The novel mechanism and therapic target of angiogenesis and regression in hemangioma.
What is it about?
Angiogenesis inhibition is vital to treat hemangioma. Propranolol (PRO) inhibition of angiogenesis may play a key role in the accelerated hemangioma involution, but the mechanisms underlying are unclear. hemangioma-derived endothelial cells (HemECs) were cultured in vitro, and a BALB/c nude mice hemangioma model was established. Viability and proliferation of HemECs, and the role of thrombospondin-1 and nuclear factor-kappa B signaling pathways were observed after PRO administration in vitro and in vivo. This study described a new mechanism of tumor angiogenesis and regression in hemangioma, and provided a new target for hemangioma treatment.
Why is it important?
We analyzed hemangioma-derived endothelial cells viability and proliferation, and the role of thrombospondin-1 and nuclear factor-kappa B signaling pathways after administration of propranolol. Our results showed a new mechanism of tumor angiogenesis and regression in hemangioma associated with thrombospondin-1 and nuclear factor-kappa B, and provided new targets for hemangioma treatment. We believe that our study makes a significant contribution to the literature because new effective therapeutic methods for the treatment of diseases such as hemangioma are necessary.
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