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Triphala ameliorates hyperuricemia-associated nephropathy by modulating the gut microbiota-glycerophospholipid-TLR4
Cong Liu1, Huan Zhang1, Huihui Zhang1
1International Cooperation Base for Active Substances in Traditional Chinese Medicine in Hubei Province, School of Pharmaceutical Sciences, South-Central Minzu University, Wuhan 430074, China.
Summary
Triphala (TRP) treats hyperuricemia (HUA) and kidney inflammation by reshaping the gut microbiota. This reduces harmful lysophospholipids, blocking the TLR4 inflammatory pathway for kidney protection.
Area of Science:
- Metabolic Disorders
- Nephrology
- Microbiome Research
- Pharmacology
Background:
- Hyperuricemia (HUA) is a growing global health issue linked to chronic kidney injury.
- Dyslipidemia exacerbates HUA-associated kidney complications.
- Triphala (TRP), a Tibetan herbal formula, shows potential for metabolic regulation in HUA, but its mechanisms require clarification.
Purpose of the Study:
- To investigate the protective effects of Triphala (TRP) against hyperuricemia-associated nephropathy.
- To elucidate the molecular mechanisms underlying TRP's therapeutic actions in HUA.
Main Methods:
- HPLC analysis identified key TRP constituents.
- An HUA mouse model was established using potassium oxonate and a yeast diet.
- A multi-omics approach (16S rRNA, metabolomics, lipidomics) assessed TRP's impact on gut microbiota and host metabolism.
- Fecal microbiota transplantation (FMT), TLR4 blockade, and in vitro assays explored the role of TRP-modulated microbiota and the LPC-TLR4 pathway.
Main Results:
- TRP reduced serum uric acid, improved renal function (serum Cr, BUN), and increased uric acid excretion.
- TRP normalized urate transporters and suppressed renal inflammatory cytokines.
- TRP reversed HUA-induced gut dysbiosis, reducing pro-inflammatory lysophospholipids (LPCs).
- TRP and FMT inhibited the TLR4/MyD88/NF-κB pathway, reducing kidney LPC accumulation.
- In vitro studies confirmed LPCs trigger TLR4 expression and TNF-α release.
Conclusions:
- TRP ameliorates HUA and renal inflammation by modulating gut microbiota to reduce pro-inflammatory LPCs.
- This action deactivates the TLR4-mediated inflammatory cascade.
- The gut microbiota-glycerophospholipid metabolism-renal inflammation axis is a potential therapeutic target for HUA.
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