Baicalin Ameliorates L-Glutamate-induced Hippocampal Oxidative Stress
Injury and Apoptosis in Mice by Regulating Nrf2/HO-1 Signaling Pathway
Abstract
Objective: To explore the effect and mechanism of baicalin on
L-Glutamate-induced oxidative stress injury in the hippocampus of mice.
Methods: Forty mice were randomly assigned to five groups:
Sham, Model, N-Acetyl-L-Cysteine (NAC), and baicalin (BA-7.5mg/kg and
BA-15mg/kg). A model of excitatory amino acid toxicity with oxidative
stress injury was induced by injecting L-Glutamate into the lateral
ventricle. The drugs were then injected intraperitoneally. Six hours
later, behavioral tests were performed. The lesions of brain were
observed using HE staining, while the apoptosis of neurons was assessed
through TUNEL staining. The levels of superoxide dismutase (SOD) and
malondialdehyde (MDA) were determined using biochemical methods. The
expression of Cytochrome C (CytC) was assessed by immunohistochemistry.
Fluorescent staining was employed to detect the expression of reactive
oxygen species (ROS). The levels of Nrf2, HO-1, SOD2 and Catalase (Cat)
were detected by qPCR and WB. Results: The behavioral tests
showed that the motion distance and pain threshold were reduced. MDA,
ROS, and CytC were increased, SOD and Cat were decreased. The CA3 region
of the hippocampus exhibited pathological changes, and the rate of
TUNEL-positive increased. Baicalin could reverse these changes,
especially BA-7.5mg/kg. Conclusion: Baicalin can reduce the
hippocampal injury induced by L-Glutamate. This may be related to the
activation of the Nrf2/HO-1 signaling pathway.