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纸质出版日期:2017
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刘玉凤, 李丹, 黄枚, 等. 紫草油膏对褥疮模型大鼠的治疗作用及机制[J]. 中国实验方剂学杂志, 2017,23(23):122-128.
LIU Yu-feng, LI Dan, HUANG Mei, et al. Therapeutic Effect of Arnebiae Radix Oil Ointment on Rat Pressure Ulcer Model and Its Mechanism[J]. Chinese journal of experimental traditional medical formulae, 2017, 23(23): 122-128.
刘玉凤, 李丹, 黄枚, 等. 紫草油膏对褥疮模型大鼠的治疗作用及机制[J]. 中国实验方剂学杂志, 2017,23(23):122-128. DOI: 10.13422/j.cnki.syfjx.2017230122.
LIU Yu-feng, LI Dan, HUANG Mei, et al. Therapeutic Effect of Arnebiae Radix Oil Ointment on Rat Pressure Ulcer Model and Its Mechanism[J]. Chinese journal of experimental traditional medical formulae, 2017, 23(23): 122-128. DOI: 10.13422/j.cnki.syfjx.2017230122.
目的:观察紫草油膏对褥疮模型大鼠的治疗作用及可能的作用机制,为其临床推广应用提供一定的实验依据。方法:采用皮下植入铁片加磁铁的方法复制大鼠褥疮模型。将造模成功的大鼠随机分为模型组、阳性(消炎生肌膏)组、紫草油膏中、高剂量组和碘剂组。另设空白组和假手术组。于造模成功后次日开始外涂给药,每日1次。连续给药3 d后,肉眼观察受压部位皮肤形态学和颜色变化;光镜下观察受压部位皮肤组织病理学变化;免疫组化法检测核转录因子-κB p65(nuclear transcription factor-κB,NF-κB p65)表达水平;水溶性四唑盐法及微板法检测大鼠血清中超氧化物歧化酶 (superoxide dismutase,SOD),丙二醛(malondialdehyde,MDA)的含量;酶联免疫吸附法(enzyme linked immunosorbent assay,ELISA)测定大鼠血清中白细胞介素-lα(interleukin-lα,IL-1α),肿瘤坏死因子-α(tumour necrosis factorα-α,TNF-α)的含量。结果:与空白组及假手术组比较,模型组大鼠受压部位发红不改变;病理观察到细胞排列紊乱,细胞间隙增宽,炎症细胞浸润等现象;血清中MDA,TNF-α,IL-1α及皮肤组织细胞核中NF-κB p65的含量明显升高(P<0.05,P<0.01),而血清中SOD的含量显著降低(P<0.01)。紫草油膏治疗3 d后,与模型组比较,受压部位皮肤组织红肿消退,状态明显好转;病理状态明显得到改善,炎症程度和数量均明显减轻或减少。紫草油膏中、高剂量组大鼠血清中SOD的含量明显高于模型组,而MDA的含量明显低于模型组(P<0.05,P<0.01);紫草油膏高剂量组较模型组血清中TNF-α,IL-1α的含量显著降低(P<0.05),细胞核中NF-κB p65蛋白表达显著降低(P<0.05)。结论:紫草油膏对褥疮模型大鼠具有一定治疗作用,其机制与抑制细胞核中NF-κB p65的表达、降低大鼠血清中IL-lα,TNF-α,MDA的含量及增加SOD含量有关。
Objective: To observe the therapeutic effect of Arnebiae Radix oil ointment (AROO) on a rat model of pressure ulcer (PU) and its possible mechanism
in order to provide the experimental evidence for clinical application. Method: Rats were randomly divided into seven groups
namely blank control group
sham group
model group
positive control group
middle-dose AROO group
high-dose AROO group and iodine group. The PU model was induced by applying magnets over irons that were implanted under the skin of rats except for blank control and sham group. AROO was applied the next day after modeling. Rats in blank control
sham group and model group were treated with normal saline
where as the other groups were given the corresponding medicines once a day. After three days of administration
the morphologic and color changes in skin were observed
and the histopathological changes in pressed skin tissues were observed under microscope. Nuclear transcription factor-κB p65(NF-κB p65) was detected by immunohistochemistry; WST-1 and microplate method were used to detect the superoxide dismutase (SOD) and malondialdehyde (MDA) in rat serum. And the levels of interleukin-lα (IL-lα) and tumor necrosis factorα-α (TNF-α) in rat serum were detected as well by enzyme linked immunosorbent assay (ELISA). Result: Compared with blank control and sham group
compressed skin parts of the rats in model group were red and swollen; and pathological observation showed that the cell lines were disordered
the cell gaps were widened
and the inflammatory cells were infiltrated. The levels of TNF-α
IL-1α and MDA in the serum and the expression of NF-κB p65 were significantly increased
while the level of SOD was reduced. After being treated with AROO for 3 days
the swelling in compressed tissues subsided
the pathological status was significantly improved
the inflammation was relieved
and the content of SOD in middle and high-dose groups was significantly higher than that of model group. However
the content of MDA was significantly lower than that of model group (P <0.05
P<0.01)
the levels of TNF-α and IL-1α in the serum of high-dose group were significantly lower than those in model group (P<0.05)
and the NF-κB p65 protein expression in high-dose group was significantly lower than model group (P<0.05). Conclusion: AROO has a therapeutic effect on rat PU model. Its mechanism is possibly related to the regulation of NF-κB p65 expression and the content of IL-1α
TNF-α
SOD and MDA in rat serum.
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