论文部分内容阅读
目的研究右美托咪定对小鼠视网膜缺血再灌注损伤的保护作用机制。方法选取8周龄C57BL/6雄性小鼠48只,按照体重随机分为3组:假手术组、模型组和实验组,每组16只。制备小鼠视网膜缺血再灌注损伤(RIRI)模型。在缺血前15 min和再灌注前5 min,实验组小鼠分别腹腔注射右美托咪定25μg·kg~(-1),假手术组和模型组腹腔注射同等剂量的0.9%Na Cl。在模型建立成功后,于再灌注24 h处死并取材。取小鼠视网膜组织匀浆液,用四唑盐试剂(WST-1)法检测超氧化物歧化酶(SOD),用TBA法检测丙二醛(MDA),用比色法测定谷胱甘肽过氧化物酶(GSH-PX),用酶联免疫吸附法检测肿瘤坏死因子α(TNF-α)、白细胞介素-6(IL-6)、1-甲基环丙烯(1-MCP)及IL-10水平。结果与假手术组比较,模型组小鼠视网膜组织中SOD为(45.47±8.16)U·mg~(-1)、GSH-PX为(264.64±27.31)U·mg~(-1),均明显降低;而MDA为(1.56±0.41)nmol·mg~(-1)、TNF-α为(2.67±0.23)ng·mL~(-1)、IL-6为(2.84±0.34)ng·mL~(-1)、MCP-1为(0.68±0.06)ng·mL~(-1)和IL-10为(0.21±0.02)ng·mL~(-1),均明显升高,差异有统计学意义(均P<0.05)。与模型组比较,实验组小鼠视网膜组织中SOD为(71.05±9.34)U·mg~(-1)、GSH-PX为(382.20±31.56)U·mg~(-1)、IL-10为(0.44±0.07)ng·mL~(-1),均明显降低;而MDA为(1.02±0.23)nmol·mg~(-1)、TNF-α为(1.53±0.20)ng·mL~(-1)、IL-6为(1.64±0.07)ng·mL~(-1)、MCP-1为(0.41±0.07)ng·mL~(-1),均明显降低,差异有统计学意义(P<0.05)。结论右美托咪定可以改善视网膜缺血再灌注损伤,其机制与抑制氧自由基所致的脂质过氧化损伤和抑制炎症因子的分泌有关。
Objective To study the protective mechanism of dexmedetomidine on retinal ischemia-reperfusion injury in mice. Methods Forty eight male C57BL / 6 mice aged 8 weeks were randomly divided into three groups according to body weight: sham operation group, model group and experimental group, with 16 rats in each group. Preparation of mouse retinal ischemia-reperfusion injury (RIRI) model. The mice in the experimental group were injected intraperitoneally with dexmedetomidine 25 μg · kg -1 at 15 min before ischemia and 5 min before reperfusion, respectively. The rats in sham operation group and model group were intraperitoneally injected with 0.9% NaCl. After successful establishment of the model, the animals were sacrificed and drawn 24 h after reperfusion. The homogenate of mouse retinal tissue was taken and the activity of superoxide dismutase (SOD) was detected by tetrazolium reagent (WST-1), malondialdehyde (MDA) by TBA method, glutathione The levels of TNF-α, IL-6, 1-methylcyclopropene (1-MCP) and IL-6 were detected by enzyme linked immunosorbent assay (ELISA) -10 level. Results Compared with sham operation group, the retinal tissue SOD in the model group was (45.47 ± 8.16) U · mg -1, GSH-PX was (264.64 ± 27.31) U · mg -1) (2.67 ± 0.23) ng · mL -1 for TNF-α and (2.84 ± 0.34) ng · mL -1 for MDA and (1.56 ± 0.41) nmol · mg -1 for MDA, (-1), (0.68 ± 0.06) ng · mL -1 for MCP-1 and (0.21 ± 0.02) ng · mL -1 for IL-10, respectively) Significance (all P <0.05). Compared with the model group, the SOD in the experimental group was (71.05 ± 9.34) U · mg -1, the GSH-PX was (382.20 ± 31.56) U · mg -1 in the experimental group and IL-10 was (0.44 ± 0.07) ng · mL ~ (-1), all of which were significantly lower than those in control group (1.02 ± 0.23) nmol · mg -1 and (-1.33 ± 0.20) ng · mL -1 1, IL-6 was (1.64 ± 0.07) ng · mL -1 and MCP-1 was (0.41 ± 0.07) ng · mL -1, both decreased significantly with a significant difference (P <0.05). Conclusion Dexmedetomidine can improve retinal ischemia-reperfusion injury, and its mechanism is related to inhibition of lipid peroxidation induced by oxygen free radicals and inhibition of the secretion of inflammatory cytokines.