[1]张汝锋,肖 虎.腺苷A2A受体拮抗剂通过PI3K途径抑制小鼠瘢痕增生的实验研究[J].中国美容医学,2022,(4):100-105.
　ZHANG Rufeng,XIAO Hu.Experimental Study on Adenosine A2A Receptor Antagonist Inhibiting Scar Hyperplasia in Mice Through PI3K Pathway[J].Medical Aesthetics and Beauty,2022,(4):100-105.
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腺苷A2A受体拮抗剂通过PI3K途径抑制小鼠瘢痕增生的实验研究()
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《中国美容医学》[ISSN:1008-6445/CN:61-1347/R]

卷:
期数:
2022年4期
页码:
100-105
栏目:
出版日期:
2022-04-10

文章信息/Info

Title:
Experimental Study on Adenosine A2A Receptor Antagonist Inhibiting Scar Hyperplasia in Mice Through PI3K Pathway
文章编号:
1008-6455（2022）04-0100-05
作者:
张汝锋; 肖 虎
(山东省立医院烧伤与创面修复科 山东 济南 250021 )
Author(s):
ZHANG Rufeng; XIAO Hu
(Department of Burn and Wound Repair,Shandong Provincial Hospital,Jinan 250021,Shandong,China)
关键词:
瘢痕增生; 腺苷A2A受体; 拮抗剂; PI3K途径; TGF-β1; 胶原
Keywords:
scar hyperplasia;  adenosine A2A receptor;  antagonist;  PI3K pathway;  TGF- 1;  collagen
分类号:
R619+.6
文献标志码:
A
摘要:
目的：探究腺苷A2A受体（A2AR）拮抗剂SCH58261对小鼠瘢痕增生的影响，并进一步分析该影响作用与PI3K途径的相关性。方法：实验1：将32只BALB/c雄性小鼠随机分为4组（n=8）。各组均制备瘢痕增生模型，第5～14天时，对照组和模型组均用生理盐水局部注射、高低剂量组分别给2mg/kg、5mg/kg A2AR拮抗剂SCH58261局部注射，每日1次、连续10d。实验2：将32只BALB/c雄性小鼠随机分为4组（n=8）。各组制备瘢痕增生模型，第5～14天，Ad-NC组局部注射Ad-NC及生理盐水,Ad-NC+模型组局部注射Ad-NC及生理盐水、Ad-NC+高剂量组局部注射Ad-NC及5mg/kg SCH58261局部注射、Ad-PI3K+高剂量组局部注射Ad-PI3K及5mg/kg SCH58261局部注射，每日1次，连续10d。采用HE染色观察增生瘢痕的组织学特征，采用Western blot检测转化生长因子-β1（TGF-β1）、Ⅰ型胶原（Col-Ⅰ）、Ⅲ型胶原（Col-Ⅲ）、p-PI3K、p-AKT的表达水平。结果：实验1：模型组出现了典型的瘢痕增生，TGF-β1、Col-I、Col-III、p-PI3K、p-AKT的表达水平均高于对照组；低剂量组和高剂量组瘢痕增生明显改善，TGF-β1、Col-I、Col-III、p-PI3K、p-AKT的表达水平均低于模型组，差异有统计学意义（P＜0.05）；实验2：过表达PI3K后，高剂量SCH58261改善瘢痕增生及抑制TGF-β1、Col-Ⅰ、Col-Ⅲ表达的作用发生逆转（P＜0.05）。结论：腺苷A2AR受体拮抗剂SCH58261能够抑制小鼠瘢痕增生，且这一作用与抑制PI3K途径有关。
Abstract:
Objective To investigate the effect of adenosine A2A receptor (A 2AR) antagonist SCH58261 on scar hyperplasia in mice, and furtherly analyze the correlation between this effect and PI3K pathway. Methods Experiment 1: 32 BALB/C male mice were randomly divided into four groups (n=8). The scar hyperplasia model was prepared in each group. At 5～14 d, the control group and the model group were injected with normal saline, and the high and low dose groups were injected with 2mg/kg and 5mg / kg A2AR antagonist SCH58261 respectively, once a day for 10 days. Experiment 2: 32 BALB/C male mice were randomly divided into four groups (n=8). The scar hyperplasia model was prepared in each group. At 5～14d, Ad-NC group was injected with Ad-NC and normal saline, ad Ad-NC+model group was injected with Ad-NC and normal saline, ad Ad-NC+high dose group was injected with Ad-NC and 5?mg / kg SCH58261, Ad-PI3K + high dose group was injected with Ad-PI3K and 5mg/kg SCH58261, once a day for 10 days.Then HE staining was used to observe the histological characteristics of hypertrophic scars, and western blot was used to detect transforming growth factor- β1 (TGF- β1), type I collagen (Col-I), type III collagen (Col-III), p-PI3K, p- The expression level of AKT. Results Experiment 1: The model group had typical scar hyperplasia, the expression levels of TGF- β1, Col-I, Col-III, p-PI3K, and p-AKT were higher than those of the control group. scar hyperplasia was obvious in the low-dose and high-dose groups improved, the expression levels of TGF-β1, Col-I, Col-III, p-PI3K, and p-AKT were lower than the model group, the difference was statistically significant (P＜0.05). Experiment 2: After overexpression of PI3K, high The effect of SCH58261 on improving scar hyperplasia and inhibiting the expression of TGF-β1, Col-I and Col-III was reversed (P＜0.05). Conclusion The adenosine A2AR receptor antagonist SCH58261 can inhibit scar hyperplasia in mice, and this effect is related to the inhibition of PI3K pathway

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更新日期/Last Update: 2022-05-06