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Updated: Jun 28, 2026

Establishing a Silicosis Rat Model via Exposure of Whole-Body to Respirable Silica
05:03

Establishing a Silicosis Rat Model via Exposure of Whole-Body to Respirable Silica

Published on: October 28, 2022

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Preliminary Study on the Effect and Molecular Mechanism of Tetrandrine in Alleviating Pulmonary Inflammation and

Yi Wang1,2, Bin Cheng1,2, Yu-Jia Lin1,2

  • 1School of Public Health, Ningxia Medical University, Yinchuan 750004, China.

Toxics
|September 27, 2023
PubMed

Insights

Tetrandrine (Tet) alleviates silica-induced lung inflammation and fibrosis by enhancing autophagy and inhibiting apoptosis. This study reveals Tet

Area of Science:

  • Pulmonary Medicine
  • Cell Biology
  • Toxicology

Background:

  • Silica (SiO2) exposure causes significant lung inflammation and fibrosis.
  • Autophagy plays a critical role in cellular response to injury.

Purpose of the Study:

  • To investigate the molecular mechanism of tetrandrine (Tet) in mitigating silica-induced pulmonary inflammation and fibrosis.
  • To explore the role of autophagy in Tet's therapeutic effects.

Main Methods:

  • C57BL/6J mice were exposed to SiO2 and treated with Tet.
  • Lung tissues were analyzed using histopathology, molecular biology, immunology, and electron microscopy.
  • Autophagy pathway markers (ATG7, LC3B, P62) and apoptosis were assessed.

Main Results:

  • Tet significantly reduced SiO2-induced lung inflammation and fibrosis.
  • Tet decreased inflammatory cytokines (TNF-α, IL-1β, MCP-1) and fibrosis markers (TGF-β1, HYP, Col-I, Fn).
  • Tet intervention improved autophagic flux, restored lysosomal function, and inhibited apoptosis.

Conclusions:

  • Tetrandrine effectively alleviates silica-induced lung inflammation and fibrosis.
  • The mechanism involves regulating autophagy pathway molecules and inhibiting apoptosis.
  • Tet represents a potential therapeutic agent for silica-induced lung diseases.
Keywords:
SiO2autophagylung inflammationpulmonary fibrosissilicosistetrandrine

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