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The Study of the Clinical Observation and the Mechanism of Infantile Hemangioma Treatment with Propranolol

Author: QinGuiZhi
Tutor: LuJianYun
School: Central South University
Course: Dermatology and Venereology
Keywords: Hemangioma Propranolol HUVEC-12 cells VEGF JNK P38
CLC: R969
Type: Master's thesis
Year: 2011
Downloads: 111
Quote: 0
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Abstract


The first part of propranolol treatment of refractory infantile hemangioma clinical Objective To observe propranolol treatment of refractory infantile hemangioma clinical efficacy and safety. To 68 cases by clinical and laboratory examinations diagnosis of refractory infantile hemangiomas in children given propranolol, 1.0 ~ 2.0mg/kg/d, 2-3 times oral monthly referral once observed and recorded hemangioma size, texture, color change, and ready to deal with the adverse reactions that occur in the course of treatment. A score of 4 to evaluate the short-term effect. Results 68 patients were followed up for 3-13 months, efficacy: Ⅰ level 8 cases, Ⅱ: 13 cases, Ⅲ grade: 29 cases, Ⅳ grade: 13 cases. 68 cases of serious adverse reactions did not occur, but did not completely fade. Conclusions of a small dose of propranolol (1 ~ 2mg/kg/d) treatment of refractory infantile hemangioma efficacy exact adverse reactions are mild, can be as intractable infantile hemangioma preferred treatment, treatment dose and treatment should be individualized medication withdrawal should be by-increasing gradually less. . Infant refractory hemangioma treated by oral propranolol lesions can not completely subsided, local scars, color off, so once the diagnosis clear, should be treated as soon as possible, if necessary, can be combined with local treatment to remove residual diseased tissue. Second part propranolol affect HUVEC-12 cells secrete VEGF intracellular signaling mechanisms Objective To study the impact of propranolol on HUVEC-12 cells (Human Umbilical Vein Endothelial cells) secrete VEGF (Vascular Endothelial Growth Factor), and related signaling pathways, and further explore the molecular biological mechanisms of propranolol treatment refractory hemangioma. Vitro cultured human umbilical vein endothelial cells (HUVEC-12) as a model, and the concentrations were 16ug/ml, 8ug/ml, 4ug/ml, 2ug/ml, 1ug/ml, 0ug/ml (blank) propranolol intervention, using the ELISA method to detect the cell culture supernatant (cultural supernatants, CS) of VEGF concentration. MTT assay VEGF promote the best concentration of vascular endothelial cell proliferation, the establishment of positive system, based on p-JNK (phosphorylated JNK) by Western blotting after the intervention of different concentrations of propranolol and p-P38 ( expression of phosphorylated P38). 1. cytotoxic effects of different concentrations of propranolol group HUVEC-12 cells in the cytotoxicity assay different concentrations of propranolol intervention, MTT test results show the experimental group and blank control group, different concentrations of propranolol on human vascular endothelial cell cytotoxicity There was no statistical significance (P gt; 0.05) different concentrations of propranolol group CS VEGF concentration propranolol intervention of VEGF concentration in group CS 16ug/ml 8ug/ml 4ug/ml, 2ug/ml, 1ug/ml with blank control group were decreased (P lt; 0.05), there is a statistically significant difference in Punai lol concentration as 8ug/ml, dropped the most obvious. 3 different concentrations of VEGF in human vascular endothelial cells proliferation in a cell proliferation assay HUVEC-12 cells accepted as 40ng/ml, 20ng/ml, 10ng/ml, 5ng/ml 2.5ng/ml of VEGF for 48h after, compared with the blank control group, VEGF in human vascular endothelial cells to promote proliferation is most obvious when the concentration of 20ng/ml (P lt; 0.001). Propranolol intervention group p-JNK and p-p38 expression: p-JNK and p-P38 signals are enhanced weakened, P-Jnk in the propranolol concentration 1ug/ml expression most obvious P-P38 at a the propranolol concentration as 4ug/ml expression most obvious, in propranolol concentration 16ug/ml both have decline. Conclusion 1. Propranolol vein endothelial cells secrete VEGF inhibition at a concentration of 8 ug / the most obvious vein endothelial cells secrete VEGF inhibition ml. 2.P38, JNK kinase propranolol affect play an important role in the process HUVEC-12 cells secrete VEGF, the lowered vascular endothelial cells intracellular JNK and P38 signaling transduction by propranolol high concentrations reduced VEGF The proliferation effect so as to promote the regression of the hemangioma.

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