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Panax notoginseng saponin attenuates the hypoxic–ischaemic injury in neonatal rats by regulating the expression of neurotrophin factors
Author(s) -
Huang Jin,
Tan YaXin,
Xue LuLu,
Du RuoLan,
Chen JunJie,
Chen Li,
Li TingTing,
Bai Xue,
Yang SiJin,
Xiong LiuLin,
Wang TingHua
Publication year - 2021
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/ejn.15428
Subject(s) - panax notoginseng , asphyxia , medicine , neurotrophin , hippocampus , neurotrophic factors , tropomyosin receptor kinase b , perinatal asphyxia , anesthesia , pathological , apoptosis , pharmacology , receptor , pathology , biology , biochemistry , alternative medicine
Neonatal hypoxic–ischaemic (HI) injury is a serious complication of neonatal asphyxia and the leading cause of neonatal acute death and chronic neurological injury, and the effective therapeutic method is lacking to improve patients' outcomes. We reported in this study that panax notoginseng saponin (PNS) may provide a treatment option for HI. HI model was established using neonatal Sprague–Dawley rats and then intraperitoneally injected with different dosage of PNS, once a day for 7 days. Histological staining and behavioural evaluations were performed to elucidate the pathological changes and neurobehavioural variation after PNS treatment. We found PNS administration significantly reduced the infarct volume of brain tissues and improved the autonomous activities of neonatal rats, especially with higher dosage. PNS treatment at 40 mg/kg reduced neuronal damage, suppressed neuronal apoptosis and depressed astroglial reactive response. Moreover, the long‐term cognitive and motor functions were also improved after PNS treatment at 40 mg/kg. Importantly, PNS treatment elevated the levels of BDNF and TrkB but decreased the expression of p75NTR both in the cortex and hippocampus of HI rats. The therapeutic efficacy of PNS might be correlated with PNS‐activated BDNF/TrkB signalling and inactivation of p75NTR expression, providing a novel potential therapy for alleviating HI injury.