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Published on: August 3, 2015
Piperazine ferulate attenuates gentamicin-induced acute kidney injury via the NF-κB/NLRP3 pathway
1State Key Laboratory of Southwestern Chinese Medicine Resources, School of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan 611137, China; School of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan 611137, China.
Background:
Piperazine ferulate (PF) is widely used in chronic nephritis and nephrotic syndrome in clinic. PF can improve diseases related inflammation by inhibiting the activation of nuclear factor kappa-B (NF-κB) signal. Acute kidney injury (AKI) is usually associated with the occurrence and development of renal inflammation. However, the nephroprotective effect and anti-inflammatory mechanisms of PF on AKI are not clear.
Purpose:
This study aimed to investigate the nephroprotective effects of PF on gentamicin (GM) induced AKI in rats and its potential mechanisms.
Methods:
Male Sprague Dawley (SD) rats were intraperitoneally injected with GM (100 mg/kg/day) with or without PF (50 and 100 mg/kg/day) for 7 consecutive days. In vitro, the NRK-52e cells were exposed to GM (7 mg/ml) with or without PF (62.5 μg/ml) treatment. The renal injury and cell damage were assessed subsequently.
Results:
Our findings showed that PF treatment can significantly improve renal function, reduce renal pathological changes, and attenuate inflammatory response in rats treated with gentamicin. Besides, PF could significantly reduce the cell damage and cellular inflammatory response. In terms of mechanisms, our study revealed that PF can evidently inhibit the activation of NF-κB and nod-like receptor family pyrin domain protein 3 (NLRP3) inflammasome. Meanwhile, it could down regulate the expressions of protein and gene of p-IKKα, p-IKKβ, p-p65, p65, p50, p105, NLRP3 and IL-1β.
Conclusion:
Our findings showed that PF may improve inflammation by inhibiting the NF-κB/NLRP3 pathway, so as to attenuate AKI.
Insights
Piperazine ferulate (PF) protects against acute kidney injury (AKI) by reducing inflammation. This study shows PF inhibits the NF-κB/NLRP3 pathway, offering a potential therapeutic strategy for kidney inflammation.
Area of Science:
- Nephrology
- Pharmacology
- Inflammation Research
Background:
- Piperazine ferulate (PF) is clinically used for chronic nephritis and nephrotic syndrome, known to reduce inflammation via nuclear factor kappa-B (NF-κB) signaling.
- Acute kidney injury (AKI) involves renal inflammation, but PF's protective effects and mechanisms in AKI remain unclear.
Purpose of the Study:
- To investigate the nephroprotective effects of Piperazine ferulate (PF) in a rat model of gentamicin (GM)-induced acute kidney injury (AKI).
- To elucidate the underlying anti-inflammatory mechanisms of PF in AKI.
Main Methods:
- Male Sprague Dawley rats received gentamicin (GM) with or without PF (50, 100 mg/kg) for 7 days.
- In vitro, NRK-52e cells were exposed to GM with or without PF treatment.
- Renal and cellular injury, alongside inflammatory markers, were assessed.
Main Results:
- PF treatment significantly improved renal function and reduced pathological damage and inflammation in GM-induced AKI rats.
- PF mitigated cell damage and inflammatory responses in vitro.
- Mechanistically, PF inhibited NF-κB and NLRP3 inflammasome activation, downregulating key inflammatory proteins and genes (p-IKKα/β, p-p65, p65, p50, p105, NLRP3, IL-1β).
Conclusions:
- Piperazine ferulate (PF) demonstrates significant nephroprotective effects against acute kidney injury (AKI).
- PF exerts its protective effects by inhibiting the NF-κB/NLRP3 inflammatory pathway.
- PF represents a potential therapeutic agent for mitigating inflammation-associated AKI.
