Related Experiment Video
Updated: Dec 10, 2025
Invasive Hemodynamic Characterization of the Portal-hypertensive Syndrome in Cirrhotic Rats
Published on: August 1, 2018
Inhibitory Effects of Beraprost Sodium in Murine Hepatic Sinusoidal Obstruction Syndrome
Makoto Nakura1, Tomoharu Miyashita2, Yasuhiko Yamamoto3
1Department of Gastroenterological Surgery, Kanazawa University Hospital, Kanazawa, Japan.
Background/Aim:
In this study, the liver sinusoidal endothelial cells (LSECs)-protective effects of beraprost sodium (BPS) were investigated using mice with monocrotaline (MCT)-induced sinusoidal obstruction syndrome (SOS).
Materials And Methods:
The mice were divided into BPS, placebo and control groups. They were killed 48 h after MCT administration, and blood samples and liver tissues were evaluated. Immunostaining was performed using anti-SE-1 and anti-CD42b antibodies, whereas plasminogen activator inhibitor (PAI-1) and endothelial nitric oxide synthase (eNOS) levels were evaluated using western blot or real-time RT-PCR.
Results:
On pathological examination, SOS-related findings were observed in zone 3 in the placebo group; however, these were significantly suppressed in the BPS group. SE-1 staining showed a consistent number of LSECs in the BPS group compared with that in the placebo group, while CD42b staining showed a significant decrease in the number of extravasated platelet aggregation (EPA) in the BPS group. PAI-1 expression was significantly lower in the BPS group than in the placebo group; however, eNOS expression was significantly higher in the BPS group than in the placebo group.
Conclusion:
Prophylactic administration of BPS is useful for suppressing the development of SOS through the protective effects of LSEC.
Insights
Beraprost sodium (BPS) protects liver sinusoidal endothelial cells (LSECs) from damage in a mouse model of sinusoidal obstruction syndrome (SOS). This finding suggests BPS is a potential therapeutic for preventing SOS development.
Area of Science:
- Hepatology
- Pharmacology
- Vascular Biology
Background:
- Sinusoidal obstruction syndrome (SOS) is a serious complication following hematopoietic stem cell transplantation.
- Liver sinusoidal endothelial cells (LSECs) are crucial for liver function and are primary targets in SOS.
- Monocrotaline (MCT) is a known toxin that induces SOS in experimental models.
Purpose of the Study:
- To investigate the protective effects of beraprost sodium (BPS) on LSECs in a mouse model of MCT-induced SOS.
- To evaluate the efficacy of BPS in preventing SOS development and its associated pathological changes.
Main Methods:
- Mice were administered MCT to induce SOS and treated with BPS or a placebo.
- Liver tissues and blood samples were collected 48 hours post-MCT administration.
- Immunostaining (SE-1, CD42b), Western blot, and real-time RT-PCR were used to assess LSEC integrity, platelet aggregation, and expression of PAI-1 and eNOS.
Main Results:
- BPS significantly suppressed SOS-related pathological findings in the liver compared to the placebo group.
- BPS maintained LSEC numbers (SE-1 staining) and reduced extravasated platelet aggregation (CD42b staining).
- BPS treatment led to decreased PAI-1 expression and increased eNOS expression.
Conclusions:
- Prophylactic administration of BPS demonstrates significant protective effects on LSECs.
- BPS is effective in suppressing the development of SOS.
- These findings highlight the therapeutic potential of BPS for SOS prevention.
More Related Videos
Related Concept Videos
01:20Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...
01:23Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...