Tang Qin-qing, Su Shi-yue, Fang Mao-yong
Department of Emergency Medicine, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China, 230022.
Biol Trace Elem Res. 2014 Jun;159(1-3):320-4. doi: 10.1007/s12011-014-9971-1. Epub 2014 Apr 29.
Oxidative stress is a main factor in the pathogenesis of severe acute pancreatitis (SAP). The ability of zinc (Zn) to retard oxidative processes has been recognized for many years. This study aims to examine the levels of free oxygen radicals and antioxidant enzyme in SAP rats and know the effect of Zn supplementation on free oxygen radicals and antioxidant system in rats with SAP. Forty-five male Wistar rats were divided into three groups-the SAP group (n=15), the Zn-treated group (n=15), and the controlled group (n=15). For the SAP group, sodium taurocholate is injected into the pancreatic duct to induce SAP; for the Zn-treated group, Zn (5 mg/kg) is subcutaneously injected immediately after injection of 5% sodium taurocholate. Firstly, the activity of erythrocyte glutathione peroxidase (GSH-Px), erythrocyte superoxide dismutase (SOD), and the content of plasma malondialdehyde (MDA), which are the toxic products of oxidative stress, is measured. Secondly, the levels of free oxygen radicals in the liver and kidney are detected. The result showed that the activity of GSH-Px and SOD was lower in the SAP group than that in the controlled group, although the content of plasma MDA increased. However, the activity of SOD and GSH-Px in the Zn-treated group was not significantly decreased after comparing with the controlled group; in the mean time, the content of MDA was not significantly increased either. Moreover, the content of free radical in liver and kidney was higher in the SAP group compared with the controlled group, but the content of free radical in the Zn-treated group was not higher than that in the controlled group (p>0.05). All of the above indicated that Zn may recover the activity of free radical-scavenging enzymes and decrease the content of free radical for the SAP group rats. In conclusion, the content of free radical increase may be one of the reasons that SAP rats are injured, and it is possible for Zn to be used to treat SAP through scavenging free radical and increasing the activity of SOD and GSH-Px of erythrocyte.
氧化应激是重症急性胰腺炎(SAP)发病机制中的一个主要因素。锌(Zn)抑制氧化过程的能力多年来已得到认可。本研究旨在检测SAP大鼠体内的游离氧自由基水平和抗氧化酶,并了解补充Zn对SAP大鼠游离氧自由基和抗氧化系统的影响。45只雄性Wistar大鼠被分为三组——SAP组(n = 15)、Zn治疗组(n = 15)和对照组(n = 15)。对于SAP组,将牛磺胆酸钠注入胰管以诱导SAP;对于Zn治疗组,在注射5%牛磺胆酸钠后立即皮下注射Zn(5 mg/kg)。首先,测量红细胞谷胱甘肽过氧化物酶(GSH-Px)、红细胞超氧化物歧化酶(SOD)的活性以及血浆丙二醛(MDA)的含量,MDA是氧化应激的毒性产物。其次,检测肝脏和肾脏中的游离氧自由基水平。结果显示,尽管血浆MDA含量增加,但SAP组中GSH-Px和SOD的活性低于对照组。然而,与对照组相比,Zn治疗组中SOD和GSH-Px的活性没有显著降低;同时,MDA的含量也没有显著增加。此外,与对照组相比,SAP组肝脏和肾脏中的自由基含量更高,但Zn治疗组中的自由基含量不高于对照组(p>0.05)。以上所有结果表明,Zn可能恢复SAP组大鼠清除自由基酶的活性并降低自由基含量。总之,自由基含量增加可能是SAP大鼠受损的原因之一,Zn有可能通过清除自由基和提高红细胞SOD及GSH-Px的活性来用于治疗SAP。