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中国应用生理学杂志 ›› 2017, Vol. 33 ›› Issue (2): 151-155.doi: 10.12047/j.cjap.5450.2017.038

• 研究论文 • 上一篇    下一篇

益气活血通络解毒方对小鼠肺缺血/再灌注损伤的作用及其机制

宋冬1,4, 郝卯林1, 项冰倩1, 罗梓垠1, 石璐2, Wu Yiming3, 王万铁1   

  1. 1. 温州医科大学缺血/再灌注损伤研究所, 浙江 温州 325035;
    2. 四川省宜宾卫生学校生理教研室, 宜宾 644000;
    3. Division of Cardiovascular Medicine University of Iowa Carver College of Medicine, Iowa City 52242, USA;
    4. 南京医科大学康达学院病理学与法医学教研室, 连云港 222000
  • 收稿日期:2016-04-28 修回日期:2016-12-07 出版日期:2017-03-28 发布日期:2018-06-20
  • 通讯作者: 王万铁,Tel:0577-86689817,E-mail:wwt@wmu.edu.cn E-mail:wwt@wmu.edu.cn
  • 基金资助:
    浙江省中医药重点研究计划(2013ZZ011);四川省宜宾市重点科技项目(2015SF035)

The effects of YHTJF on lung ischemia/reperfusion injury in mice

SONG Dong1,4, HAO Mao-lin1, XIANG Bing-qian1, LUO Zi-yin1, SHI Lu2, Wu Yiming3, WANG Wan-tie1   

  1. 1. Ischemia/Reperfusion Injury Research Institute, Wenzhou Medical University, Wenzhou 325035, China;
    2. Department of Physiology of Yibin Health School, Yibin 644000, China;
    3. Division of Cardiovascular Medicine University of Iowa Carver College of Medicine, Iowa City 52242, USA;
    4. Department of Pathology and Forensic Medicine of KangDa College of Nanjing Medical University, Lianyungang 222000, China
  • Received:2016-04-28 Revised:2016-12-07 Online:2017-03-28 Published:2018-06-20
  • Supported by:
    浙江省中医药重点研究计划(2013ZZ011);四川省宜宾市重点科技项目(2015SF035)

摘要: 目的:探讨益气活血通络解毒方(YHTJF)对小鼠的肺部缺血/再灌注(I/R)损伤,及对I/R引起的氧化应激反应的作用。方法:成年雄性10~12周龄C57BL/6J小鼠70只,体重(21~25) g,采用在体左肺门夹闭法复制缺血/再灌注损伤模型。随机分为7组:正常对照组(C),羧甲基纤维素钠carboxyl methyl cellulose-Na(CMC-Na)+正常对照组(CC),羧甲基纤维素钠+假手术组(CS),羧甲基纤维素钠+I/R模型组(CIR),羧甲基纤维素钠+YHTJF低、中、高浓度干预组(CYL、CYM、CYH)。CN、CS、CIR组术前连续7 d腹腔注射CMC溶液,CYL、CYM、CYH组术前连续7d腹腔注射低、中、高浓度的YHTJF溶液。术毕,取左肺测定肺组织干湿比(W/D)及总肺含水量(TLW),行肺组织损伤评估(IQA),光镜观察肺组织形态学结构改变。TUNEL测组织细胞凋亡指数(AI)。检测血清超氧化物歧化酶(SOD)、丙二醛(MDA)、髓过氧化物酶(MPO)。结果:相比C组,CC组和CS组所有检测指标均无明显差异,CIR组的W/D、TLW、IQA、AI明显升高(P < 0.01),肺组织形态学破坏显著;MDA含量、MPO活力明显升高,SOD活性显著降低。与CIR组比较,CYL组、CYM组、CYH组W/D、TLW、IQA、AI的表达均明显下降(P < 0.01),组织损伤明显减轻,CYM组各项指标数值改善最明显,组织损伤最轻;3个用药组的MDA含量、MPO活力明显下降,SOD活性显著升高,其中中剂量用药组氧化应激指标变化最突出。结论:YHTJF可有效减轻小鼠缺血/再灌注性肺损伤,以中剂量效果为最佳,其机制可能与其抑制体内氧化应激反应、减轻肺组织细胞凋亡有关。

关键词: 益气活血通络解毒方, 小鼠, 肺缺血/再灌注损伤, 氧化应激, 细胞凋亡

Abstract: Objective: To explore whether yiqi huoxue tongluo jiedu fang (YHTJF, Traditional Chinese Medicine) alleviates the injury during lung ischemia/reperfusion (I/R) in mice through inhibiting oxidative stress or not. Methods: C57BL/6J male mice (n=70) were randomly divided into 7 groups:control (C), carboxyl methyl cellulose-Na(CMC·Na) + normal control (CC), carboxyl methyl cellulose-Na + sham (CS), carboxyl methyl cellulose-Na + I/R (CIR), carboxyl methyl cellulose-Na + YHTJF-Low, CMC-Na + YHTJF-Middle, CMC-Na + YHTJF-High (CYL, CYM, CYH). The mice in CYL, CYM and CYH group were treated with YHTJF by intraperitoneal injection every day, while the carboxyl methyl cellulose-Na was administered with the same volume of CYL in CC, CS and CIR group. After 3 h-reperfusion, the left lung tissues were harvested to determine the lung wet/dry weight (W/D), the total lung water content (TLW), and the index of quantita-tive evaluation for alveolar damage (IQA). Morphological observation and terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL) were applied to evaluate the structural changes and the apoptosis index (AI) of the lung tissues. The expressions superoxide of dis-mutase(SOD), malondialdehyde(MDA) and myeloperoxidase(MPO) in the lung tissues were detected by kits. Results: Compared with group C, the W/D, TLW, IQA, AI, lung tissue structural changes, and the expressions of MDA and MPO in group I/R were increased obviously (P < 0.01), and the expression of SOD was decreased, while there was no significant difference between group CC and CS. Compared with group I/R, the parameters of these experiments in group CYL, CYM, CYH were all decreased, and the expression of SOD was increased, while the reduction in group CYM was the most remarkable among them (P < 0.01). Conclusion: YHTJF may attenuate the I/R injury of the lung by the inhibition of apoptosis via ROS pathway.

Key words: YHTJF, lung ischemia/reperfusion injury, reactive oxygen species (ROS), apoptosis, mice

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