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Triptolide ameliorates fine particulate matter-induced podocytes injury via regulating NF-κB signaling pathway
Qiang Wan1, Zhongyong Liu2, Ming Yang3
1Department of Medical Cardiology, The Affiliated Hospital of Jiangxi University of Traditional Chinese Medicine, Nanchang, 330006, China. wanqiang109559140@163.com.
Background:
PM2.5 is associated closely with an increased risk of membranous nephropathy (MN), however, whether PM2.5 could induce podocytes injury, the underlying pathology for MN, has not be thoroughly studied. Triptolide, an active component in Tripterygium wilfordii Hook F, is frequently used to treat MN in China, but its effects on PM2.5-induced podocytes injury is still largely unknown. Therefore, we evaluated the effects of PM2.5 on podocytes, and explored whether triptolide could improve PM2.5-induced podocytes injury and the possible underlying mechanisms.
Results:
Podocytes were incubated with PM2.5 after being pre-treated with triptolide, viability, apoptosis rate and migratory capacity of podocytes were determined by CCK-8 assay, flow cytometry and Transwell assay, respectively. Additionally, the levels of lactate dehydrogenase (LDH), malondialdehyde (MDA), and superoxide dismutase (SOD) in podocytes, the cytoskeleton of podocytes, the protein expressions of nephrin, podocin, Bcl-2, Bax, nuclear factor kappa-B/p65 (NF-κB/p65) and phospho-inhibitor of NF-κB (p-IκBα) were measured. Our data showed that PM2.5 treatment significantly increased the disorganization of F-actin stress fibers, the damaged structural integrity of nucleus, the deranged and dissociated cytoskeleton in podocytes, increased the podocytes apoptosis rate, the levels of MDA and LDH, markedly up-regulated the protein expression of Bax, NF-κB/p65 and p-IκBα, down-regulated the protein expression of nephrin, podocin and Bcl-2, and significantly decreased the level of SOD, the migration rate and the viability of podocytes, compared with those of the untreated podocytes. These effects of PM2.5 on podocytes, however, were reversed by triptolide administration.
Conclusion:
These results suggest that triptolide could prevent against PM2.5-induced podocytes injury via suppressing NF-κB signaling pathway.
Insights
Triptolide prevents against PM2.5-induced podocyte injury by suppressing the NF-κB signaling pathway. This study investigates the protective effects of triptolide on podocyte damage caused by fine particulate matter (PM2.5).
Area of Science:
- Nephrology
- Environmental Health
- Cell Biology
Background:
- Particulate matter (PM2.5) exposure is linked to increased risk of membranous nephropathy (MN).
- PM2.5's direct impact on podocyte injury, a key factor in MN, requires further investigation.
- Triptolide, a traditional Chinese medicine component, is used for MN but its effect on PM2.5-induced podocyte injury is unknown.
Purpose of the Study:
- To evaluate the effects of PM2.5 on podocyte injury.
- To explore the potential protective effects of triptolide against PM2.5-induced podocyte damage.
- To elucidate the underlying molecular mechanisms of triptolide's action.
Main Methods:
- Podocytes were treated with PM2.5, with or without triptolide pre-treatment.
- Cell viability, apoptosis, migration, lactate dehydrogenase (LDH), malondialdehyde (MDA), and superoxide dismutase (SOD) levels were assessed.
- Cytoskeletal structure and protein expressions (nephrin, podocin, Bcl-2, Bax, NF-κB/p65, p-IκBα) were analyzed.
Main Results:
- PM2.5 exposure caused significant podocyte injury, including cytoskeletal damage, increased apoptosis, elevated MDA and LDH, and altered protein expressions (increased Bax, NF-κB/p65, p-IκBα; decreased nephrin, podocin, Bcl-2).
- PM2.5 also reduced cell viability, SOD levels, and migratory capacity.
- Triptolide administration reversed these detrimental effects of PM2.5 on podocytes.
Conclusions:
- Triptolide demonstrates a protective effect against PM2.5-induced podocyte injury.
- The mechanism involves the suppression of the nuclear factor-kappa B (NF-κB) signaling pathway.
- Findings suggest triptolide as a potential therapeutic agent for conditions involving PM2.5-related podocyte damage.
