The cFb were isolated and extracted from 1－3 old SD rats by trypsin digestion and differential adhesion method. After culture and passage， the 2－3 generations of cFb were taken for experimental study. The cells were divided into normal glucose control group （5.5 mmol·L^－1 D-glucose）， high glucose group （25 mmol·L^－1 D-glucose），high glucose +15 mg·L^－1 FRGTS group （F15 group）， and high glucose +30 mg·L^－1 FRGTS group （F30 group）. MTT assay was used to detect the proliferation activities of cFb in various groups， ELISA method was used to detect the levels of collagen Ⅰ and collagen Ⅲ proteins in the cFb supernatant in various groups， Real-time fluorescence quantitative PCR（RT-qPCR） was used to detect the expression levels of Smad3 and Smad7 mRNA， and Western blotting method was used to detect the expression levels of urotensin Ⅱ（UⅡ）， transforming growth factor beta 1 （TGF-β1）， Smad3 and Smad7 proteins in the cFb in various groups.

Compared with normal glucose control group， the proliferation activities of cFb in high glucose group was significantly increased （P<0.01）， and the levels of collagen Ⅰ and collagen Ⅲ proteins were significantly increased （P<0.01）.compared with high glucose group， the proliferation abilities of cFb in F15 and F30 groups were decreased （P<0.05）， and the inhibitory effect of F30 group was stronger than that of F15 group. After 24 h of intervention with FRGTS， the levels of collagen Ⅰ and collagen Ⅲproteins in the cFb supernatant were significantly lower than those in high glucose group （P<0.05）， and the effect of F30 group was more significant than that of F15 group. Compared with normal glucose control group， the expression levels of UⅡ and TGF-β1 proteins in the cFb in high glucose group were significantly increased （P<0.01），the mRNA and protein expression levels of Smad3 were significantly increased （P<0.01），and the mRNA and protein expression levels of Smad7 were significantly decreased （P<0.05）；compared with high glucose group， after 24 h of intervention with FRGTS， the expression levels of UⅡ and TGF-β1 proteins in the cFb in F15 group and F30 group were significantly decreased （P<0.01），the mRNA and protein expression levels of Smad3 were significantly decreased （P<0.01）， the mRNA and protein expression levels of Smad7 were significantly increased （P<0.05 or P<0.01），and the effect in F30 group was better than that in F15 group.

FRGTS can effectively inhibit the fibrosis induced by high glucose and protect the myocardium of diabetic rats， and its mechanism may be related to inhibiting the activation of UⅡ in the cFb and regulating the TGF-β1/Smads pathway.