Journal of ethnopharmacology · 2025
Saorilao Qingfei Zhike Capsule alleviated inflammation and bronchial remodeling in LPS and CS-induced COPD via MAPK signaling pathway.
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Wang Yanan, Han Fengyu, Ye Lisha, ShangGuan Tongqiang, Fan Shengci, She Yihuan, Yu Xiuling, Wang Dongmei, Wang Baolian
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Chronic obstructive pulmonary disease (COPD) is a persistent inflammatory airway disease primarily caused by prolonged exposure to toxic gases or particles. The Saorilao Qingfei Zhike Capsule (SRL), derived from a traditional Mongolian medicine recipe, has demonstrated promising clinical efficacy in treating chronic bronchitis. However, its potential role in COPD treatment remains unclear.
AIM OF THE STUDY: This study aimed to assess the potential of SRL in treating COPD and further related mechanisms by utilizing network pharmacology and experimental validation.
MATERIALS AND METHODS: The study induced COPD in mice through intratracheal instillation of LPS combined with exposure to CS. From day 57 to day 84, the mice were treated with distilled water, NAC, or SRL at doses of 200, 400, and 800 mg/kg. Lung function indices and histopathological examinations were used to evaluate the therapeutic efficacy of the treatments. Furthermore, network pharmacology, along with in vitro and in vivo experiments, was conducted to explore the potential mechanisms by which SRL against COPD.
RESULTS: The study demonstrated that SRL improved lung function and reduced lung index in COPD mice. Histopathological analysis revealed that SRL decreased apoptosis, collagen accumulation, airway inflammation, and excessive mucus production, highlighting its therapeutic potential in COPD treatment. RT-PCR analysis showed a marked decrease in the expression of Pro-Col I, Pro-Col III, TIMP-1, and TIMP-2 in SRL-treated COPD mice. Furthermore, Western blot analysis indicated a substantial increase in the expression levels of p-Smad3, p-P38 and p-JNK in the lung tissue of COPD mice compared to normal controls, suggesting activation of the MAPK pathway, which was consistent with network pharmacology predictions. Additionally, SRL treatment obviously suppressed the phosphorylation of these proteins and significantly reduced α-SMA expression.
CONCLUSION: It was firstly reported that SRL exhibited promising therapeutic potential for treating COPD, possibly through the activation of the MAPK pathway.
AIM OF THE STUDY: This study aimed to assess the potential of SRL in treating COPD and further related mechanisms by utilizing network pharmacology and experimental validation.
MATERIALS AND METHODS: The study induced COPD in mice through intratracheal instillation of LPS combined with exposure to CS. From day 57 to day 84, the mice were treated with distilled water, NAC, or SRL at doses of 200, 400, and 800 mg/kg. Lung function indices and histopathological examinations were used to evaluate the therapeutic efficacy of the treatments. Furthermore, network pharmacology, along with in vitro and in vivo experiments, was conducted to explore the potential mechanisms by which SRL against COPD.
RESULTS: The study demonstrated that SRL improved lung function and reduced lung index in COPD mice. Histopathological analysis revealed that SRL decreased apoptosis, collagen accumulation, airway inflammation, and excessive mucus production, highlighting its therapeutic potential in COPD treatment. RT-PCR analysis showed a marked decrease in the expression of Pro-Col I, Pro-Col III, TIMP-1, and TIMP-2 in SRL-treated COPD mice. Furthermore, Western blot analysis indicated a substantial increase in the expression levels of p-Smad3, p-P38 and p-JNK in the lung tissue of COPD mice compared to normal controls, suggesting activation of the MAPK pathway, which was consistent with network pharmacology predictions. Additionally, SRL treatment obviously suppressed the phosphorylation of these proteins and significantly reduced α-SMA expression.
CONCLUSION: It was firstly reported that SRL exhibited promising therapeutic potential for treating COPD, possibly through the activation of the MAPK pathway.