Protective effect of Isoliquiritigenin on skin ischemia-reperfusion injury in rats

被引:1
|
作者
Zhou, Guifang [1 ]
Li, Anju [2 ]
Guo, Qiuling [1 ]
Song, Chuanmin [3 ]
Zhang, Youwen [2 ]
机构
[1] Jinan Jigang Hosp, Dept Oncol & Tradit Chinese Med, Jinan 250132, Shandong, Peoples R China
[2] Jinan Municipal Hosp Tradit Chinese Med, Dept Peripheral Vasc Dis, Jinan 250012, Shandong, Peoples R China
[3] Jinan Municipal Hosp Tradit Chinese Med, Dept Anesthesiol, Jinan 250012, Shandong, Peoples R China
关键词
skin ischemia-reperfusion (I; R) injury; isoliquiritigenin; oxidative stress; inflammation; OXIDATIVE STRESS; INFLAMMATORY RESPONSE; LATE-PHASE; ISCHEMIA/REPERFUSION; CHALLENGES; THERAPY; DAMAGE; SHOCK; FLAP;
D O I
10.1163/22238980-bja10031
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Skin ischemia-reperfusion (I/R) injury is a serious condition that compromises skin flap surgery and leads to organ dysfunction. It arose due to restoration of blood supply after prolonged ischemia. The present study was conducted to explore the possible protective Isoliquiritigenin (ISL) on skin ischemia-reperfusion injury in rats. The ISL was administered to rats in the dose of 10 mg/ kg, 20 mg/kg, and 30 mg/kg. The effect of ISL was quantified on the skin tissue of rats following the I/R injury on various indices of inflammation, oxidative stress, and apoptosis together with the effect on skin survival. ISL improves the survival of skin which is further confirmed by the histopathological analysis. It also causes a reduction of apoptosis as shown by TUNEL staining. The level of oxidative stress was found significantly reduced by restoring the MDA, SOD, and GSH levels near to normal. The level of inflammation was also decreased as suggested by reduced level of cytokines, such as TNF-alpha, IL-1 beta, and IL-6. The ISL also causes a significant reduction of COX-2 and iNOS in western blot analysis. Collectively, our study has shown a beneficial effect of ISL against skin I/R injury via multiple mechanisms of action, such as attenuation of oxidative stress, inflammation, and apoptosis.
引用
收藏
页码:90 / 98
页数:9
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