Objective: To investigate the regulatory effect of the water extract from Mori Folium on the gene expressions of Toll-like receptors (TLRs) in the liver from diabetic mice

and explore its action mechanism. Method: ICR mice were randomly divided into normal group (n=6) and diabetic group. The mice in diabetic group received high-fat and high-sugar fodder for 10 weeks and injection with 100 mg·kg-1 streptozotocin (STZ) for 3 days continuously to establish the diabetic mice models. The successfully modeled mice were then randomly divided into model group

metformin gorup (600 mg·kg-1)

Mori Folium groups (high dose 8 g·kg-1

middle dose 4 g·kg-1

and low dose 2 g·kg-1) for 10 weeks

n=6 in each group. The drugs were given by ig administration

and the fasting blood glucose was detected every week. Oral glucose tolerance test was conducted in the mid and later phases of experiment. After ig administration for 10 weeks

serum insulin (INS)

total cholesterol (T-CHO)

triglyceride (TG) and tumor necrosis factor-α (TNF-α) were detected

and the expression level of TLR 1-9 in the liver was measured with quantitative real-time PCR. Result: After the diabetic model mice were treated with Mori Folium water extract

their water intake was reduced; fasting blood glucose was significantly reduced; glucose tolerance was improved; blood fat was significantly reduced; insulin concentration was dramatically increased; insulin resistance was improved; and serum TNF-α level was reduced (P<0.05

P<0.01). Quantitative Real-time PCR data showed that TLR1

TLR2

TLR3

TLR7

TLR8 and TLR9 mRNA expression levels were significantly increased in livers of the diabetic rats (P<0.05

P<0.01

as compared with normal group)

and TLR5 expression level in model group was significantly lower than that in normal group. In addition

the expression levels of TLR7

TLR8 and TLR9 in liver of Mori Folium middle dose group were significantly lower than those in model group (P<0.05

P<0.01). Conclusion: The water extract of Mori Folium could ameliorate diabetes

and its mechanism may be partly related to inhibiting the TLRs expression in the liver.