主管单位:中华人民共和国
国家卫生健康委员会
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英文作者:Yang Yi Yang Nan Li Juanjuan Fu Lijuan Guo Zhenhua He Wenwei
英文单位:Department of Anesthesiology the First Affiliated Hospital of Dali University Yunnan Province Dali 671000 China
英文关键词:Liverinjury;Dexmedetomidine;Pneumoperitoneum;Inflammation;Oxidativestress
目的 研究右美托咪定(DEX)对气腹后脂多糖诱导肝损伤模型小鼠肝功能的保护作用。方法 将40只无特定病原体级小鼠完全随机分为对照组(不进行处理)、气腹组、气腹+脂多糖处理组及气腹+脂多糖+DEX处理组,各10只。检测比较各组肝功能指标[丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)]、炎症因子指标[白细胞介素(IL)-1、IL-4、IL-6、肿瘤坏死因子α(TNF-α)]、氧化应激指标[活性氧、丙二醛、诱导型一氧化氮合酶(iNOS)、超氧化物歧化酶(SOD)]表达水平。结果 气腹+脂多糖处理组和气腹+脂多糖+DEX处理组的ALT和AST水平均明显高于对照组及气腹组,气腹+脂多糖+DEX处理组的ALT和AST水平均明显低于气腹+脂多糖处理组[(68±5)U/L比(106±9)U/L、(56±5)U/L比(77±8)U/L],差异均有统计学意义(均P<0.05)。气腹+脂多糖处理组和气腹+脂多糖+DEX处理组的IL-1、IL-4、 IL-6、TNF-α mRNA水平,活性氧、丙二醛、iNOS mRNA和SOD mRNA水平均明显高于气腹组,气腹+脂多糖+DEX处理组的以上指标水平均明显低于气腹+脂多糖处理组,差异均有统计学意义(均P<0.05)。结论 DEX可以保护气腹后脂多糖诱导肝损伤模型小鼠的肝功能,减轻炎症反应以及氧化应激。
Objective To investigate the protective effect of dexmedetomidine(DEX) on liver function in model mice undergoing lipopolysaccharide(LPS)-inducing liver injury after pneumoperitoneum. Methods Totally 40 specific pathogen free mice were randomly divided into the control group (no treatment), the pneumoperitoneum group, the pneumoperitoneum+LPS group and the pneumoperitoneum+LPS+DEX group, with 10 mice in each group. The levels of liver function indexes[alanine aminotransferase(ALT), aspartate aminotransferase(AST)], inflammatory factors indexes [interleukin(IL)-1, IL-4, IL-6, tumor necrosis factor-α(TNF-α)], oxidative stress indexes[reactive oxygen species, malondialdehyde, inducible nitric oxide synthase(iNOS), superoxide dismutase(SOD)] were detected and compared among the groups. Results ALT and AST levels of the pneumoperitoneum+LPS group and the pneumoperitoneum+LPS+DEX group were significantly higher than those of the control group and the pneumoperitoneum group, and ALT and AST levels of the pneumoperitoneum+LPS+DEX group were significantly lower than those of pneumoperitoneum+LPS group[(68±5)U/L vs (106±9)U/L, (56±5)U/L vs (77±8)U/L], with significant differences (all P<0.05). The levels of IL-1, IL-4, IL-6, TNF-α mRNA, reactive oxygen species, malondialdehyde, iNOS mRNA and SOD mRNA of the pneumoperitoneum+LPS group and the pneumoperitoneum+LPS+DEX group were significantly higher than those of the pneumoperitoneum group, and those of the pneumoperitoneum+LPS+DEX group were significantly lower than those of the pneumoperitoneum+LPS group(all P<0.05). Conclusion DEX can protect the liver function of model mice with LPS-inducing liver injury after pneumoperitoneum, and reduce inflammatory reaction and oxidative stress.
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