Pentadecapeptide BPC-157 Prevents and Completely Reverses Monocrotaline-Induced Pulmonary Hypertension in Rats

Monocrotaline is a substance known to cause selective injury to the vascular endothelium of the lungs, leading to a serious condition called pulmonary arterial hypertension. This condition is characterized by massive thickening of the precapillary artery's smooth muscle layer, right-side heart hypertrophy (cor pulmonale), and can lead to right-heart failure and death. The stable gastric pentadecapeptide BPC-157 is considered a prototype cytoprotective agent with known benefits for maintaining endothelial integrity, preventing thrombosis, and exhibiting anti-inflammatory effects. Researchers hypothesized that its endothelium-protective and other beneficial properties could offer a novel therapeutic approach to both prevent the onset and reverse the progression of this severe cardiopulmonary disease model.

The study used a rat model of pulmonary arterial hypertension, induced by a single subcutaneous injection of monocrotaline (80 mg/kg). The intervention peptide, BPC-157, was administered at two different doses (10 μg/kg or 10 ng/kg) via two routes: once-daily intraperitoneal injection or continuously in drinking water. Treatment regimens were either 'early' (starting on day 1 and lasting for 14 or 30 days) to test prevention, or 'delayed' (starting on day 14 and lasting until day 30) to test reversal of established disease. The primary endpoints were markers of pulmonary hypertension and cardiac distress, including blood vessel wall thickness, total vessel area, heart frequency, QRS axis deviation, QT interval prolongation, and right ventricle systolic pressure.

Rats receiving only monocrotaline developed the full syndrome of severe pulmonary hypertension, right-heart hypertrophy, clinical deterioration, and in some cases, death. In stark contrast, all BPC-157 treatment regimens, regardless of dose, route, or timing, successfully counteracted the monocrotaline-induced pathology. The early administration regimens completely prevented the development of pulmonary hypertension. Remarkably, the delayed treatment regimen, initiated after the disease was already established, demonstrated a rapid attenuation and then complete elimination of advanced pulmonary hypertension. The study documented consistent beneficial effects across all measured parameters, including right ventricle systolic pressure, heart hypertrophy, and ECG abnormalities like QRS axis deviation and QT interval prolongation.

With the delayed BPC-157 regimen, advanced pulmonary hypertension was rapidly attenuated and then completely eliminated.

Written by TitrateLab, separately from the study summarized above.