Objective: To investigate the effect of Baichanting compound(BCT) on neuroethology

oxidative stress response

and dopamine (DA) content in mice with Parkinson's disease(PD) induced by 1-methyl-4-phenyl-1

2

3

6-tetrahydropyridine (MPTP)

and discuss the possible mechanism of BCT's neuroprotection effect in PD models. Method: Male C57BL/6 mice were processed with MPTP-HCl (30 mg·kg-1·d-1

ip

0.9% normal saline solution) for 5 days to establish PD mice models;the mice were randomly divided into normal group

model group

levodopa and benserazide tablets group(62.50 mg·kg-1·d-1)

BCT high-dose

middle-dose and low-dose groups (363.00

181.50

95.75 mg·kg-1·d-1). All treatment groups were dissolved with 0.5% carboxyl methyl cellulose (CMC-Na);BCT compound was ig given once daily for 20 days.The pole and independent activity experiments were done to observe the mice behavior change.The content of DA in corpus striatum was detected by UPLC-MS-MS method.Superoxide dismutase (SOD)

glutathione-peroxidase (GSH-Px)

monoamine oxidase-B (MAO-B)

and malondialdehyde (MDA) levels in midbrain substantia nigra tissues were detected by chemical colorimetry method. Result: Compared with the normal group

pole climbing time was significantly longer in model group(P<0.05)

autonomic activity significantly reduced(P<0.05)

content of DA in corpus striatum

SOD and GSH-Px levels significantly reduced (P<0.01)

MDA and MAO-B levels significantly increased (P<0.01). Compared with the model group

neural behavior was improved significantly(P<0.05)

the content of DA in corpus striatum

the activity of SOD and GSH-Px were increased significantly(P<0.01

P<0.01)

and MDA and MAO-B levels were significantly reduced (P<0.01) in PD model mice after the treatment of BCT. Conclusion: BCT can significantly improve neurobehavioral change and the content of striatal DA in PD mice by improving the body's ability to resist oxidation and scavenging free radicals.It is the possible mechanism of neuroprotective potential for BCT in PD model.