Acute lung injury (ALI) and its more severe form, acute respiratory distress syndrome (ARDS), are life-threatening pulmonary disorders with extremely high mortality rates, for which effective and safe therapeutic strategies remain limited. The development of targeted and biocompatible drug delivery systems is urgently needed to control pulmonary inflammatory cascades while minimizing systemic toxicity. Plant-derived extracellular vesicles offer a naturally safe and anti-inflammatory platform for therapeutic delivery. Ginsenoside Rb1 (GRb1), a major bioactive compound from ginseng, possesses potent anti-inflammatory and anti-apoptotic properties, whereas lemon-derived EVs (LEVs) exhibit intrinsic antioxidant and anti-inflammatory effects. Here, we engineered a multifunctional, biocompatible drug delivery platform, GRb1@LEVs-cRGD, in which ginsenoside Rb1 is incorporated into and fused with LEVs to form hybrid bio-nanovesicles, while the vesicle surface is functionalized with cyclic RGD (cRGD) peptides to target integrin αvβ3 highly expressed in inflamed pulmonary tissues, thereby enhancing site-specific delivery. In vitro and in vivo studies confirmed that GRb1@LEVs-cRGD effectively inhibited M1 macrophage polarization, suppressed inflammatory cascades, and preserved epithelial-endothelial integrity. Furthermore, exogenous cholesterol loading improved vesicle stability, maintained the pH gradient, and enhanced the loading efficiency of tigecycline and vancomycin by six-fold. In murine models of bacterial pneumonia induced by carbapenem-resistant Klebsiella pneumoniae and methicillin-resistant Staphylococcus aureus, antibiotic-loaded GRb1@LEVs-cRGD efficiently accumulated at infection sites and exhibited synergistic anti-inflammatory and bactericidal effects. Overall, this study demonstrates that GRb1@LEVs-cRGD is a safe, targeted, and multifunctional therapeutic platform with significant potential for ALI/ARDS treatment.

01 May 2026·EUROPEAN JOURNAL OF PHARMACOLOGY

Ginsenoside Rb1 alleviates cerebral ischaemia/reperfusion injury by suppressing oxidative stress and excessive autophagy via ATM-CHK2-Beclin 1 pathway

Article

Author: Cai, Biao ; Shan, Xiaoying ; Lei, Yuanyuan ; Yuan, Yuqi ; Li, Yuqing ; Wei, Liangli ; Wang, Guangyun

Recent studies have demonstrated that ginsenoside Rb1 (GRb1) exhibits neuroprotective effects against cerebral ischaemia/reperfusion (I/R) injury. However, whether GRb1 modulates autophagy and oxidative stress induced by cerebral I/R remains unclear. This study aims to determine whether GRb1 attenuates cerebral I/R injury by suppressing autophagy and oxidative stress via regulation of the ATM-CHK2-Beclin 1 pathway. Middle cerebral artery occlusion/reperfusion (MCAO/R) in 60 SPF C57BL/6 mice and oxygen-glucose deprivation/reperfusion (OGD/R) in rat pheochromocytoma (PC12) cells were employed to evaluate the protective effects of GRb1 on neurological injury, autophagy, and oxidative stress. Molecular mechanisms were validated using Western blot, immunofluorescence, and pharmacological inhibitors. The results showed that GRb1 alleviated neurological impairments, decreased cerebral infarct volume, and reduced histological damage in MCAO/R mice. Besides, GRb1 alleviated cell injury and reduced intracellular ROS production in PC12 cells induced by OGD/R. Furthermore, during MCAO/R and OGD/R, GRb1 suppressed autophagy and oxidative stress. Moreover, GRb1 treatment also decreased p-ATM/ATM and p-CHK2/CHK2 ratio and increased Beclin 1-Bcl-2 interaction both in vivo and in vitro. Molecular docking further elucidated that the mechanism by which GRb1 improves cerebral ischaemia maybe related to its direct binding to ATM, which in turn inhibited the phosphorylation of ATM. Additionally, the drug affinity response target stability (DARTS) and cellular thermal shift assay (CETSA) were also performed to suggest that GRb1 directly interacts with ATM. Collectively, these findings demonstrated that GRb1 reduced ischemic stroke-induced oxidative stress and autophagy through ATM-CHK2-Beclin 1 pathway, and GRb1 may be a protective medication for the treatment of cerebral ischaemia.

