ArticleSichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition2025
[Molecular Mechanisms of Intervention With Lishukang Capsule in a Rat Model of High-Altitude Pulmonary Edema].
Article in Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objective: To investigate the molecular targets and signaling pathways involved in the therapeutic effects of Lishukang Capsule (LSK) in a rat model of high-altitude pulmonary edema (HAPE) using a proteomics-based approach. Methods: A total of 60 male Wistar rats were randomly assigned to a control group, a HAPE model group, 3 LSK treatment groups receiving low-, medium-, and high-dose LSK, respectively, and a Results: The medium-dose LSK group exhibited significant anti-HAPE effects. Findings from the proteomic analysis revealed, in the comparison with the control group, 267 DEPs were identified in the HAPE group. In the comparison with the HAPE group, 225 DEPs were identified in the medium-dose LSK group. A total of 112 DEPs in the control group were normalized following LSK treatment in the medium-dose LSK group. In addition, GO enrichment analysis of proteins differentially expressed between the HAPE and LSK group showed that these DEPs were mainly enriched in 12 biological processes, 2 cellular components, and 5 molecular functions. KEGG pathway analysis showed that LSK activated pathways associated with cell adhesion molecules, glycosaminoglycan biosynthesis, DNA replication/nucleotide excision repair, transcriptional dysregulation in cancer, and Herpes simplex virus type 1 (HSV-1) infection, while inhibiting pathways associated with glycerophospholipid metabolism. Some differentially expressed proteins with potential functions were verified by Western blotting, including AGPAT5, NCAM1, SRSF3, and PLA2. These differentially expressed proteins were significantly expressed in the normal group, HAPE group, and LSK group, and the validation results were consistent with proteomic findings, indicating the high reliability of the proteomic results. Conclusion: LSK exerts a significant protective effect against HAPE. Proteomic analysis suggests that its therapeutic action may be mediated through activating pathways involved in cell adhesion molecules, glycosaminoglycan biosynthesis, DNA replication/nucleotide excision repair, transcriptional dysregulation in cancer, and HSV-1 infection, alongside inhibition of pathways associated with glycerophospholipid metabolism. The key DEPs identified in these pathways may play crucial roles in the preventive and therapeutic effects of LSK on HAPE.
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