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Astragaloside IV Pretreatment Alleviates Pulmonary Ischemia-Reperfusion Injury via the TLR4/MyD88/NF-κB p65 Pathway
Xiao-Rui Tian1, Jun-Hui Zhao1, Xia-Hui Yin1
1Department of Pharmaceutical Engineering, South China Agricultural University, Guangzhou, Guangdong, China.
Phytotherapy Research : PTR
|September 4, 2025
Summary
Astragaloside IV (ASIV) protects against lung ischemia-reperfusion injury by inhibiting the TLR4/MyD88/NF-κB pathway. ASIV binds to TLR4-MD-2, reducing inflammation and cellular damage in a rat model.
Area of Science:
- Pharmacology
- Immunology
- Cell Biology
Background:
- Lung ischemia-reperfusion injury (PIRI) is a significant clinical challenge.
- Astragaloside IV (ASIV) has demonstrated protective effects against lung injury in previous studies.
- The precise molecular mechanisms underlying ASIV's protective effects require further elucidation.
Purpose of the Study:
- To investigate whether ASIV attenuates PIRI by inhibiting the Toll-like receptor 4 (TLR4)/MyD88/NF-κB p65 signaling pathway.
- To compare the protective efficacy of ASIV with other agents like DEX and NAC.
- To elucidate the binding interaction between ASIV and TLR4-MD-2.
Main Methods:
- In vitro studies using oxygen-glucose deprivation/reoxygenation (OGD/R) to induce cell injury.
- In vivo PIRI model in Sprague-Dawley rats, monitoring lung injury markers and oxidative stress.
- Evaluation of TLR4/MyD88/NF-κB p65 pathway activation at mRNA and protein levels.
- Molecular docking, binding affinity calculations, and surface plasmon resonance (SPR) to assess ASIV-TLR4-MD-2 interaction.
Main Results:
- ASIV demonstrated superior protection against OGD/R-induced cell injury compared to DEX and NAC, with a synergistic effect with TAK-242.
- In vivo, ASIV treatment significantly reduced lung tissue damage, decreased oxidative stress markers (MDA, MPO), and increased antioxidant levels (T-SOD, GSH-PX).
- ASIV administration led to significant downregulation of TLR4, MyD88, NF-κBp65, and p-NF-κBp65 protein expression.
- Molecular docking predicted strong binding of ASIV to TLR4-MD-2 (free binding energy of -8.0 kcal·mol⁻¹), confirmed by SPR (KD of 2.17 × 10⁻⁶ M).
Conclusions:
- ASIV effectively alleviates PIRI by specifically binding to TLR4-MD-2.
- This binding suppresses the activation of the TLR4/MyD88/NF-κB p65 inflammatory pathway.
- ASIV represents a promising therapeutic agent for mitigating lung ischemia-reperfusion injury.
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