Objective: To explore the effect of baicalin zinc (HBZn) in repairing BNB in mice by alleviating anti-oxidative stress and activating hematogenous factors in optic nerve injury. Method: A model of optic nerve injury in mice was established by unilateral interlocking carotid artery

and the mice were divided into 7 groups

namely ischemia group

sham operated group

HBZn group (3.75

6.5

13 mg·kg-1)

HB group

and zinc gluconate group. Each group was administered by gavage for 5 days before operation. Optic nerve crush injury was made on every group

except for sham group. Mitochondrias were observed under electron microscope; superoxide dismutase (SOD)

malondialdehyde (MDA)

and myeloperoxidase (MPO) of plasma were measured by colorimetric. The expressions of immunoglobulin G(IgG)

Fibriogen and matrix metallo protein9(MMP-9) were detected by Western blot. MMPs/TIMPs were detected by qPCR. Result: HBZn can effectively prevent the injury of mitochondria

reduce the concentrations of MDA and MPO

increase the concentration of SOD

compared with HB group and znic gluconate group (P < 0.05). HBZn can reduce the expressions of IgG

Fibriogen and MMP-9 more effectively than ischemia group

suppress the expression of the MMPs family and adjust the balance of MMPs/TIMPs. Conclusion: HBZn can protect the optic nerve injury in mice

and its mechanism may be correlated with the ability to resist oxidative stress and the activating MMP-9

IgG and Fibriogen. HBZn has better anti-oxidative and repairing abilities than monomer baicalin and trace element zinc.