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[Puerarin alleviates lipopolysaccharide-induced acute kidney injury in mice by modulating the SIRT1/NF-κB pathway]
1School of Basic Medical Sciences, Xiangnan University, Chenzhou 423000, China.
Objective:
To investigate the role of the SIRT1/NF-κB pathway in mediating the effect of puerarin against lipopolysaccharide (LPS)-induced acute kidney injury (AKI).
Methods:
Fifteen BALB/C mice were randomized into control group, LPS group and puerarin treatment group, and in the latter two groups, the mice were given an intraperitoneal injection of LPS (5 mg/kg), followed by daily injection of normal saline for 3 days or injection of puerarin (25 mg/kg) given 1 h later and then on a daily basis for 3 days. On day 5 after modeling, the kidney tissues were taken for histological observation and detection of cell apoptosis. The renal function indexes including urea nitrogen (BUN), serum creatinine (Scr) and kidney injury molecule 1 (KIM-1) and the levels of tumor necrosis factor (TNF-α) and interleukin 1β (IL-1β) were measured, and the expressions of SIRT1 and NF-κB-p65(acetyl K310) in the renal tissues were detected.
Results:
Intraperitoneal injection of LPS caused obvious glomerular capillary dilatation, hyperemia, renal interstitial edema, and renal tubular epithelial cell swelling and deformation in the mice. The mouse models of LPS-induced AKI also showed significantly increased renal tubular injury score and renal cell apoptosis (P < 0.01) with increased serum levels of BUN, Scr, KIM-1, TNF-α and IL-1β (P < 0.01), enhanced renal expressions of TNF-α, IL-1β and NF-κB p65(acetyl K310) (P < 0.01) and lowered renal expression of SIRT1 (P < 0.05). Treatment with puerarin effectively alleviated LPS-induced renal interstitial edema and renal tubular epithelial cell shedding, lowered renal tubular injury score (P < 0.01) and renal cell apoptosis rate (P < 0.01), and decreased serum levels of BUN, Scr, KIM, TNF-α and IL-1β (P < 0.01). Puerarin treatment significantly reduced TNF-α, IL-1β and NF-κB p65 (acetyl K310) expression in the renal tissue (P < 0.05) and increased SIRT1 expression by 17% (P < 0.05) in the mouse models.
Conclusion:
Puerarin can effectively alleviate LPS-induced AKI in mice possibly by modulating the SIRT1/NF-κB signaling pathway.
Insights
Puerarin effectively treats lipopolysaccharide (LPS)-induced acute kidney injury (AKI) in mice. It works by modulating the SIRT1/NF-κB pathway, reducing inflammation and cell damage.
Area of Science:
- Biochemistry
- Pharmacology
- Nephrology
Context:
- Lipopolysaccharide (LPS) is a potent inducer of inflammation and cellular damage, commonly used to model acute kidney injury (AKI).
- The SIRT1/NF-κB signaling pathway plays a critical role in inflammatory responses and cellular survival.
- Puerarin, a natural flavonoid, has demonstrated various pharmacological properties, including anti-inflammatory effects.
Purpose:
- To elucidate the protective mechanisms of puerarin against LPS-induced AKI in a murine model.
- To investigate the involvement of the SIRT1/NF-κB signaling pathway in puerarin's renoprotective effects.
Summary:
- LPS injection induced significant kidney damage, characterized by histological alterations, increased apoptosis, elevated serum biomarkers (BUN, Scr, KIM-1), and heightened levels of TNF-α and IL-1β.
- LPS challenge also led to increased acetylation of NF-κB p65 and decreased expression of SIRT1 in renal tissues.
- Puerarin treatment ameliorated these pathological changes, reduced inflammatory markers, decreased apoptosis, and restored SIRT1 expression while inhibiting NF-κB activation.
Impact:
- These findings suggest that puerarin exerts renoprotective effects against LPS-induced AKI by activating SIRT1 and suppressing the NF-κB signaling pathway.
- Puerarin represents a potential therapeutic agent for managing AKI, particularly when associated with inflammatory insults.
- The study highlights the therapeutic potential of targeting the SIRT1/NF-κB axis in kidney disease.
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