Objective:To explore the therapeutical effect of Tetramethylpyrazine on chronic allograft nephropathy of rat

reveal the relationship with CAN

then discovering mechanism of action that delaying the proceeding of CAN of rat

which provide a new way of therapy to extend survival time of transplanting kidney. Methods: We used Fisher rats as donors and Lewis rats as recipients to establish the model of CAN. 75 rats with transplanting kidney were divided into 3 groups: Ciclosporin group

TMP associating with Ciclosporin group and black group; every group for 25 rats. Renal cell apop totic index was examined by means of terminal deoxynucleotidyl transferase2mediated d-UTP nick end labeling (TUNEL). The expressions of Bcl-2 and Bax in kidney was immunohistochemically evaluated and. The kidney histology were observed by light microscope. Results:The rats of black group were died in two weeks. Ciclosporin group

appearance the histopathological changes of CAN since 4th week

it is thus evident that typical histopathological changes of CAN at 12th week. TMP associating with Ciclosporin group was later. There was significant difference(P<0.05). By Tetramethylpyrazine treatment

the apoptotic index (13.2 ±2.7 vs 28.9 ±4.4

P<0.05) and the expression of Bax (7. 12 ±0. 11 vs 13. 45 ±0. 61

P<0.05)were decreased significantly

and the expression of Bcl-2 (15.32 ±0. 22 vs 6. 89 ±0. 14

P<0.05) was increased significantly as compared with that in Ciclosporin group. Conclusion: Tetramethylpyrazine can slowed the proceeding of CAN. and protective mechanism may be partly through inhibition of cell apoptosis byregulating the expressions of apoptosis related genes Bcl-2 and Bax.