目的 觀察番茄紅素對SD大鼠在體心臟缺血再灌注損傷的影響，并探求其作用機制。方法 SD大鼠隨機分為假手術(shù)組，缺血再灌注損傷組，番茄紅素5、15 mg/kg+缺血再灌注損傷組。番茄紅素組術(shù)前15 d開始ig給藥，其他組給予生理鹽水，1次/d。制備大鼠缺血再灌注損傷模型后再灌3 h，收集血液，測定血清中心肌酶譜相關(guān)指標(biāo)肌酸激酶（CK）和乳酸脫氫酶（LDH）、氧化應(yīng)激相關(guān)指標(biāo)超氧化物歧化酶（SOD）和丙二醛（MDA），以及炎癥相關(guān)指標(biāo)腫瘤壞死因子α（TNF-α）和白介素1β（IL-1β）的水平，Western blotting法檢測心肌中生存素的表達(dá)。再灌24 h后取心臟，依文思藍(lán)–氯化三苯基四氮唑雙染色測定心肌梗死面積。結(jié)果 與缺血再灌注損傷組比較，番茄紅素可顯著減小心肌缺血再灌注損傷后心肌梗死面積（P<0.05），顯著降低缺血再灌注損傷后血清中CK、LDH水平（P<0.05），顯著升高缺血再灌注損傷后血清中SOD水平而降低MDA水平（P<0.05），顯著降低缺血再灌注損傷后血清中TNF-α和IL-1β水平（P<0.05），顯著逆轉(zhuǎn)缺血再灌注損傷下調(diào)的生存素表達(dá)（P<0.05）。結(jié)論 番茄紅素對SD大鼠在體心肌缺血再灌注損傷具有保護(hù)作用，其機制與減輕缺血再灌注損傷后氧化應(yīng)激損傷、抑制炎癥反應(yīng)和激活生存素通路有關(guān)。

Objective To study the protective effect of lycopene on the myocardial ischemia reperfusion injury (IRI) in SD rat model, and to explore the protective mechanisms. Methods SD rats were randomly divided into Sham, IRI, and lycopene 5, 15 mg/kg + IRI groups. The rats were ig administered with lycopene for 15 d before operation, and the other groups were ig administered with saline, once daily, for 15 d. When the IRI model was established, reperfusion was carried out for 3 h. Then the blood was collected, and the serum levels of related index of myocardial enzymes such as CK and LDH, related indexes of oxidative stress such as SOD and MDA, and relevant indicators of inflammation such as TNF-α and IL-1β were detected. The survivin expression was detected by Western blotting. After 24 h reperfusion, the area of myocardial infarction was detected by Evans blue-TTC double staining method.Results Compared with Sham group, lycopene treatment could significantly decrease the area of myocardial infarction (P < 0.05), significantly decrease the serum levels of CK and LDH (P < 0.05), significantly increase serum level of SOD, but decrease the level of MDA (P < 0.05), and significantly reverse the down-regulated survivin expression induced by IRI (P < 0.05). Conclusion Lycopene has protective effect against myocardial IRI, and its mechanism is not only related to the inhibition of inflammatory and oxidative stress response, but also related to the activation of survivin.