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Resveratrol delays polycystic kidney disease progression through attenuation of nuclear factor κB-induced
Ming Wu1, Junhui Gu1, Shuqin Mei1
1Kidney Institute, Department of Nephrology, Shanghai Changzheng Hospital, Second Military Medical University, Shanghai, China.
Insights
Resveratrol effectively reduced polycystic kidney disease (PKD) markers in rats by inhibiting inflammation and nuclear factor-kappa B (NF-κB) signaling. This suggests resveratrol as a potential therapeutic agent for treating PKD.
Area of Science:
- Nephrology
- Pharmacology
- Molecular Biology
Background:
- Inflammation is a key factor in polycystic kidney disease (PKD) pathogenesis.
- The potential of anti-inflammatory compounds for PKD treatment requires further investigation.
Purpose of the Study:
- To evaluate the efficacy of resveratrol, an anti-inflammatory compound, in treating PKD.
- To elucidate the mechanism of action of resveratrol in PKD, focusing on the nuclear factor-kappa B (NF-κB) pathway.
Main Methods:
- Treatment of polycystic kidney disease (PKD) rats with resveratrol or vehicle.
- In vitro studies using human autosomal dominant (AD) PKD cells and 3D cell cultures.
- In vivo studies using zebrafish models to assess cyst formation.
- Inhibition of nuclear factor-kappa B (NF-κB) using QNZ in cellular and zebrafish models.
Main Results:
- Resveratrol significantly reduced blood urea nitrogen, creatinine, kidney weight, and cyst volume in PKD rats.
- Resveratrol decreased proliferation and macrophage infiltration in cystic kidneys, alongside reduced pro-inflammatory factors (MCP-1, TNF-α, CFB) and NF-κB activity.
- Resveratrol and NF-κB inhibition suppressed inflammatory markers and cyst formation in cellular, 3D, and zebrafish models.
Conclusions:
- The nuclear factor-kappa B (NF-κB) signaling pathway is implicated in polycystic kidney disease (PKD) inflammation.
- Targeting inflammation with resveratrol presents a promising therapeutic strategy for future PKD treatment.
Background:
Inflammation plays an important role in polycystic kidney disease (PKD). The current study aimed to examine the efficacy of the anti-inflammatory compound resveratrol in PKD and to investigate its underlying mechanism of action.
Methods:
Male Han:SPRD (Cy/+) rats with PKD were treated with 200 mg/kg/day resveratrol or vehicle by gavage for 5 weeks. Human autosomal dominant (AD) PKD cells, three-dimensional (3D) Madin-Darby canine kidney cells and zebrafish were treated with various concentrations of resveratrol or the nuclear factor κB (NF-κB) inhibitor QNZ.
Results:
Resveratrol treatment reduced blood urea nitrogen levels and creatinine levels by 20 and 24%, respectively, and decreased two-kidney/total body weight ratio by 15% and cyst volume density by 24% in Cy/+ rats. The proliferation index and the macrophage infiltration index were reduced by 40 and 43%, respectively, in resveratrol-treated cystic kidneys. Resveratrol reduced the levels of the pro-inflammatory factors monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-α (TNF-α) and complement factor B (CFB) in Cy/+ rat kidneys in parallel with the decreased activity of NF-κB (p50/p65). The activation of NF-κB and its correlation with pro-inflammatory factor expression were confirmed in human ADPKD cells and kidney tissues. Resveratrol and QNZ inhibited the expression of MCP-1, TNF-α and CFB and reduced NF-κB activity in ADPKD cells. Moreover, NF-κB blockage minimized the inhibition of inflammatory factor production by resveratrol treatment. Furthermore, resveratrol or QNZ inhibited cyst formation in the 3D cyst and zebrafish models.
Conclusions:
The NF-κB signaling pathway is activated and partly responsible for inflammation in polycystic kidney tissues. Targeting inflammation through resveratrol could be a new strategy for PKD treatment in the future.
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