Abstract
Neonatal hypoxic-ischemic brain damage (HIBD) is the main cause of severe neurological diseases and death in newborns. Macamide B is an effective monomer extracted from Maca (Lepidium meyenii Walpers), which has important biological activities such as neuroprotection and neuromodulation. The purpose of this study was to investigate whether Macamide B can exert neuroprotective effects on HIBD in newborn mice by regulating Silent information regulator factor 2-related enzyme 1 (SIRT1). A modified Rice-Vannucci method was used to construct the HIBD model of newborn mice. The pups were divided into the following groups: sham group, HI group, and Macamide B group. On the first and third days after hypoxic-ischemic (HI), immunofluorescence and Western blot experiments were used to detect the expression level of SIRT1 in the brain tissue of infants. The results of the immunofluorescence experiment showed that compared with the sham group, the expression level of SIRT1 is significantly decreased in HI group pups, while the expression level of SIRT1 in pups pretreated with Macamide B increased significantly. The results of Western blot experiments are consistent with the results of immunofluorescence experiments. Our data indicate that Macamide B may exert a neuroprotective effect on HIBD in newborn mice by up-regulating the expression of SIRT1. Macamide B may become a new medicine effective in preventing and treating HIBD.
Highlights
Neonatal hypoxic-ischemic damage (HIBD) is brain damage caused by Perinatal hypoxia
Macamide B can increase the expression of Silent information regulator factor 2-related enzyme 1 (SIRT1) protein in brain tissue of hypoxic-ischemic newborn mice
The results showed that SIRT1 was clearly labeled with neuronal cells (NeuN), astrocytes (GFAP) and microglia cells (IBA-1), indicating that SIRT1 protein was expressed in neuronal cells, astrocytes and microglia cells in the brain of HI damaged mice
Summary
Neonatal hypoxic-ischemic damage (HIBD) is brain damage caused by Perinatal hypoxia. Umbilical cord prolapse, amniotic fluid embolism, and uterine rupture are the common cause of mortality in HIBD [1,2,3]. Neonatal HIBD can cause acute death and chronic mental dysfunction, even survivors will suffer from the loss of motor ability, cognitive function, and sensory function, which will cause difficulties in learning and living in the future [4, 5]. The clinical treatment of HIBD mainly adopts therapeutic hypothermia [6], but few of active and effective treatments intervene and promote nerve repair. HIBD brings pain to the infant and brings a burden to family and country. It is urgent to explore effective treatment measures for HIBD
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