hubarb ( RO ) has been shown to be effec-tive in slowing the
progression of CRF in diabeticrats, but its mechanism
was not very clear. Thisstudy was
designed to investigate the effects of ROon STZ -induced diabetic rats. 24 SD rats
wererandomly divided into 3 groups: untreated diabeticgroup (n= 8),RO treated group (started to
haveRO at 8 hrs after bollus
injection of STZ,n= 8) ,normal control (n = 8). Results: (1) The
meanmesangial area in untreated diabetic rats increasedmarkedly on 28th day after STZ
injection (2. 50±0. 25 vs 0. 857 ± 0. 06,P<0. 01 ). RO treatmentprevented the mesangial
expansion as compared tountreated group. (1. 13± 0. 14 vs 2. 50± 0. 25 ,P<0. 05). (2)￣
3H-proline incorporation rate of thegloumeruli in the untreated diabetic rats glomelulishowed a
tendency to increase on 7th day and 28thday of the experirnent,and this tendency was
sup-pressed by RO
treatment. (P<0. 1) . (3)Theamount of glomelular fibronectin (Fn) in
untreat-ment diabetic rats increased significantly on 7th dayafter STZ injection (34.64±4. 72 vs
20. 72 ± 0.88 ,P<0. 01) , this abnormal increase of Fn was re-duced by RO treatment. (6. 18±
0. 47 vs 34. 64 ±4.72, P < 0. 01). (4)The weight of untreatment dia-betic rats decreascd
significantly (115. 3 ± 2. 70 vs133. 5± 17. 1 P< 0. 05 ) and urinary protein excre-tion was
markedly increased ( 685. 8± 78. 3 vs 54. 8± 26. 9 P< 0. 05 ). These abnormalities were
im-proved by the treatment of RO ( 296. 5 ± 64. 1 vs685. 8± 78. 3 P<0. 05). Conclusion: RO
decreas-es the production of renal ECM in STZ- induceddiabetic rats. It might be beneficial to
the treatmentof diabetic nephropathy.