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Abstract Title:

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

Abstract Source:

Phytomedicine. 2021 Jul 9 ;91:153650. Epub 2021 Jul 9. PMID: 34332282

Abstract Author(s):

Wenwen Liu, Lanmei Liang, Qi Zhang, Ying Li, Sishan Yan, Tang Tang, Yuqing Ren, Juxian Mo, Fanna Liu, Xiaoyan Chen, Tian Lan

Article Affiliation:

Wenwen Liu

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 μM) 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 10μM) 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 μM) 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 μM) 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.

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Sayer Ji
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