文章摘要
王丽娜.丹红注射液对感染性休克大鼠肺损伤的保护作用机制[J].安徽医药,2022,26(9):1715-1718.
丹红注射液对感染性休克大鼠肺损伤的保护作用机制
Protective mechanism of Danhong injection on lung injury in rats with septic shock
  
DOI:10.3969/j.issn.1009-6469.2022.09.005
中文关键词: 肺损伤  休克,脓毒性  丹红注射液  核因子-κB  肿瘤坏死因子-α  白细胞介素-6  大鼠,Sprague-Dawley
英文关键词: Lung injury  Shock, septic  Danhong injection  NF-kappa B  Tumor necrosis factor-alpha  Interleukin-6  Rats, Sprague-Dawley
基金项目:
作者单位
王丽娜 承德市第三医院感染一科河北承德067000 
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中文摘要:
      目的观察丹红注射液(DHI)对感染性休克(SS)大鼠肺损伤的保护作用,并探讨其作用机制。方法2018年4月至2019年8月,48只健康雄性SD大鼠采用随机数字表法分为对照组、模型组、DHI干预组和阳性对照组,12只/组。采用腹腔注射脂多糖构建内毒素性休克致肺损伤模型;造模成功后,DHI干预组经腹腔注射2 mL/kg DHI,阳性对照组经腹腔注射1 mL/kg地塞米松,模型组和对照组大鼠均予以等体积生理盐水。通过苏木精-伊红(HE)染色观察大鼠肺组织病理改变;测量肺组织湿干质量比(W/D);采用酶联免疫吸附测定(ELISA)检测肺组织中肿瘤坏死因子-α(TNF-α)、白细胞介素(IL)-6含量水平;采用免疫组织化学法检测肺组织核因子-κB(NF-κB)及κB抑制因子α(IκB-α)蛋白表达。结果模型组大鼠肺组织W/D较对照组增加[(5.56±0.51)比(4.02±0.37)],DHI干预组肺组织W/D较模型组降低[(4.72±0.44)比(5.56±0.51)](P<0.05),DHI干预组与阳性对照组W/D[(4.72±0.44)比(4.45±0.46)]比较差异无统计学意义(P>0.05);模型组TNF-α[(0.66±0.08)μg/g比(0.23±0.06)μg/g],IL-6[(128.04±10.35)ng/g比(38.17±6.82)ng/g]含量较对照组升高(P<0.05),DHI干预组TNF-α[(0.41±0.06)μg/g比(0.66±0.08)ng/g],IL-6[(66.38±6.20)ng/g比(128.04±10.35)ng/g]含量较模型组下调(P<0.05),阳性对照组肺组织TNF-α[(0.38±0.07)μg/g比(0.41±0.06)μg/g],IL-6[(60.54±5.27)ng/g比(66.38±6.20)ng/g]含量与DHI干预组比较差异无统计学意义(P>0.05);与对照组比较,模型组NF-κB(p65)及IκB-α呈强阳性免疫反应,与模型组比较,DHI干预组NF-κB(p65)及IκB-α阳性反应减弱,阳性细胞百分比下降(P<0.05),DHI干预组与阳性对照组NF-κB(p65)及IκB-α阳性细胞百分比差异无统计学意义(P>0.05)。结论DHI可能通过抑制NF-κB活化,减少TNF-α、IL-6等促炎细胞因子表达,在SS大鼠肺损伤中发挥保护作用。
英文摘要:
      Objective To observe protective effect of Danhong injection (DHI) on lung injury in rats with septic shock (SS), and to explore its action mechanism.Methods The starting and ending time of this experiment was from April 2018 and August 2019, 48 healthy male SD rats were assigned into control group, model group (LPS), DHI intervention group (LPS+DHI) and positive control group (LPS+DEX) according to random number table method, 12 cases in each group. The models of rats with endotoxin shock induced lung injury were constructed by intraperitoneal injection of lipopolysaccharides (LPS). After successful modeling, LPS+DHI group was intraperitoneally injected with 2 mL/kg DHI, LPS+DEX group was intraperitoneally injected with 1 mL/kg dexamethasone (DEX), LPS group and control group were given same volume of normal saline. The pathological changes of lung tissues were observed by HE staining.The wet-dry ratio (W/D) of lung tissues was measured. The levels of tumor necrosis factor-α (TNF-α) and interleukin (IL)-6 in lung tissues were detected by enzyme-linked immunosorbent assay (ELISA). The expressions of nuclear factor κB (NF-κB) and κB suppressor α (IκB-α) proteins in lung tissues were detected by immunohistochemistry.Results W/D of lung tissue in model group was higher than that in control group [(5.56±0.51) vs. (4.02±0.37), W/D of lung tissue in DHI intervention group was lower than that in model group [(4.72±0.44) vs. (5.56±0.51)] (P<0.05). There was no significant difference in W/D between DHI intervention group and positive control group [(4.72±0.44) vs. (4.45±0.46)] (P>0.05). The levels of TNF- α [(0.66 ± 0.08) μg/g vs. (0.23 ± 0.06) μg/g] and IL-6 [(128.04 ±10.35) ng/g vs. (38.17 ± 6.82) ng/g] in model group were higher than those in control group (P<0.05), the levels of TNF-α and IL-6 in DHI intervention group were lower than those in model group [(0.41 ± 0.06) μg/g vs. (0.66 ± 0.08) ng/g, (66.38 ± 6.20) ng/g vs. (128.04 ±10.35) ng/g] (P<0.05). There was no significant difference in TNF-α [(0.38 ± 0.07) μg/g vs. (0.41 ± 0.06) μg/g] or IL-6 [(60.54 ± 5.27)ng/g vs. (66.38 ± 6.20) ng/g] between positive control group and DHI intervention group (P>0.05). Compared with control group, NF-κB(p65) and IκB-α showed strongly positive immune response in model group. Compared with model group, positive responses of NF-κB(p65) and IκB-α were decreased in DHI intervention group, and percentage of positive cells was decreased (P<0.05). There was no significant difference in percentage of NF-κB (p65) or IκB-α positive cells between DHI intervention group and positive control group (P>0.05).Conclusion DHI may play protective roles against lung injury in SS rats by inhibiting NF-κB activation, and reducing expres1sions of pro-inflammatory cytokines such as TNF-α and IL-6.
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