Baicalein alleviates high glucose-induced mesangial cell fibrosis and inflammation in diabetic nephropathy: roles of AMPK activation and TGF-β1 inhibition.

Authors

Hongtao Tan, Yingshan Li, Yicong Li, Junxian Chen, Weiwei Yuan

Published in

Genes & genomics. Jul 01, 2026. Epub Jul 01, 2026.

Abstract

Diabetic nephropathy (DN), a major diabetic microvascular complication, is the primary cause of end-stage renal disease worldwide. It is characterized by mesangial cell fibrosis and chronic inflammation, which current treatments cannot completely reverse. Baicalein, a major flavonoid from Scutellaria baicalensis Georgi, has anti-inflammatory and antifibrotic activities, but its role and mechanism in high glucose (HG)-induced mesangial cell injury (a key DN feature) remain unclear.
This study investigated baicalein's effects on rat glomerular mesangial cells (HBZY-1) and validated key findings in human primary glomerular mesangial cells.
CCK-8 assay identified 10-20 μM as baicalein's non-cytotoxic range (cell viability ≥ 90%).
Further experiments demonstrated that baicalein dose-dependently inhibited HG-induced increases in fibrotic markers (α-SMA, FN, COL1A1) at both mRNA (qRT-PCR) and protein levels (Western blot, immunofluorescence), and reduced proinflammatory cytokines (IL-6, TNF-α, MCP-1) at transcriptional (qRT-PCR) and secretory levels (ELISA). Western blot analysis demonstrated that baicalein dose-dependently activated the AMPK pathway by increasing p-AMPK/AMPK at Thr172 and inhibited the TGF-β/Smad pathway by reducing TGF-β1 and p-Smad2/3/Smad2/3. Using the AMPK inhibitor Compound C, we confirmed baicalein's anti-fibrotic, anti-inflammatory, and TGF-β/Smad-inhibitory effects were closely associated with AMPK activity. Molecular docking showed baicalein stably bound the AMPK β-subunit's C-terminal domain (PDB ID: 4EAK), suggesting a potential interaction that may contribute to AMPK activation.
Baicalein protects against HG-induced mesangial cell injury via an AMPK-associated mechanism linked to the suppression of fibrosis and inflammation, highlighting it as a promising DN therapeutic candidate for further preclinical and clinical study.

PMID:
42384354
Bibliographic data and abstract were imported from PubMed on 01 Jul 2026.

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