Ginsenoside Rb1 alleviates hypoxic brain injury in neonatal mice through ERK pathway
10.16557/j.cnki.1000-7547.2025.03.001
- VernacularTitle:人参皂苷Rb1通过ERK通路改善新生小鼠缺血缺氧性脑损伤
- Author:
Feihong YANG
1
;
Chao LIN
1
;
Xiangyu SUN
1
;
Yongqiang WANG
1
;
He LI
1
;
Lili LI
1
;
Yue YONG
1
;
Jiangang SONG
1
Author Information
1. 上海中医药大学曙光医院麻醉科,上海 201203
- Publication Type:Journal Article
- Keywords:
hypoxic-ischemic encephalopathy(HIE);
ginsenoside Rb1;
oligodendrocytes;
myelin regeneration;
ERK signaling pathway;
mouse
- From:
Chinese Journal of Neuroanatomy
2025;41(3):261-271
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the neuroprotective effects of ginsenoside Rb1 in neonatal mice with Hypoxic Ischemia(HI)and analyze its potential molecular mechanisms.Methods:Seven-day-old C57BL/6 neonatal mice were randomly assigned to three groups:Sham group,hypoxic-ischemic(HI)model group,and HI model+ginsenoside Rb1 intervention group(HI+Rb1),with 10 mice per group.The modified Rice-Vannucci method was used to establish the HI model,and ginsenoside Rb1(20 mg/kg)was administered via intraperitoneal injection for 7 consecutive days post-surgery(once per day).Brain damage was assessed on days 7 and 14 post-surgery by evaluating cortical neurons and glial cell numbers,as well as the activation status of the ERK signaling pathway.Additionally,in utero electroporation(IUE)was used to overexpress the ERK signaling pathway in the cortical neurons,and the impact of ERK activation on glial cell development was observed.Further,IUE was used to overexpress ERK in the cortex of P0 neonatal mice,fol-lowed by the HI model on day 7 to analyze the effects of enhanced ERK signaling on oligodendrocyte development and myelin regeneration.Results:Compared to the HI group,the HI+Rb1 intervention group showed significant improve-ment in motor ability,reduction in brain injury area,less mature neuron loss,and increased newborn neurons.Addi-tionally,the number of oligodendrocytes in the cortex was increased,and the activation of the ERK signaling pathway was enhanced.In mice with overexpression of the ERK signaling pathway in the cortex,there was a significant increase in oligodendrocytes.In the HI model with ERK overexpression,an increased number of oligodendrocyte precursor cells were found around the brain injury area,consistent with the results of ginsenoside Rb1 intervention.Conclusion:Gin-senoside Rb1 exerts neuroprotective effects in neonatal mice with hypoxic-ischemic brain injury,potentially through the enhancement of ERK signaling,promoting oligodendrocyte proliferation and myelin regeneration.
