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Published on: August 23, 2024

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Thymol alleviates AGEs-induced podocyte injury by a pleiotropic effect via NF-κB-mediated by RhoA/ROCK signalling

Qinglian Wang1, Zhenwei Shen2, Guanghui Qi3

  • 1Department of Nephrology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, China.

Cell Adhesion & Migration
|February 8, 2020
PubMed

Insights

Thymol offers protective effects against advanced glycation end product (AGE)-induced injury in human podocytes. It suppresses the RhoA-NF-κB pathway, reducing inflammation and apoptosis for potential therapeutic use.

Area of Science:

  • Nephrology
  • Cell Biology
  • Pharmacology

Background:

  • Advanced glycation end products (AGEs) are key contributors to diabetic complications.
  • Diabetic nephropathy involves podocyte injury and apoptosis.
  • Understanding protective mechanisms against AGE-induced damage is crucial.

Purpose of the Study:

  • To investigate the protective effects of thymol on AGE-induced injury in human podocytes (HPCs).
  • To elucidate the underlying mechanisms of thymol's action, focusing on the RhoA/NF-κB pathway.

Main Methods:

  • Human podocytes were stimulated with AGEs.
  • Thymol treatment was administered to assess its effects.
  • Western blot analysis was used to examine protein expression (RhoA, ROCK, vimentin, nephrin, podocin, p65, IκBα).
  • siRNA targeting RhoA was employed to confirm pathway involvement.

Main Results:

  • AGE stimulation activated the RhoA/NF-κB pathway, leading to inflammation, apoptosis, and cytoskeletal disruption.
  • Thymol treatment suppressed inflammatory responses, apoptosis, and cytoskeletal abnormalities.
  • Thymol restored podocin expression and reduced cell migration.
  • Thymol normalized the expression of RhoA, ROCK, vimentin, nephrin, podocin, and modulated p65/IκBα phosphorylation.
  • siRNA-mediated RhoA knockdown mimicked thymol's protective effects.

Conclusions:

  • Thymol effectively inhibits AGE-induced podocyte injury by suppressing the RhoA-NF-κB pathway.
  • Thymol demonstrates potential as a therapeutic agent for diabetic nephropathy.
  • Targeting the RhoA-NF-κB pathway is a viable strategy for mitigating AGE-induced podocyte damage.
Keywords:
RhoA/ROCK pathwayThymoladvanced glycation end products (AGE)human podocytesnuclear factor-kappa B (NF-κB)

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