novel therapeutic approach for sevoflurane -induced nerve damage.