[Suppressive effects of GTW treatment on mesangial lesions in experimental irreversible glomerulosclerosis].
OBJECTIVE
To examine suppressive effects of multi-glycoside of Tripterygium wilfordii Hook. f. (GTW)on mesangial injury induced by two-injecti on of anti-Thy1. 1 monoclonal antibody(mAb) 1-22-3 in vitro.


METHODS
We established the irreversible model of glomerulosclerosis with anti-Thy1. 1 mAb 1-22-3. After 42 days of oral treatment with GTW (50 mg x kg(-1) BW)and vehicle (distilled water), to observe effects of GTW on proteinuria, renal function, mesangial morphological change, and mRNA expressions of collagen type I and TGF-beta by light microscope (LM), immunofluorescence (IF), and Reverse Transcription Polymerase Chain Reaction (RT-PCR).


RESULTS
GTW ameliorated proteinuria (from day24 to day 42) and mesangial proliferation [total cell number, GTW group 65.67+/-3.43 vs. control group 87.02+/-2.41, P < 0.05; matrix expansion, GTW group 1.20+/-0.06 vs. control group 2.77+/-0.23, P < 0.05; alpha-smooth muscle actin(alpha-SMA) expression, GTW group 1.75+/-0.33 vs. control group 2.62+/-0.15, P < 0.05; collagen type I expression, GTW group 1.68+/-0.31 vs. control group 2.06+/-0.24, P < 0.05], moreover, significantly reduced the glomerular expression of mRNA for collagen type 1(53.5% to the control group, P < 0.05)and TGF-beta(14.7% to the control group, P < 0.05)on day 42day.


CONCLUSIONS
GTW can not only decrease proteinuria, but also ameliorate mesangial alterations probably by the reduction of cytokines. GTW may be a promising agent for the prevention of progressive and irreversible glomerulosclerosis.
Wan
Yi-gang
YG
The Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing 210008, Jiangsu, China. wyg68918@sina.com
Sun
Wei
W
Shmizu
Fujio
F
Gu
Liu-bao
LB
Suziki
Koichi
K
Karasawa
Tamaki
T
Kawachi
Hiroshi
H
D000185:Actinin / Q000378:metabolism; D000818:Animals; D024042:Collagen Type I / Q000096:biosynthesis* / Q000235:genetics; D005260:Female; D005920:Glomerular Mesangium / Q000378:metabolism / Q000473:pathology*; D015432:Glomerulonephritis, Membranoproliferative / Q000378:metabolism* / Q000473:pathology; D006027:Glycosides / Q000302:isolation & purification / Q000494:pharmacology*; D010946:Plants, Medicinal / Q000737:chemistry; D011507:Proteinuria / Q000188:drug therapy; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D051381:Rats; D017208:Rats, Wistar; D016212:Transforming Growth Factor beta / Q000096:biosynthesis / Q000235:genetics; D029757:Tripterygium / Q000737:chemistry
D024042:Collagen Type I; D006027:Glycosides; D012333:RNA, Messenger; D016212:Transforming Growth Factor beta; D000185:Actinin