Abstract: Objective To investigate the preventive and therapeutic effects of baicalein (BAI) on experimental autoimmune encephalomyelitis (EAE) in mice and its effects on polarization and inflammatory factors of microglia in central nervous system. Methods Fifty female C57BL/6 mice were randomly divided into the blank control group, the EAE model group and the BAI low, medium and high dose groups, with 10 mice in each group. The blank control group was not treated, and EAE model was established in the other groups. BAI low, medium and high dose groups were given BAI (75, 150 and 300 mg·kg-1·d -1) by gavage respectively, while the blank control group and the EAE model group were given the same volume of normal saline by gavage for 14 consecutive days. The neurological deficit and inflammatory demyelination of spinal cord were observed. The immunofluorescence double staining was used to detect the expression of inducible nitric oxide synthase (iNOS) in M1 type microglia, arginase 1 (Arg1) in M2 type microglia and divergence index (RI) in Iba-1 positive microglia of spinal cord of mice. The real time fluorescent quantitative RT-PCR was used to detect iNOS, Arg1 and mRNA of TNF-α, IL-10 expression of spinal cord of mice. Results No disease was found in the blank control group, but the other groups all had the disease in varying degrees. Compared with the EAE model group, the onset latency and peak time were prolonged (P＜0.05), the peak neurological dysfunction score was decreased (P＜0.05), the demyelination degree of spinal cord was reduced, the expression level of iNOS in Iba-1 positive microglia was decreased (P＜0.05), the expression of Arg1 was increased (P＜0.05) and the RI value was decreased in the BAI intervention groups (P＜0.05). The morphology of microglia tended to be M2 polarization. The mRNA expressions of iNOS and TNF-α of spinal cord decreased (P＜0.05), but the mRNA expression of Arg1 and IL-10 increased (P＜0.05). The higher the dose of BAI, the more obvious the effect. Conclusion BAI can prevent and treat EAE in a dose-dependent manner in mice. Its mechanism may be related to the correction of M1/M2 microglia cell imbalance and regulation of the inflammatory factors TNF-α and IL-10 expression.

Key words: scutellaria baicalensis, encephalomyelitis, autoimmune, experimental, microglia, demyelinating diseases, nitric oxide synthase, arginase, baicalein