文献类型：期刊文献

英文题名：TRX-1 CAN REPAIR THE ISCHEMIA REPERFUSION FLAP BY ANTI-OXIDATION MECHANISM AND INHIBITION OF ASK-MAPK PATHWAY

作者：Tao, Yongming[1];Wang, Jia[2];Liu, Yanhong[1];Pan, Jianxi[3];Ma, Zhixiang[1];Zhen, Wenjun[3]

第一作者：Tao, Yongming

通信作者：Wang, J[1]

机构：[1]Lanzhou Chinese Med Orthopaed Hosp, Dept & Land & Foot Surg, Lanzhou 730030, Gansu, Peoples R China;[2]Gansu Univ Tradit Chinese Med, Affiliated Hosp, Dept Rheumatol, Lanzhou 730020, Gansu, Peoples R China;[3]Lanzhou Hosp Tradit Chinese Med, Dept Orthopaed, Lanzhou 730030, Gansu, Peoples R China

第一机构：Lanzhou Chinese Med Orthopaed Hosp, Dept & Land & Foot Surg, Lanzhou 730030, Gansu, Peoples R China

通信机构：[1]corresponding author), Gansu Univ Tradit Chinese Med, Affiliated Hosp, Dept Rheumatol, Lanzhou 730020, Gansu, Peoples R China.|[10735b845793de6ae2b30]甘肃中医药大学第二附属医院;[10735]甘肃中医药大学;

年份：2019

卷号：35

期号：6

起止页码：3121

外文期刊名：ACTA MEDICA MEDITERRANEA

收录：;Scopus(收录号：2-s2.0-85074918240);WOS:【SCI-EXPANDED(收录号:WOS:000496261400037)】；

语种：英文

外文关键词：Thioredoxin-1; Antioxidant; ASK-MAPK; Ischemia-Reperfusion

摘要：Objective: To investigate the protective effect of thioredoxin-1 (Trx-1) on ischemia reperfusion flap and analyze the possible mechanism. Methods: Using human immortalized keratinocytes (HaCAT cells) as study cells, the optimal CoCl2 concentration and time was used to induce cell hypoxia in vitro. Cells were divided into hypoxia non-intervention group (CoCl2 was added into the cell culture medium to induce cytochemical hypoxia), hypoxia intervention group (CoCl2 was added into the cell culture medium to induce cytochemical hypoxia and rhTrx-1 was added for drug intervention), and negative control group (conventional cell culture medium was added to the cell culture medium). Cell viability was studied by CCK-8 method. Total protein was extracted and its concentration was determined. Expression levels of apoptosis-related proteins were analyzed by Western Blotting. Results: The concentration of CoCl2 was 80 mu mol/L, and the cell activity was about 50% of that of the control group when treated with HaCAT cells for 24h, which was used as the concentration of follow-up experiments. After CoCl2 was applied to HaCAT cells for 24h, the expression levels of apoptosis-related proteins ASK1 and c-PARP in the non-hypoxia intervention group were significantly higher than those in the control group, and the expression levels ofTrx-1 were significantly lower than those in the control group (P < 0.05). The expression levels of apoptosis related proteins ASK1 and c-PARP in the hypoxia intervention group were significantly lower than those in the non-hypoxia intervention group, and the expression levels ofTrx-1 were significantly higher than those in the non-hypoxia intervention group (P<0.05). Conclusion: Trx-1 preconditioning can reduce the ischemia reperfusion injury of the flap, and its mechanism may be related to the scavenging of reactive oxygen species and the inhibition of ASK-MAPK cell apoptosis signaling pathway, soTrx-1 can be used as the drug intervention target to reduce the ischemia reperfusion injury of the flap.