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作 者:吴建龙[1] 巨积辉[1] 周广良[1] 金光哲[1] 李志敏[1] 侯瑞兴[1]
机构地区:[1]苏州大学附属瑞华医院手外科,江苏苏州215104
出 处:《中国临床解剖学杂志》2014年第6期698-703,707,共7页Chinese Journal of Clinical Anatomy
基 金:江苏省"333工程"培养资金资助项目(BRA2014091)
摘 要:目的探讨P38MAPK抑制剂SB202190对皮瓣缺血再灌注损伤发展及TNF-α与IL-10表达水平的影响。方法取12-14周龄健康Wistar大鼠48只,随机分为对照组(Ⅰ组)、缺血再灌注组(Ⅱ组)、生理盐水组(Ⅲ组)、P38抑制剂组(Ⅳ组),每组12只。制作大鼠腹部轴型皮瓣缺血再灌注损伤模型。术后7d,测定皮瓣存活率,检测大鼠血清TNF-α、IL-10浓度,切取皮瓣通过免疫组织化学方法检测P38MAPK与P-P38MAPK的表达。结果术后第7天,Ⅳ组皮瓣存活率显著高于Ⅱ、Ⅲ组(P〈0.05),与Ⅰ组无统计学差异(P〉0.05)。与Ⅱ、Ⅲ组相比,Ⅳ组P38MAPK与P-P38MAPK表达显著降低,血清TNF-α浓度明显降低,但IL-10浓度增高(P〈0.05)。相关分析结果表明:皮瓣存活率与TNF-α浓度显著负相关,与IL-10浓度相关不显著。P38MAPK、P-P38MAPK评分与TNF-α浓度均显著正相关,与IL-10浓度相关不显著。结论 SB202190可抑制皮瓣内P38MAPK信号通路,降低TNF-α浓度,减轻缺血再灌注损伤,提高皮瓣存活率。Objective To explore the P38 MAPK inhibitor SB202190 on IRI development and TNF- α、IL-10 expression levels in flap. Methods Forty-eight Wistar rats aged 12-14 weeks old, were randomly divided into control group (group Ⅰ ), ischemia-reperfusion group (group Ⅱ), saline group (group Ⅲ), P38 MAPK inhibitor group (group Ⅳ). The superficial epigastric artery flap ischemia reperfusion injury model was made in the left lower quadrant abdominal of each rat. The flaps were harvested 7 days after injection to receive immunohistochemistry observation, and P38MAPK, P-P38MAPK scoring. The TNF-α and IL-10 levels of the superficial epigastric vein were tested. Results The survival rates of the flaps 7 days after operation in group Ⅳwas higher than in group Ⅱ and Ⅲ significantly(P〈0.05). The expression of P38MAPK and P-P38MAPK in groupiv was lower than that in groupⅡ and In. The expression of TNF-α in group Ⅳ was lower than that in group Ⅱ and Ⅲ, but the IL- 10 content in group Ⅳ was higher than that in group Ⅱ and Ⅲ. Pearson correlation analysis showed that there was a significant negative correlation between flap survival rates and TNF-α level; there was a significant positive correlation between P38MAPK, P-P38MAPK scoring and TNF-α level. Conclusion The intraperitoneal use of P38 MAPK inhibitor SB202190 can decrease of the plasma TNF-α level, and improve skin flap survival from the Ischemia- reperfusion injury by preventing the activation of P38MAPK pathway.
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