Search

Objective To observe and investigate the therapeutic effect of scorpion ointment on early hypertrophic scar in rabbit ear model. Methods From October 2019 to October 2020, 8 New Zealand white rabbits were randomly divided into control group and treatment group, 4 rabbits in each group. The rabbit ear hypertrophic scar model was established. The scorpion ointment was used in the treatment group and the PBS was used in the control group. At 7 and 28 days after treatment, the tissues of each group were taken for HE staining, Masson's trichrome staining and immunohistochemistry. Results At 28 days after rabbit ear model established, the wounds of rabbit ears in each group were completely healed and hypertrophic scar was formed. Significant hyperplasia of scars was found in the control group. In the treatment group, the scar volume was gradually decreased, and the texture and color were improved. The results of HE staining and Masson's trichrome staining showed that the degree of tissue fibrosis was significantly reduced after treatment with scorpion ointment (P<0.05). Compared with the control group, the immunohistochemistry results showed that the expression of CD31 and vascular endothelial growth factor (VEGF) in the treatment group at 7 and 28 days were significantly decreased (P<0.05). Conclusion Scorpion ointment can treat hypertrophic scar by reducing the degree of fibrosis and down regulating the expression of CD31 and VEGF. [ABSTRACT FROM AUTHOR]

Objective To explore whether miR-9 can inhibit the growth of hypertrophic scar fibroblasts by targeting PI3K. Methods From September 2020 to September 2021, 12 healthy adult New Zealand long-eared rabbits were randomly divided into control group (6 rabbits) and scar group (6 rabbits). The histological morphology of both groups was detected by HE staining. The mRNA expression of miR-9 and PI3K in tissues was detected by real-time fluorescent quantitative PCR, and the expression of miR-9 and PI3K was analyzed by Pearson's correlation coefficient. The human hypertrophic scar fibroblasts (HSFb) were divided into psiCHECK-WT-PI3K+miR-9 control group, psiCHECK-WT-PI3K+miR-9 mimic group, psiCHECK-MUT-PI3K+miR-9 control group and psiCHECK-MUT-PI3K+ miR-9 mimic group. The corresponding sequences were transfected respectively. The expression of luciferase and renilla luciferase were detected by luciferase reporter gene assay at 48 h after transfection. The HSFb was divided into miR-9 control group and miR-9 mimic group. At 0, 12, 24, 36 and 48 h after transfection, the cell proliferation was detected by MTT. At 24 h after treatment, the cell apoptosis was detected by Annexin V-FITC/PI kit, and the expression of PI3K, caspase 3 and Bcl-2 protein was detected by protein immunoblotting. The number of samples in cell experiment was 3. The data were analyzed by t-test and Pearson's correlation coefficient. Results In HE staining, the excessive proliferation of fibroblasts and inflammatory cell infiltration were found in scar tissue. The model was successfully constructed. Compared with the control group, the miR-9 expression was significantly down-regulated (t=11.020, P<0.05) and PI3K expression was significantly up-regulated in the scar group (t=10.840, P<0.05). Pearson's correlation analysis showed that the expression of miR-9 and PI3K was negatively correlated in all tissues. At 48 h after transfection, the PI3K activity in the psiCHECK-WT-PI3K + miR-9 mimic group was significantly lower than that in the psiCHECK-WT-PI3K+miR-9 control group (t=8.648, P=0.001). The PI3K activity in the psiCHECK-MUT-PI3K+miR-9 control group was similar to that in the psiCHECKMUT-PI3K+miR-9 mimic group (t=2.053, P=0.109). At 12, 24, 36 and 48 h after transfection, the proliferation ability of miR-9 mimic group was significantly lower than that of the miR-9 control group (P<0.05). At 24 h after transfection, the early apoptotic rate of HSFb in the miR-9 mimic group was higher than that in the miR-9 control group (t=11.210, P=0.001). MiR-9 can down regulate the expression of PI3K, inhibit the expression of Bcl-2 and up regulate the content of caspase 3. Conclusion MiR-9 is down-regulated in the hypertrophic scar tissue, which can inhibit the growth of HSFb by targeting PI3K. [ABSTRACT FROM AUTHOR]