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刘芹, 陈岩, 胡国鑫, 彭锦, 刘健, 樊晓光, 牟林, 王亨, 崔文娟, 乔鲁军. HOTAIR靶向miR-138介导TLR4依赖性信号通路对脓毒症大鼠炎症和氧化应激作用机制[J]. 中国公共卫生, 2021, 37(2): 293-297. DOI: 10.11847/zgggws1124218
引用本文: 刘芹, 陈岩, 胡国鑫, 彭锦, 刘健, 樊晓光, 牟林, 王亨, 崔文娟, 乔鲁军. HOTAIR靶向miR-138介导TLR4依赖性信号通路对脓毒症大鼠炎症和氧化应激作用机制[J]. 中国公共卫生, 2021, 37(2): 293-297. DOI: 10.11847/zgggws1124218
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LIU Qin, CHEN Yan, HU Guo-xin, . Effect and mechanism of long-chain noncoding RNA HOTAIR targeting micRNA-138 on inflammatory response and oxidative stress induced by LPS in septic rats[J]. Chinese Journal of Public Health, 2021, 37(2): 293-297. DOI: 10.11847/zgggws1124218
Citation: LIU Qin, CHEN Yan, HU Guo-xin, . Effect and mechanism of long-chain noncoding RNA HOTAIR targeting micRNA-138 on inflammatory response and oxidative stress induced by LPS in septic rats[J]. Chinese Journal of Public Health, 2021, 37(2): 293-297. DOI: 10.11847/zgggws1124218
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HOTAIR靶向miR-138介导TLR4依赖性信号通路对脓毒症大鼠炎症和氧化应激作用机制

Effect and mechanism of long-chain noncoding RNA HOTAIR targeting micRNA-138 on inflammatory response and oxidative stress induced by LPS in septic rats

    摘要
  • 摘要:
      目的  探讨长链非编码RNA HOTAIR靶向miR-138并介导TLR4依赖性信号通路对脂多糖(LPS)诱导的脓毒症大鼠炎症反应和氧化应激的影响及其作用机制。
      方法  将大鼠按体重随机分为4组：对照组、模型组、shRNA对照组和shHOTAIR组，每组10只；腹腔注射脂多糖(5 mg/kg)建立脓毒症大鼠模型，采用RT-PCR法检测lncRNA HOX反义转录RNA（HOTAIR）和miR-138表达情况；苏木素 – 伊红染色观察各组大鼠肝、肺组织的病理损伤情况，试剂盒法检测肿瘤坏死因子α（TNF-α）、白细胞介素 – 6（IL-6）、IL-4和IL-10及超氧化物歧化酶（SOD）、丙二醛（MDA）和谷胱甘肽（GSH）表达水平，TLR4、NF-κB P65的磷酸化情况。
      结果  与对照组比较，模型组大鼠肺组织中HOTAIR表达升高、miR-138表达下降(P < 0.05)。与对照组比较，模型组大鼠肝、肺组织出现明显的病理改变；与模型组比较，shHOTAIR组大鼠肝、肺组织病理改变明显减轻。与对照组比较，模型组大鼠血清中TNF-α、IL-6、MDA含量明显升高，IL-4、IL-10、SOD和GSH含量明显下降(P < 0.05)；与模型组比较，shHOTAIR组大鼠血清中TNF-α、IL-6、MDA含量明显下降，IL-4、IL-10、SOD和GSH含量明显升高(P < 0.05)。
      结论  HOTAIR通过靶向miR-138并介导TLR4依赖性的信号通路，抑制脂多糖诱导的脓毒症大鼠炎症反应和氧化应激。

     

    Abstract:
      Objective  To investigated the effect and mechanism of long-chain noncoding RNA (lncRNA) HOX transcript antisense RNA (HOTAIR) targeting microRNA-138 (miRNA-138) and mediating Toll-like receptors 4 (TLR4)-dependent signaling pathway on inflammatory response and oxidative stress induced by lipopolysaccharide (LPS) in septic rats.
      Methods  Sixty male Sprague-Dawley rats were randomly divided into four groups according to body weight (10 in each group): control group, model group, short-hairpin RNA (shRNA) control group and short hairpin RNA targeting HOTAIR (shHOTAIR) group. LPS (5 mg/kg) was injected intraperitoneally to establish a rat sepsis model. The expression of HOTAIR and miRNA-138 were detected by real-time reverse-transcriptase PCR (RT-PCR). Hematoxylin-eosin staining was used to observe the pathological changes of liver and lung tissues in rats of each group. The expressions of tumor necrosis factor-alpha (TNF-α), interleukin 6, 4, 10 (IL-6, IL-4, IL-10), superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH), and the phosphorylation of TLR4 and nuclear factor kappa B (NF-kB/p65) were detected using kit assays.
      Results  Compared with those of the control group, the HOTAIR was overexpressed but miRNA-138 was underexpressed in lung tissues of model rats (both P < 0.05); obvious pathological changes were observed in liver and lung tissues of the model rats. Compared with those of the model rats, the pathological changes of the liver and lung tissues of the rats with shHOTAIR treatment were significantly alleviated. Compared with those of the control rats, serum TNF-α, IL-6 and MDA of the model rats increased significantly, while serum IL-4, IL-10, SOD and GSH decreased significantly (P < 0.05 for all); in comparison with those of the model rats, serum TNF-α, IL-6 and MDA of the rats of shHOTAIR group decreased significantly, but serum IL-4, IL-10, SOD and GSH increased significantly (all P < 0.05).
      Conclusion  HOTAIR inhibits inflammatory response and oxidative stress induced by LPS in septic rats by targeting miR-138 and mediating TLR4-dependent signaling pathway.

     

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