# Targeting Pulmonary Hypertension: Elucidating Sophocarpine’s Protective Role via Preclinical Models

**Authors:** Feng Xie, Jie Feng, Kai Li, Yi Chen, Leilei Han, Yanqing Wu

PMC · DOI: 10.1155/mi/5524066 · Mediators of Inflammation · 2026-02-23

## TL;DR

This study explores how sophocarpine protects against pulmonary hypertension in preclinical models, showing it reduces inflammation and artery pressure.

## Contribution

The study experimentally validates sophocarpine's protective effects and mechanisms in pulmonary hypertension models.

## Key findings

- Sophocarpine reduced pulmonary artery pressure and inflammation in PH models.
- It alleviated apoptosis and restored pulmonary artery remodeling balance.
- Sophocarpine shows promise as a therapeutic agent for pulmonary hypertension.

## Abstract

Pulmonary hypertension (PH) is a serious disease that manifests itself as elevated pressure within the pulmonary arteries. The onset of PH is usually insidious, and if left untreated, it may lead to heart failure and even life‐threatening conditions. Recent studies have shown that sophocarpine (SOP) has significant effects on antioxidant, anti‐inflammatory, antifibrotic, and hemodynamic improvement, and it may become an emerging drug for the treatment of PH. However, the specific mechanism of action of SOP still requires further experimental validation.

We established in vivo and in vitro models of PH and treated them with varying concentrations of SOP. To visualize the changes in rats and cells, we used scratch assay, flow cytometry, Western blotting, pulmonary artery pressure measurement, biochemical analysis, enzyme‐linked immunosorbent assay (ELISA), ultrasound scanning, hematoxylin and eosin (HE) staining, and Masson’s trichrome staining.

Our results showed that SOP significantly alleviated the inflammatory response and apoptosis induced by PH, reduced pulmonary artery pressure, and restored the balance of pulmonary artery remodeling. These effects were found to be effective in alleviating PH.

Our study provides clear evidence that SOP has a significant protective effect in the PH model and is expected to be a promising therapeutic agent for PH.

## Linked entities

- **Chemicals:** sophocarpine (PubChem CID 115269)
- **Diseases:** pulmonary hypertension (MONDO:0005149)
- **Species:** Rattus norvegicus (taxon 10116)

## Full-text entities

- **Genes:** Il1b (interleukin 1 beta) [NCBI Gene 24494] {aka IL-1F2}, Tnf (tumor necrosis factor) [NCBI Gene 24835] {aka RATTNF, TNF-alpha, Tnfa}, NQO1 (NAD(P)H quinone dehydrogenase 1) [NCBI Gene 1728] {aka DHQU, DIA4, DTD, NMOR1, NMORI, QR1}, Hmox1 (heme oxygenase 1) [NCBI Gene 24451] {aka HEOXG, Heox, Hmox, Ho-1, Ho1, hsp32}, Nos2 (nitric oxide synthase 2) [NCBI Gene 24599] {aka Nos2a, iNos}, Gapdh (glyceraldehyde-3-phosphate dehydrogenase) [NCBI Gene 24383] {aka BARS-38, Gapd}, Edn1 (endothelin 1) [NCBI Gene 24323] {aka Et1}, GCLC (glutamate-cysteine ligase catalytic subunit) [NCBI Gene 2729] {aka CNSHA7, GCL, GCS, GLCL, GLCLC}, Sod1 (superoxide dismutase 1) [NCBI Gene 24786] {aka CuZnSOD}, Il6 (interleukin 6) [NCBI Gene 24498] {aka ILg6, Ifnb2}, Bax (BCL2 associated X, apoptosis regulator) [NCBI Gene 24887], Tlr4 (toll-like receptor 4) [NCBI Gene 29260], NFE2L2 (NFE2 like bZIP transcription factor 2) [NCBI Gene 4780] {aka IMDDHH, NRF2, Nrf-2}, Vim (vimentin) [NCBI Gene 81818], HMOX1 (heme oxygenase 1) [NCBI Gene 3162] {aka HMOX1D, HO-1, HSP32, bK286B10}, Casp3 (caspase 3) [NCBI Gene 25402] {aka CPP32-beta, Lice, Yama}, Bcl2 (BCL2, apoptosis regulator) [NCBI Gene 24224] {aka Bcl-2}, Nfe2l2 (NFE2 like bZIP transcription factor 2) [NCBI Gene 83619]
- **Diseases:** pain (MESH:D010146), Inflammation (MESH:D007249), fibrosis (MESH:D005355), dyspnea (MESH:D004417), pulmonary damage (MESH:D008171), hypoxic (MESH:D002534), Hy (MESH:D000860), spinal cord dislocation (MESH:D013118), PAH (MESH:D000081029), HP (MESH:C537262), thrombus (MESH:D013927), toxicity (MESH:D064420), vascular injury (MESH:D057772), RV dysfunction (MESH:D018497), cardiac remodeling (MESH:D020257), structural damage to the heart (MESH:D006331), RV hypertrophy (MESH:D017380), heart failure (MESH:D006333), PH (MESH:D006976), immune dysregulation (OMIM:614878), necrotic (MESH:D009336), HPASMCs (MESH:D018235), Endothelial hyperplasia (MESH:D006965)
- **Chemicals:** paraffin (MESH:D010232), saline (MESH:D012965), polyacrylamide (MESH:C016679), sodium pentobarbital (MESH:D010424), monocrotaline (MESH:D016686), isoflurane (MESH:D007530), water (MESH:D014867), prostacyclin (MESH:D011464), SDS (MESH:D012967), alkaloid (MESH:D000470), Hematoxylin (MESH:D006416), CCK8 (-), PI (MESH:D011419), MDA (MESH:D008315), SOP (MESH:C035933), lipid (MESH:D008055), paraformaldehyde (MESH:C003043), MCT (MESH:C000709826), CO2 (MESH:D002245), formaldehyde (MESH:D005557), ROS (MESH:D017382), Eosin (MESH:D004801), PVDF (MESH:C024865)
- **Species:** Homo sapiens (human, species) [taxon 9606], Rattus norvegicus (brown rat, species) [taxon 10116]
- **Mutations:** C) for 24, C1062S
- **Cell lines:** HPASMCs — Homo sapiens (Human), Finite cell line (CVCL_6775)

## Full text

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## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC12927990/full.md

## References

43 references — full list in the complete paper: https://tomesphere.com/paper/PMC12927990/full.md

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Source: https://tomesphere.com/paper/PMC12927990