#8343. Hypaphorine exerts anti-inflammatory effects in sepsis induced acute lung injury via modulating DUSP1/p38/JNK pathway
September 2026 | publication date |
Proposal available till | 10-05-2025 |
4 total number of authors per manuscript | 0 $ |
The title of the journal is available only for the authors who have already paid for |
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Journal’s subject area: |
Medicine (all); |
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Abstract:
Sepsis is a systemic inflammatory response syndrome attributed to infection, while sepsis-induced acute lung injury (ALI) has high morbidity and mortality. Here, we aimed to explore the specific mechanism of hypaphorines anti-inflammatory effects in ALI. Lipopolysaccharide (LPS) was adopted to construct ALI model both in vivo and in vitro. BEAS-2B cell viability and apoptosis was testified by the MTT assay and flow cytometry. Reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) were performed to examine the expression of proinflammatory cytokines (IL-1?, IL-6, TNF-?, and IL-18), and Western blot was adopted to examine the expression of the apoptosis-related proteins (Bax, Bcl2, and Caspase3) and the DUSP1/p38/JNK signaling pathway. At the same time, lung injury score, lactate dehydrogenase (LDH) and myeloperoxidase (MPO) activity were monitored. The dry/wet weight method was used to examine lung edema, and the total protein content in BALF was determined to test pulmonary vascular permeability.
Keywords:
acute lung injury; dual-specific phosphatase 1; hypaphorine; inflammation; sepsis
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