【摘要】 目的：探究腺苷A_2A受体(A_2AR)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2 mg/kg、5 mg/kgA_2AR拮抗剂SCH58261局部注射，每日1次、连续10 d。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,AdNC+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5 mg/kgSCH58261局部注射、Ad-PI3K+高剂量组局部注射Ad-PI3K及5 mg/kgSCH58261局部注射，每日1次，连续10 d。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A_2AR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。更多还原

【Abstract】 Objective To investigate the effect of adenosine A_2A 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 A_2AR 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 A_2AR receptor antagonist SCH58261 can inhibit scar hyperplasia in mice, and this effect is related to the inhibition of PI3K pathway.更多还原