Acta Pharmacologica Sinica 2006 September; 27 (9): 1222-1230; doi: 10.1111/j.1745-7254.2006.00360.x

 
Original Article
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Ginkgo biloba extract suppresses hypertrophy and extracellular matrix accumulation in rat mesangial cells1
 

Jian-yun WANG2, Xiao-xing YIN2,6, Yun-ming WU2, Dao-quan TANG2, Yuan-yuan GAO2, Mei-rong WAN4, Xiao-yu HOU3, Bei ZHANG5

2Department of Pharmacy, 3Provincial Key Lab for Brain Diseases Bioinformation, Xuzhou Medical College, Xuzhou 221002, China; 4Center-Laboratory, Affiliated Hospital of Xuzhou Medical College, Xuzhou 221002, China; 5Department of Obstetrics and Gynecology, The Third People's Hospital of Xuzhou, Xuzhou 221002, China

 

Aim: To observe the effects of Ginkgo biloba extract (EGb) on the hypertrophy of mesangial cells and the accumulation of extracellular matrix (ECM) in mesangial cells.

 

Methods: Cultured mesangial cells were allotted into 7 groups: normal group, solvent control group, high glucose group, low dose of EGb group, moderate dose of EGb group, high dose of EGb group, and captopril group. Activities of cell antioxidases, S phase percentage and G0/G1 phase percentage, collagen IV and laminin, Smad2/3 and Smad7, TGF-β1 mRNA were measured by different methods.

 

Results: For EGb-treated groups, when compared with high glucose group, the cell percentage of S phase was raised and the percentage of G0/G1 was lowered. The intensity of oxidative stress was weakened. The expression of Smad2/3 was greatly decreased and Smad7 was increased. Collagen IV, laminin and TGF-β1 mRNA were also reduced.


Conclusion:
EGb can suppress cell hypertrophy and the accumulation of ECM in rat mesangial cells, which means it could play a vital role in the delay of glomerulosclerosis in diabetic nephropathy.

 

Keywords: ginkgo biloba extract; glomerulosclerosis; oxidative stress; TGF-β1; Smads

 
1 Project supported by College Natural Science Research Foundation of Jiangsu Province (No 03KJ13360143).

6 Correspondence to Dr Xiao-xing YIN.
Phn/Fax 86-516-326-2136.
E-mail yinxx@xzmc.edu.cn
Received 2006-01-13     Accepted 2006-03-31

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