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Updated: Jan 27, 2026

Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells
Published on: May 22, 2014
Luteolin attenuates high glucose-induced podocyte injury via suppressing NLRP3 inflammasome pathway
Qian Yu1, Minda Zhang2, Lifen Qian1
1Department of Pharmacology, School of Pharmacy, China Pharmaceutical University, Nanjing, Jiangsu 210009, PR China.
Aims:
Diabetic nephropathy is a growing health concern, which is reported to be associated with inflammation. Luteolin has been explored for the treatment of some diabetic complications. Although several studies have verified the effect of luteolin on diabetic nephropathy, the mechanism by which the therapeutic effects of luteolin on diabetic nephropathy has not been established. Therefore, we aimed to investigate the effect of luteolin on diabetic nephropathy and its underlying mechanism.
Main Methods:
We used western blot, Real-time PCR, immunofluorescence and flow cytometry to analyze the effects of luteolin on podocyte injury and NOD-like receptor family and pyrin domain-containing protein 3 (NLRP3) inflammasome activation in high glucose (HG) condition. Reactive oxygen species (ROS) generation was measured by flow cytometry and malondialdehyde (MDA) level. To investigate the potential mechanism, we examined cell apoptosis upon transfection of siNLRP3.
Key Findings:
We showed that luteolin treatment could protect podocyte against HG-induced cell apoptotic and mitochondrial membrane potential collapse. In addition, luteolin significantly reduced NLRP3 inflammasome formation and subsequent interleukin-1β (IL-1β) secretion in HG-induced MPC-5 cells. Interestingly, siNLRP3 abolished the effect of luteolin on cell apoptosis, suggesting that the anti-apoptotic effect was found to be mostly related to NLRP3 inflammasome.
Significance:
In summary, our data demonstrated the abilities of luteolin to inhibit podocyte injury and NLRP3 inflammasome activation, which could be used in the treatment of diabetic nephropathy.
Insights
Luteolin protects against diabetic nephropathy by inhibiting podocyte injury and NLRP3 inflammasome activation. This suggests luteolin
Area of Science:
- Nephrology
- Pharmacology
- Molecular Biology
Background:
- Diabetic nephropathy is a significant complication of diabetes, linked to inflammation.
- Luteolin shows potential in managing diabetic complications, but its mechanism in nephropathy is unclear.
Purpose of the Study:
- To investigate the therapeutic effects of luteolin on diabetic nephropathy.
- To elucidate the underlying mechanism of luteolin's action, focusing on podocyte injury and NLRP3 inflammasome activation.
Main Methods:
- Utilized western blot, Real-time PCR, immunofluorescence, and flow cytometry to assess podocyte injury and NLRP3 inflammasome activation.
- Measured reactive oxygen species (ROS) and malondialdehyde (MDA) levels.
- Investigated the role of NLRP3 inflammasome in luteolin's anti-apoptotic effects via siNLRP3 transfection.
Main Results:
- Luteolin protected podocytes from high glucose-induced apoptosis and mitochondrial dysfunction.
- Luteolin significantly reduced NLRP3 inflammasome assembly and interleukin-1β (IL-1β) secretion.
- Inhibition of NLRP3 inflammasome abolished luteolin's anti-apoptotic effects, highlighting its central role.
Conclusions:
- Luteolin demonstrates protective effects against podocyte injury in diabetic nephropathy.
- Luteolin's therapeutic potential is mediated through the inhibition of NLRP3 inflammasome activation.
- Luteolin represents a promising therapeutic agent for treating diabetic nephropathy.
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