目的：研究红丝线多糖（PRP）对鼠源肝星状HSCs-T6 细胞的增殖抑制作用及其机制。方法：用质量浓度为0（空白对照）、

50、100、200 μg/ml 的PRP分别培养鼠源肝星状HSCs-T6 细胞24、48 h 后，采用MTT法测定细胞活力并计算细胞增殖抑制率，采用

免疫组化法测定细胞上清液中羟脯氨酸（Hyp）的含量；培养48 h 后，采用免疫组化法测定细胞中α-平滑肌肌动蛋白（α-SMA）的表

达水平，采用Western blot法测定细胞转化生长因子β（1 TGF-β1）和信号传导蛋白（Smad3）的蛋白表达水平。结果：与空白对照比

较，50、100、200 μg/ml PRP 均可抑制HSCs-T6 细胞增殖，培养24、48 h 后细胞的增殖抑制率分别为39.84％～69.31％、45.16％～

82.93％，且与培养时间和质量浓度呈正相关；各质量浓度PRP培养24 h后细胞上清液中Hyp含量为178.36～93.25 μg/ml，48 h后为

131.94～68.74 μg/ml，与培养时间和质量浓度呈负相关；PRP 培养48 h 后TGF-β1、Smad3 的蛋白表达水平降低（P＜0.01）。结论：

PRP对大鼠肝星状HSCs-T6 细胞的增殖有抑制作用，其机制可能与其使内源性TGF-β通路失活从而减少胶原蛋白的生成有关。

OBJECTIVE：To study inhibitory effect of Lycianthes biflora polysaccharide on the proliferation of hepatic stellate

HSCs-T6 cells in rats and its mechanism. METHODS：After treated with 0（blank control），50，100，200 μg/ml L. biflora polysaccharide

for 24 and 48 h，the activity of hepatic stellate HSCs-T6 cells in rats was determined by MTT assay and inhibitory rate of

cell proliferation was calculated；the content of Hyp in supernatant was detected by immunohistochemical assay. After 48 h，the expression

of cellular α-smooth muscle actin（α-SMA）was measured by immunohistochemical assay；both transforming growth factor

β1（TGF-β1）and Smad3 were measured by Western blot assay. RESULTS：Compared to blank control，50，100 and 200 μg/ml

L. biflora polysaccharide could inhibit the proliferation of HSCs-T6 cells；cell inhibitory rates were 39.84％-69.31％ and

45.16％-82.93％ respectively after treated for 24 and 48 h，which were positively associated with time and concentration. The contents

of Hyp in supernatant were 178.36-93.25 μg/ml and 131.94-68.74 μg/ml respectively after treated with different concentrations

of PRP for 24 and 48 h，which were negatively associated with time and concentration. The protein level of TGF-β1 and Smad3 decreased

after treated with L. biflora polysaccharide for 48 h（P＜0.01）. CONCLUSIONS：L. biflora polysaccharide can inhibit the

proliferation of hepatic stellate HSCs-T6 cells in rats，and its mechanism is associated with the inactivation of endogenous TGF-β

pathway for reducing collagen production.