Therapeutic potential of pro-angiogenic BPC157 is associated with VEGFR2 activation and up-regulation.
Hsieh. Ming-Jer MJ; Liu. Hsien-Ta HT; Wang. Chao-Nin CN; Huang. Hsiu-Yun HY; Lin. Yuling Y; Ko. Yu-Shien YS; Wang. Jong-Shyan JS; Chang. Vincent Hung-Shu VH; Pang. Jong-Hwei S JS
Key Findings
- BPC‑157 increased vessel density in both the chick chorioallantoic membrane assay and in vitro endothelial tube formation.
- In rats with hind‑limb ischemia, BPC‑157 accelerated blood‑flow recovery and raised the number of blood vessels in the muscle.
- BPC‑157 up‑regulated VEGFR2 expression, promoted its internalization, and activated the VEGFR2‑Akt‑eNOS signaling pathway; these effects were blocked by an endocytosis inhibitor.
Practical Outcomes
- For the biohacker community, BPC‑157 may have potential as a tool to enhance tissue repair and improve blood supply to damaged areas, complementing its known gut‑healing benefits. However, the evidence is limited to animal and cell studies, with no human dosing or safety data, so any use for angiogenesis should be considered experimental and approached with caution.
Summary
The study shows that BPC‑157 can stimulate the growth of new blood vessels and speed up blood‑flow recovery in injured muscle in animal models. It does this by increasing the amount and activity of the VEGFR2 receptor on endothelial cells, which then triggers downstream signals that promote vessel formation.
Abstract
BPC 157, a pentadecapeptide with extensive healing effects, has recently been suggested to contribute to angiogenesis. However, the underlying mechanism is not yet clear. The present study aimed to explore the potential therapeutic effect and pro-angiogenic mechanism of BPC 157. As demonstrated by the chick chorioallantoic membrane (CAM) assay and endothelial tube formation assay, BPC 157 could increase the vessel density both in vivo and in vitro, respectively. BPC 157 could also accelerate the recovery of blood flow in the ischemic muscle of the rat hind limb as detected by laser Doppler scanning, indicating the promotion of angiogenesis. Histological analysis of the hind limb muscle confirmed the increased number of vessels and the enhanced vascular expression of vascular endothelial growth factor receptor 2 (VEGFR2) in rat with BPC 157 treatment. In vitro study using human vascular endothelial cells further confirmed the increased mRNA and protein expressions of VEGFR2 but not VEGF-A by BPC 157. In addition, BPC 157 could promote VEGFR2 internalization in vascular endothelial cells which was blocked in the presence of dynasore, an inhibitor of endocytosis. BPC 157 time dependently activated the VEGFR2-Akt-eNOS signaling pathway which could also be suppressed by dynasore. The increase of endothelial tube formation induced by BPC 157 was also inhibited by dynasore. This study demonstrates the pro-angiogenic effects of BPC 157 that is associated with the increased expression, internalization of VEGFR2, and the activation of VEGFR2-Akt-eNOS signaling pathway. BPC 157 promotes angiogenesis in CAM assay and tube formation assay. BPC 157 accelerates the blood flow recovery and vessel number in rats with hind limb ischemia. BPC 157 up-regulates VEGFR2 expression in rats with hind limb ischemia and endothelial cell culture. BPC 157 promotes VEGFR2 internalization in association with VEGFR2-Akt-eNOS activation. BPC 157 promotes angiogenesis in CAM assay and tube formation assay. BPC 157 accelerates the blood flow recovery and vessel number in rats with hind limb ischemia. BPC 157 up-regulates VEGFR2 expression in rats with hind limb ischemia and endothelial cell culture. BPC 157 promotes VEGFR2 internalization in association with VEGFR2-Akt-eNOS activation.
Study Information
pubmed
2016
2016-11-15T00:00:00.000Z
10.1007/s00109-016-1488-y
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