Abstract
Neonatal hypoxic–ischemic (HI) brain injury is a detrimental disease, which results in high mortality and long-term neurological deficits. Nevertheless, the treatment options for this disease are limited. Thus, the aim of the present study was to assess the role of liraglutide in neonatal HI brain injury in rats and investigate the associated mechanisms. The results showed that treatment with liraglutide significantly reduced infarct volume and ameliorated cerebral edema, decreased inflammatory response, promoted the recovery of tissue structure, and improved prognosis following HI brain injury. Moreover, treatment with liraglutide inhibited apoptosis and promoted neuronal survival both in the rat model and following oxygen-glucose deprivation (OGD) insult. LY294002, an inhibitor of phosphoinositide 3-kinase (PI3K), partially reversed these therapeutic effects, suggesting that the PI3K/protein kinase B (Akt) pathway was involved. In conclusion, our data revealed that treatment with liraglutide exerts neuroprotection after neonatal HI brain injury via the PI3K/Akt/glycogen synthase kinase-3β (GSK3β) pathway and may be a promising therapy for this disease.
Highlights
Despite the advancements in medical technology and nursing, hypoxic–ischemic (HI) brain injury in newborns is associated with a high disability rate and mortality
We examined the neuroprotective role of liraglutide in neonatal brain damage induced by HI injury, and we determined whether the phosphoinositide 3-kinase (PI3K)/Akt/glycogen synthase kinase-3β (GSK3β) signaling pathway is involved in this process
The oxygen-glucose deprivation (OGD) + Liraglutide + LY294002 group showed an increase in the number of transferase dUTP nick end labeling (TUNEL)-positive apoptotic cells (Figures 7A,B). in vivo, the results showed the same trend as those obtained in vitro
Summary
Despite the advancements in medical technology and nursing, hypoxic–ischemic (HI) brain injury in newborns is associated with a high disability rate and mortality. Surviving infants suffer from various degrees of neurological deficits (e.g., epilepsy, learning difficulties, cerebral palsy, and mental retardation), which require long-term or even lifelong recovery (Al-Macki et al, 2009). The physical and mental pain, as well as the high cost of HI encephalopathy, has been. Liraglutide Exerts Neuroprotection a constant source of stress for the families of patients with HI brain injury. Hypothermia, as a standard treatment, plays an important role in reducing the rates of mortality and disability, to some extent; it has a narrow therapeutic window of 6 h (Chiang et al, 2017). The development of more effective and safer treatment strategies is warranted
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