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- Title
Triptolide protects podocytes from puromycin aminonucleoside induced injury in vivo and in vitro.
- Authors
Chun-Xia Zheng; Zhao-Hong Chen; Cai-Hong Zeng; Wei-Song Qin; Lei-Shi Li; Zhi-Hong Liu
- Abstract
Extracts of Tripterygium wilfordii Hook F have been used to treat glomerulonephritis for more than 30 years in China with dramatic antiproteinuric effects. Triptolide, a diterpene triepoxide, is one of the major active components of these extracts. To clarify its antiproteinuric effects we induced podocyte injury by puromycin aminonucleoside. Triptolide effectively reduced the proteinuria induced by puromycin in nephrotic rats without reducing the glomerular filtration rate. The antiproteinuric effect was associated with improvement in the foot process effacement, a decrease in the podocyte injury marker desmin as well as the restoration of nephrin and podocin expression and distribution. In cultured mouse podocytes triptolide pretreatment prevented the puromycin-induced disruption of the actin cytoskeleton and microfilament-associated synaptopodin while protecting nephrin and podocin expression. Triptolide suppressed reactive oxygen species generation and p38 mitogen-activated protein kinase activation while restoring RhoA signaling activity. These results show that triptolide ameliorates puromycin aminonucleoside-mediated podocyte injury in vivo and in vitro.Kidney International (2008) 74, 596–612; doi:10.1038/ki.2008.203; published online 28 May 2008
- Publication
Kidney International, 2008, Vol 74, Issue 5, p596
- ISSN
0085-2538
- Publication type
Academic Journal
- DOI
10.1038/ki.2008.203