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Xiaoqinglong Decoction Protects the Lungs of AECOPD Mice through the AMPK/mTOR Signaling Pathway
Qingsong Huang1, Hongjing Yang1, Chuantao Zhang1
1Department of Respimiceory Medicine, Hospital of Chengdu University of Traditional Chinese Medicine, No. 39, Twelve Bridge Road, Jinniu District, Chengdu, Sichuan 610075, China.
Method:
Male C57BL/6J mice were used to establish AECOPD model by cigarette smoke and bacterial exposure. Mice were randomly divided into normal control (NC), AECOPD, XQLD, Compound C (Com C), Com C + XQLD, and Clarithromycin (CLA) groups. After treatment, the pulmonary function was evaluated by whole-body plethysmograph. The lung histopathology was observed by HE staining. The serum levels of IL-6, TNF-α, and COX-2 were detected by ELISA assay. The apoptotic index was measured by TUNEL assay, and the protein expressions of Bax, Bcl-2, Caspase-3, GRP78, and CHOP in the lung tissues were measured by western blot assay.
Results:
XQLD treatment can improve pulmonary function (PF), ameliorate lung injury, and suppress inflammation and apoptosis of lung tissues. In addition, XQLD also markedly attenuated endoplasmic reticulum stress (ERS) and activated AMPK/mTOR pathway in the lung tissues of mice with AECOPD. However, the AMPK inhibitor Compound C decreased the protective effect of XQLD in AECOPD mice.
Conclusion:
These findings suggested that XQLD has protective effect against inflammation and apoptosis in AECOPD mice by attenuating ER stress via AMPK/mTOR pathway.
Insights
XQLD treatment protects against acute exacerbations of chronic obstructive pulmonary disease (AECOPD) by reducing lung inflammation and apoptosis. It achieves this by alleviating endoplasmic reticulum stress through the AMPK/mTOR pathway.
Area of Science:
- Pulmonology
- Pharmacology
- Cellular Biology
Background:
- Acute exacerbations of chronic obstructive pulmonary disease (AECOPD) involve significant lung injury, inflammation, and apoptosis.
- Understanding the molecular mechanisms underlying AECOPD is crucial for developing effective therapeutic strategies.
- Endoplasmic reticulum stress (ERS) and the AMPK/mTOR pathway are implicated in various inflammatory lung diseases.
Purpose of the Study:
- To investigate the therapeutic potential of XQLD in a mouse model of AECOPD.
- To elucidate the underlying mechanisms of XQLD's protective effects, focusing on inflammation, apoptosis, ERS, and the AMPK/mTOR pathway.
Main Methods:
- An AECOPD mouse model was established using cigarette smoke and bacterial exposure.
- Mice were treated with XQLD, Compound C (an AMPK inhibitor), or Clarithromycin.
- Pulmonary function, lung histopathology, inflammatory markers (IL-6, TNF-α, COX-2), apoptosis (TUNEL assay), and protein expression (Bax, Bcl-2, Caspase-3, GRP78, CHOP) were assessed.
Main Results:
- XQLD treatment significantly improved pulmonary function, reduced lung injury, and suppressed inflammation and apoptosis in AECOPD mice.
- XQLD markedly attenuated endoplasmic reticulum stress (ERS) and activated the AMPK/mTOR pathway in lung tissues.
- The co-administration of Compound C diminished the protective effects of XQLD, indicating the involvement of the AMPK pathway.
Conclusions:
- XQLD demonstrates significant protective effects against inflammation and apoptosis in AECOPD.
- These protective effects are mediated by the attenuation of endoplasmic reticulum stress via the activation of the AMPK/mTOR pathway.
- XQLD represents a potential therapeutic agent for managing AECOPD.