01 Mar 2026·PHYTOMEDICINE

Qingfei Jiedu Huatan formula protects against pneumonia by activating Nrf2 to suppress alveolar epithelial apoptosis

Article

Author: Zhang, Qin ; Shan, Baixi ; Jiang, Yuhang ; Zhao, Peng ; Li, Jiansheng ; Cao, Haiyang ; Cheng, Yumeng ; Xing, Xiaoxiang

BACKGROUND:

Qingfei Jiedu Huatan Formula (QJHF) has demonstrated efficacy in reducing the clinical stabilization time for pneumonia patients, decreasing ICU durations, and enhancing patients' quality of life.

OBJECTIVE:

Protecting the alveolar epithelial barrier is a proven strategy for improving pneumonia outcomes. This study aims to investigate the protective effects and underlying mechanisms of QJHF on the alveolar epithelial barrier in pneumonia.

METHODS:

A mouse model of pneumonia and acute lung injury was established via tracheal instillation of Klebsiella pneumoniae and LPS to evaluate the therapeutic effects of QJHF. Additionally, a TNF-α-induced alveolar epithelial cell barrier injury model was employed to explore the molecular mechanisms underlying QJHF's protective effects. Transcriptomics combined with network analysis was utilized to identify the active components and mechanisms of action for QJHF. Molecular docking and molecular dynamics analyses elucidated the binding interactions between Ginsenoside Rb1 (GRb1) and target proteins, while the application of Nrf2 inhibitor and siRNA clarified the role of Nrf2 activation in GRb1-mediated alveolar barrier protection.

RESULTS:

QJHF significantly ameliorates Klebsiella pneumoniae-induced pneumonia in mice by improving lung tissue damage, reducing inflammatory cell infiltration, and decreasing levels of pro-inflammatory factors such as TNF-α, IL-1β, and IL-6. Additionally, QJHF upregulates the expression of cell junction proteins ZO-1 and OCLN, thereby protecting the alveolar epithelial barrier. Similarly, QJHF mitigates LPS-induced lung damage, inflammation, and alveolar epithelial barrier dysfunction. Through integrating serum component profiling, network pharmacology, and lung transcriptomics revealed that 12 constituents in QJHF may interact with Nrf2 to modulate oxidative stress and apoptosis signaling pathways. Both in vitro and in vivo studies demonstrate that GRb1, one of the 12 components, significantly protects against TNF-α-induced alveolar epithelial cell barrier dysfunction and LPS-induced lung inflammation and alveolar barrier damage in mice. Furthermore, GRb1 can inhibit TNF-α-induced ROS levels and apoptosis in alveolar epithelial cells. Molecular dynamics stimulation and luciferase assays demonstrate that GRb1 can bind to and activate Nrf2, promoting its interaction with antioxidant response elements. Additionally, rotenone can counteract the protective effect against apoptosis in the alveolar epithelial cell barrier by increasing cellular ROS levels. Similarly, siRNA can significantly impair GRb1's protective effects against TNF-α-induced damage to the alveolar epithelial cell barrier. Nrf2 inhibitors notably attenuated GRb1's amelioration of LPS-induced lung inflammation and alveolar barrier damage in mice.

CONCLUSION:

This study confirms that QJHF and its active component GRb1 can activate Nrf2 to inhibit oxidative stress and apoptosis in alveolar epithelial cells, thereby protecting the alveolar epithelial barrier and ameliorating pulmonary inflammation and damage in mice with pneumonia.

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Indication	Highest Phase	Country/Location	Organization	Date
Arthritis	Discovery	South Korea	Oscotec, Inc.	-

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