ReferenceID 4501

Effects of andrographolide on renal tubulointersticial injury and fibrosis. Evidence of its mechanism of action

Phytomedicine

BACKGROUND: Diabetic nephropathy (DN) is associated with renal interstitial injury and fibrosis. Our previous study showed that andrographolide protected against the progression of DN and high glucose (HG)-induced mesang

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Reference Id
4501
Evidence Id
21091
Core Evidence Id
21091
Source Reference Id
2280
Herb2 Reference Id
HBREF003077
Subject Paper Key
HBIN016019_34332282
Pubmed Id
34332282
Doi
10.1016/j.phymed.2021.153650
Paper Title
Effects of andrographolide on renal tubulointersticial injury and fibrosis. Evidence of its mechanism of action
Paper Abstract
BACKGROUND: Diabetic nephropathy (DN) is associated with renal interstitial injury and fibrosis. Our previous study showed that andrographolide protected against the progression of DN and high glucose (HG)-induced mesangial dysfunction. However, the protective effects of andrographolide on renal tubular epithelial cells have not been fully elucidated. PURPOSE: To determine the protective effects of andrographolide on renal tubular damage and explore the underlying mechanism. STUDY DESIGN: Human tubular epithelial cells (HK-2 cells) were treated with andrographolide (5 and 10 muM) under HG conditions. Diabetic mice were treated with andrographolide (i.p. 2 and 4 mg/kg, twice per week). METHODS: Western blotting, reverse transcription-polymerase chain reaction (RT-PCR), immunofluorescence and flow cytometry were used to analyze the effects of andrographolide on renal tubular injury and fibrotic mechanisms in HK-2 cells. The protective effects of andrographolide against renal tubulointerstitial injury and fibrosis were investigated in diabetic mice fed a high-fat diet (HFD). Renal interstitial tissue was collected at sacrifice for immunohistochemistry, immunofluorescence analysis, RT-PCR and Western blotting to analyze the effects of andrographolide on renal tubular injury and fibrosis. RESULTS: In vitro assay results indicated that andrographolide (5 and 10 muM) effectively inhibited HG-induced apoptosis, epithelial-mesenchymal transition (EMT) and collagen deposition in HK-2 cells. Mechanistically, HG stimulated mitochondrial reactive oxygen species (mtROS)-mediated NOD-like receptor family and pyrin domain-containing protein 3 (NLRP3) inflammasome activation and EMT in tubular epithelial cells, and andrographolide (5 and 10 muM) inhibited these effects by ameliorating mitochondrial dysfunction. In vivo, treatment with andrographolide (2 and 4 mg/kg) inhibited renal tubular cell apoptosis, EMT and tubulointerstitial fibrosis, mitochondrial dysfunction and NLRP3 inflammasome activation in diabetic mice. CONCLUSION: Andrographolide (5 and 10 muM) prevents HG-induced renal tubular cell damage, and andrographolide (2 and 4 mg/kg) protects against the progression of diabetic tubular injury and fibrosis in mice by suppressing mitochondrial dysfunction and NLRP3 inflammasome activation.
Journal
Phytomedicine
Publish Year
2021
Experiment Subject
mouse; human; hk-2 cells
Experiment Type
Animal & Cell Experiment
Phenotype Related
Renal Tubular Injury; Diabetic; Diabetic Tubular Injury; Mesangial Dysfunction; Tubulointerstitial Fibrosis; Fibrosis; Mitochondrial Dysfunction; Diabetic Nephropathy; Renal Interstitial Injury; Renal Tubulointerstitial Injury
Paper Title Cn
Paper Title En
Effects of andrographolide on renal tubulointersticial injury and fibrosis. Evidence of its mechanism of action
Bilingual Status
semi_complete