The Bufei Nashen Pill Alleviates COPD by Targeting Endoplasmic Reticulum Stress Through the PERK/eIF2α Signaling Pathway

BACKGROUND: Evidence supporting the therapeutic efficacy of Bufei Nashen pill (BFNSP) for chronic obstructive pulmonary disease (COPD) is currently limited. We evaluated BFNSP's effects on COPD progression and elucidated its potential mechanisms through LC/MS analysis of its active components. METHODS: Following the establishment of a rat COPD model, animals received graded BFNSP doses. Pulmonary function testing quantified respiratory parameters, while HE staining revealed histological changes in lung tissue. ELISA was used to measure TGF-β1, IL-6, IL-8, and IL-1β concentrations in BALF, as well as MDA, SOD, and GSH levels in lung tissue. Immunofluorescence staining was used to detect the levels of GRP78 and CHOP expression. Protein expression levels of GRP78, CHOP, p-PERK, p-eIF2α, and p-ATF4 in lung tissue were analyzed using Western blotting. The results were further confirmed through in vitro cellular assays. RESULTS: The study found that BFNSP improved pulmonary ventilation, reduced lung tissue damage, decreased inflammatory factor secretion, and alleviated oxidative and endoplasmic reticulum stress in COPD rats by inhibiting the PERK/eIF2α signaling pathway, potentially slowing COPD progression. CONCLUSION: BFNSP mitigates COPD progression by regulating endoplasmic reticulum stress via the suppression of the PERK/eIF2α signaling pathway.

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Publication Details

Journal
Immunity Inflammation and Disease
Published
2026-04-01
DOI
https://doi.org/10.1002/iid3.70418
Primary Topic
Endoplasmic Reticulum Stress and Disease
Type
article
Field-Weighted Citation Impact
0.00
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article

The Bufei Nashen Pill Alleviates COPD by Targeting Endoplasmic Reticulum Stress Through the PERK/eIF2α Signaling Pathway

Tengfei He, Changxi Zhang, Anni Zhang
Immunity Inflammation and Disease
Endoplasmic Reticulum Stress and Disease
article

The Bufei Nashen Pill Alleviates COPD by Targeting Endoplasmic Reticulum Stress Through the PERK/eIF2α Signaling Pathway

Tengfei He, Changxi Zhang, Anni Zhang
article en

Abstract

BACKGROUND: Evidence supporting the therapeutic efficacy of Bufei Nashen pill (BFNSP) for chronic obstructive pulmonary disease (COPD) is currently limited. We evaluated BFNSP's effects on COPD progression and elucidated its potential mechanisms through LC/MS analysis of its active components. METHODS: Following the establishment of a rat COPD model, animals received graded BFNSP doses. Pulmonary function testing quantified respiratory parameters, while HE staining revealed histological changes in lung tissue. ELISA was used to measure TGF-β1, IL-6, IL-8, and IL-1β concentrations in BALF, as well as MDA, SOD, and GSH levels in lung tissue. Immunofluorescence staining was used to detect the levels of GRP78 and CHOP expression. Protein expression levels of GRP78, CHOP, p-PERK, p-eIF2α, and p-ATF4 in lung tissue were analyzed using Western blotting. The results were further confirmed through in vitro cellular assays. RESULTS: The study found that BFNSP improved pulmonary ventilation, reduced lung tissue damage, decreased inflammatory factor secretion, and alleviated oxidative and endoplasmic reticulum stress in COPD rats by inhibiting the PERK/eIF2α signaling pathway, potentially slowing COPD progression. CONCLUSION: BFNSP mitigates COPD progression by regulating endoplasmic reticulum stress via the suppression of the PERK/eIF2α signaling pathway.

Immunity Inflammation and DiseaseVol. 14(4)
Ningxia Hui Autonomous Region Peoples Hospital (CN), Ningxia Medical University (CN), Ningxia Medical University General Hospital (CN), Beijing Friendship Hospital (CN), Inner Mongolia Autonomous Region Hospital of Traditional Chinese Medicine (CN), The Fourth People's Hospital of Ningxia Hui Autonomous Region (CN)
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Endoplasmic Reticulum Stress and Disease
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The Bufei Nashen Pill Alleviates COPD by Targeting Endoplasmic Reticulum Stress Through the PERK/eIF2α Signaling Pathway — Tengfei He, Changxi Zhang, et al. · Immunity Inflammation and Disease (2026) | TGRS Research Map | TGRS