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首页> 外文期刊>European review for medical and pharmacological sciences. >Ulinastatin improves myocardial ischemia-reperfusion injury in rats through endoplasmic reticulum stress-induced apoptosis pathway
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Ulinastatin improves myocardial ischemia-reperfusion injury in rats through endoplasmic reticulum stress-induced apoptosis pathway

机译：UlinaTaTin通过内质网胁迫诱导的凋亡途径改善了大鼠的心肌缺血再灌注损伤

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OBJECTIVE: To investigate the protective role of ulinastatin (UTI) on myocardial ischemia-reperfusion (I/R) injury in rats via endoplasmic reticulum stress (ERS)-induced apoptosis pathway. MATERIALS AND METHODS: A total of 60 rats were randomly divided into normal group (n=20), myocardial I/R model group (model group, n=20), and myocardial I/R model+UTI treatment group (treatment group, n=20). The myocardial function indicators [creatinine (Scr) and creatine kinase (CK)] were detected. Enzyme-linked immunosorbent assay (ELISA) was performed to measure serum levels of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and matrix metalloproteinase-9 (MMP-9). Meanwhile, the contents of reactive oxygen species (ROS), superoxide dismutase (SOD), and malondialdehyde (MDA) in rat left ventricular tissues were determined by ELISA as well. The cardiac function indexes were determined via magnetic resonance imaging (MRI) and echocardiography (ECG). Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL) staining assay was carried out to detect the apoptosis of myocardial tissues. Additionally, the expression levels of endoplasmic reticulum stress and apoptosis genes were measured through quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR) assay and Western blotting analysis, respectively. RESULTS: Serum levels of alanine aminotransferase (ALT), CK, and Scr in model group were significantly higher than those in normal group (p0.05). Besides, rats in model group had significantly lowered SOD, ejection fraction (EF, %), and fractional shortening (FS, %) than those in normal group (p0.05). In addition, remarkably increased contents of TNF-α, IL-6, MMP-9, MDA, and ROS, as well as higher left ventricular end-diastolic diameter (LVEDd) and left ventricular end-systolic diameter (LVESd) were observed in model group in comparison with normal group (p0.05). TUNEL staining results revealed that there were more apoptotic cells in model group than that in the other two groups (p0.05). Expression levels of cysteine aspartic acid-specific protease 12 (Caspase-12) and glucose-regulated protein 78 (GRP78) were evidently higher in model group than those in normal group (p0.05), while the expression level of B-cell lymphoma 2 (Bcl-2) was clearly lower in model group than that in normal group (p0.05). UTI treatment partially reversed the above expression changes (p0.05). CONCLUSIONS: UTI has a protective effect against myocardial I/R injury in rats by repressing the occurrence of ERS-induced apoptosis.
机译：目的：探讨乌司汀（UTI）对通过内质网胁迫（ERS）诱导的凋亡途径对大鼠心肌缺血再灌注（I / R）损伤的保护作用。材料和方法：将60只大鼠随机分为正常组（n = 20），心肌I / R模型组（模型组，n = 20）和心肌I / R型+ UTI治疗组（治疗组， n = 20）。检测心肌功能指示剂[肌酐（SCR）和肌酸激酶（CK）]。进行酶联免疫吸附测定（ELISA）以测量肿瘤坏死因子-α（TNF-α），白细胞介素-6（IL-6）和基质金属蛋白酶-9（MMP-9）的血清水平。同时，通过ELISA确定了大鼠左心室组织中反应性氧物质（ROS），超氧化物歧化酶（SOD）和丙二醛（MDA）的含量。通过磁共振成像（MRI）和超声心动图（ECG）确定心功能指标。末端脱氧核苷酸转移酶介导的脱氧尿苷三磷酸 - 生物素碎片末端标记（TUNEL）染色测定以检测心肌组织的凋亡。另外，通过定量逆转录聚合酶链反应（QRT-PCR）测定和蛋白质印迹分析，测量内质网应激和凋亡基因的表达水平。结果：模型组中丙氨酸氨基转移酶（ALT），CK和SCR的血清水平明显高于正常组（P <0.05）。此外，模型组的大鼠显着降低了SOD，喷射分数（EF，％）和分数缩短（FS，％），而不是正常组（P <0.05）。另外，TNF-α，IL-6，MMP-9，MDA和RO的显着增加，以及较高的左心室尿道直径（LVEDD）和左心室最终收缩直径（LVESD）的含量显着增加模型组与正常组相比（P <0.05）。 TUNEL染色结果表明，模型组中有比其他两组更高的细胞细胞（P <0.05）。模型组在模型组中显然高于正常组（P <0.05），表达水平的表达水平明显较高（P <0.05），而B细胞淋巴瘤的表达水平模型组中的2（Bcl-2）显然比正常组中的模型组显然（P <0.05）。 UTI治疗部分反转了上述表达变化（P <0.05）。结论：通过抑制诱导的细胞凋亡的发生，UTI对大鼠心肌I / R损伤具有保护作用。

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