Literature DB >> 27871079

Triptolide Attenuates Inflammatory Response in Membranous Glomerulo-Nephritis Rat via Downregulation of NF-κB Signaling Pathway.

Ying Zhou1, Yan Hong, Haihua Huang.   

Abstract

BACKGROUND/AIMS: Triptolide (TPL), a main active ingredient of Tripterygium wilfordii has been shown to exert anti-inflammatory effect. The role of TPL on glomerular diseases remains unclear.
METHODS: This study aims to investigate the potential anti-inflammatory effect of TPL in rats with membranous glomerulonephritis (MGN).
RESULTS: Our data showed that the pathological kidney damage was significantly alleviated by TPL treatment in MGN rats. We also found that MGN rats exhibited significantly higher (p < 0.01) level of inflammatory cytokines (TNF-α, IL-1β and MCP-1) than those in normal group, while these inflammatory cytokines levels were significantly reduced in TPL treatment group compared with model group. Additionally, we found that TPL treatment could significantly decrease the malondialdehyde (MDA) level while enhanced superoxide dismutase (SOD) activity. Meanwhile, we also found that IκB kinase inhibitor (IMD-0354) could significantly reduce the accumulation of inflammation damage and oxidative lesions. Furthermore, we observed that both TPL and IMD-0354 treatment could block IκBα degradation and suppress mRNA and protein level of nuclear factor (NF) -κB p65.
CONCLUSION: Together, all above results suggest that inflammatory response could be attenuated by TPL and this is partly due to the inhibition of NF- κB signaling pathway.
© 2016 The Author(s) Published by S. Karger AG, Basel.

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Year:  2016        PMID: 27871079     DOI: 10.1159/000452591

Source DB:  PubMed          Journal:  Kidney Blood Press Res        ISSN: 1420-4096            Impact factor:   2.687


  35 in total

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Review 8.  Triptolide: pharmacological spectrum, biosynthesis, chemical synthesis and derivatives.

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10.  Triptolide Suppresses Glomerular Mesangial Cell Proliferation in Diabetic Nephropathy Is Associated with Inhibition of PDK1/Akt/mTOR Pathway.

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