Current medicinal chemistry · 2026
Mechanistic Insights into Ginkgo Biloba Extract's Anti-Inflammatory Effects in COPD: Regulation of Th1/Th2 Balance via the p38 MAPK Pathway.
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Zhang Pengfei, Liao Lijun, Dong Xiaojun, Peng Zheng, Huang Shigao, Guo Dongwei, Sun Hao
Аннотация
OBJECTIVE: To investigate the anti-inflammatory and therapeutic effects of Ginkgo biloba extract (GBE) on chronic obstructive pulmonary disease (COPD), and to elucidate the underlying molecular mechanism by which GBE modulates the p38 mitogen-activated protein kinase (MAPK) signaling pathway and maintains the balance of T helper 1 (Th1)/T helper 2 (Th2) cells, thereby alleviating pulmonary inflammation, alveolar destruction and airway remodeling in COPD.
METHODS: Rats were randomly assigned to one of six groups: a blank group, a COPD model group, a high-dose GBE group (14 mg/kg/day), a medium-dose GBE group (7 mg/kg/day), a low-- dose GBE group (3.5 mg/kg/day), and a p38 MAPK inhibitor group, with 15 rats in each group. Except for the blank group, COPD models were established in the other groups using cigarette smoke (CS) inhalation combined with intratracheal lipopolysaccharide (LPS) instillation. Following the establishment of the models, the respective treatments were administered to each group. After the drug interventions, histological examination using HE staining, enzyme-linked immunosorbent assay (ELISA), flow cytometry, quantitative real-time polymerase chain reaction (PCR), and Western blot analysis were performed to explore the underlying mechanisms.
RESULTS: Different doses of GBE and the p38 MAPK inhibitor alleviated alveolar destruction and airway remodeling in COPD rats, reducing inflammatory infiltration around alveoli and bronchi. Compared with the COPD model group, all GBE dose groups and the p38 MAPK inhibitor group inhibited p38 MAPK signaling and the activation of upstream regulatory factors (TLR3, MKK3, MKK6) (p<0.05), reduced CD4+ T cell differentiation toward Th1 (p<0.05), suppressed secretion of inflammatory cytokines interferon-γ (IFN-γ) and interleukin-2 (IL-2) (p<0.05), and mitigated immune-inflammatory damage to alveoli and bronchi.
DISCUSSION: The core pathological issues of COPD include immune-inflammatory imbalance, destruction of alveolar structure, and airway remodeling. This study indicates that GBE can act simultaneously on these three core aspects. This research links GBE with the p38 MAPK signaling pathway and the regulation of Th1/Th2 balance. It improves airway remodeling by regulating the p38 MAPK pathway and corrects immune-inflammatory disorders by maintaining the Th1/Th2 balance, providing clear molecular mechanism support for the action of GBE, rather than merely remaining at the level of phenomenon observation.
CONCLUSION: GBE alleviates COPD immune-inflammatory responses, prevents alveolar destruction, and attenuates airway remodeling by regulating the p38 MAPK signaling pathway to maintain Th1/Th2 balance, thereby exerting therapeutic effects on COPD.
METHODS: Rats were randomly assigned to one of six groups: a blank group, a COPD model group, a high-dose GBE group (14 mg/kg/day), a medium-dose GBE group (7 mg/kg/day), a low-- dose GBE group (3.5 mg/kg/day), and a p38 MAPK inhibitor group, with 15 rats in each group. Except for the blank group, COPD models were established in the other groups using cigarette smoke (CS) inhalation combined with intratracheal lipopolysaccharide (LPS) instillation. Following the establishment of the models, the respective treatments were administered to each group. After the drug interventions, histological examination using HE staining, enzyme-linked immunosorbent assay (ELISA), flow cytometry, quantitative real-time polymerase chain reaction (PCR), and Western blot analysis were performed to explore the underlying mechanisms.
RESULTS: Different doses of GBE and the p38 MAPK inhibitor alleviated alveolar destruction and airway remodeling in COPD rats, reducing inflammatory infiltration around alveoli and bronchi. Compared with the COPD model group, all GBE dose groups and the p38 MAPK inhibitor group inhibited p38 MAPK signaling and the activation of upstream regulatory factors (TLR3, MKK3, MKK6) (p<0.05), reduced CD4+ T cell differentiation toward Th1 (p<0.05), suppressed secretion of inflammatory cytokines interferon-γ (IFN-γ) and interleukin-2 (IL-2) (p<0.05), and mitigated immune-inflammatory damage to alveoli and bronchi.
DISCUSSION: The core pathological issues of COPD include immune-inflammatory imbalance, destruction of alveolar structure, and airway remodeling. This study indicates that GBE can act simultaneously on these three core aspects. This research links GBE with the p38 MAPK signaling pathway and the regulation of Th1/Th2 balance. It improves airway remodeling by regulating the p38 MAPK pathway and corrects immune-inflammatory disorders by maintaining the Th1/Th2 balance, providing clear molecular mechanism support for the action of GBE, rather than merely remaining at the level of phenomenon observation.
CONCLUSION: GBE alleviates COPD immune-inflammatory responses, prevents alveolar destruction, and attenuates airway remodeling by regulating the p38 MAPK signaling pathway to maintain Th1/Th2 balance, thereby exerting therapeutic effects on COPD.