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Protocatechualdehyde attenuates obstructive nephropathy through inhibiting lncRNA9884 induced inflammation
Jieke Yang1, Jianchun Li1, Ruizhi Tan1
1Research Center of Intergated Traditional Chinese and Western Medicine, and Department of Nephrology, Affiliated Traditional Medicine Hospital, Southwest Medical University, Luzhou, China.
Abstract:
Persistent chronic inflammation and fibrosis product accumulation aggravate tubulointerstitial fibrosis (TIF), leading to the progression of chronic kidney disease. The aim of this study was designed to investigate the effect of protocatechualdehyde (PCA), a natural phenolic acid compound isolated from Salvia miltiorrhiza, on the unilateral ureteral obstruction (UUO)-induced fibrosis and inflammation and to elucidate the underlying mechanism in primary renal tubular epithelial cells (TECs). Results from the histology suggested that the moderate to severe deteriorations of renal dysfunction and the pathological changes in UUO could be relieved by PCA treatment. Mechanistic studies revealed that the effect of PCA was associated with the downregulation of Smad3 and NF-κB driven fibrosis and inflammation respectively. It is worth noting that PCA could inhibit the aberrant expression of inflammation cytokines such as iNOS, MCP-1, TNF-α in UUO, and IL-1β-treated TECs. In addition, PCA also suppressed the expression of Smad3-dependent long noncoding RNA (lncRNA), 9884. Importantly, when overexpressing of lncRNA9884 in TECs by transfection of pcDNA3.1-lncRNA9884 plasmid, it revealed significant reversal of protein expression levels as that observed with only PCA, suggesting that PCA inhibits inflammation by mediating lncRNA9884/MCP-1 signaling pathway. Collectively, the current study establishes a foundational basis for PCA in future treatment of obstructive nephropathy.
Insights
Protocatechualdehyde (PCA) effectively treats kidney fibrosis and inflammation caused by ureteral obstruction. PCA works by downregulating key fibrotic and inflammatory pathways, including the lncRNA9884/MCP-1 signaling pathway.
Area of Science:
- Nephrology
- Pharmacology
- Molecular Biology
Background:
- Tubulointerstitial fibrosis (TIF) progression in chronic kidney disease is driven by inflammation and fibrosis.
- Unilateral ureteral obstruction (UUO) is a common model for studying kidney fibrosis and inflammation.
Purpose of the Study:
- To investigate the therapeutic effects of protocatechualdehyde (PCA) on UUO-induced kidney fibrosis and inflammation.
- To elucidate the underlying molecular mechanisms of PCA action in renal tubular epithelial cells (TECs).
Main Methods:
- Histological analysis of kidney tissues from UUO model mice treated with PCA.
- Investigation of molecular pathways including Smad3, NF-κB, and inflammatory cytokines (iNOS, MCP-1, TNF-α, IL-1β).
- Analysis of long noncoding RNA (lncRNA) 9884 expression and its role in PCA's anti-inflammatory effects.
Main Results:
- PCA treatment ameliorated renal dysfunction and pathological changes in UUO mice.
- PCA downregulated Smad3 and NF-κB signaling, reducing fibrosis and inflammation.
- PCA inhibited inflammatory cytokines and suppressed Smad3-dependent lncRNA9884 expression.
- Overexpression of lncRNA9884 reversed PCA's effects, indicating PCA acts via the lncRNA9884/MCP-1 pathway.
Conclusions:
- PCA demonstrates significant therapeutic potential for obstructive nephropathy.
- PCA exerts its protective effects by modulating Smad3, NF-κB, and the lncRNA9884/MCP-1 signaling pathway.
- This study provides a mechanistic basis for PCA as a treatment for kidney fibrosis and inflammation.
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