Study on the protective mechanism of neuropeptide S in neonates with hypoxic ischemic encephalopathy

Abstract

Hypoxic-ischemic brain damage (HIBD) is a severe complication of neonatal asphyxia that contributes significantly to neonatal mortality, cerebral palsy, and delays in intellectual and motor development. Neuropeptide S (NPS) plays a role in the regulation of various physiological processes. This study aimed to determine the morphological localization of NPS in hypothalamic target neurons during HIBD, providing a basis for further investigation of HIBD. Seven-day-old SD neonatal male rats were assigned to a sham group and a model group to establish the HIBD model. Then, the rats in the model group were further averagely divided into the NPS group and the normal saline group. Immunohistochemical staining of Fos immunoreactivity (Fos-IR) found that NPS administration resulted in a significant increase in the count of Fos-IR neurons in the suprachiasmatic nucleus (122%), paraventricular nucleus (108%), dorsal tuberomammillary nucleus (174% and 386%), ventromedial hypothalamic nucleus (116%), arcuate nucleus (167%), perifornical nucleus (320%), ventral tuberomammillary nucleus (441%), and lateral hypothalamic area (278%) (P < 0.0001), compared to the normal saline group. During HIBD, NPS can protect the above neurons and activate the above target neurons in the hypothalamus to participate in the sleep and wake cycle, mood, diet, circadian rhythm, temperature and neuroendocrine regulation.