Abstract: Ｏｂｊｅｃｔｉｖｅ：To explore effect of telmisartan in a mouse model of peritoneal fibrosis,role of metadherin (Mtdh) and autophagy in this model were studied.
Ｍｅｔｈｏｄｏｌｏｇｙ：A mouse peritoneal fibrosis model was established by daily intraperitoneal injection of 3 ml of 425％ glucose dialysate for 28 days. Eighteen C57BL／6J mice were randomized into control group, model group and telmisartan treatment group. Masson staining was used to observe peritoneal thickness; immunohistochemical staining and Western Blot were used to detect expression of Fibronectin (Fib), Collagen Ⅰ (Col Ⅰ), Ecadherin, TGFβ1, Mtdh and LC3A／B in each group. In the vitro experiment, human peritoneal mesothelial cell line (HMrSV5 cells) was stimulated with TGFβ1 and transfected with a siRNA targeting Mtdh, expressions of extracellular matrix proteins, LC3A／B and Mtdh were detected with Western blotting.
Ｒｅｓｕｌｔｓ：Compared with control mice, mice exposed to peritoneal dialyate showed increased thickening of peritoneal membrane within the anterior abdominal wall, accompanied by elevated levels of Fib, Col Ⅰ, TGFβ1, Mtdh, decreased levels of Ecadherin and LC3A／BⅡ. While in telmisartan treated mice, the peritoneal thickness was reduced, and expression of Fib, 
ColⅠ, TGFβ1, Mtdh were significantly suppressed, and the expression of Ecadherin, LC3A／BⅡ were significantly increased. In vitro, siRNAmediated knockdown of Mtdh obviously reversed TGFβ1 induced expressions of ColⅠ and Mtdh,accompanied by upregulation of LC3A／BⅡ.
Ｃｏｎｃｌｕｓｉｏｎ：Telmisartan can inhibit Mtdh expression, promote autophagy and ameliorate peritoneal fibrosis.

Key words: telmisartan,autophagy,peritoneal fibrosis