Effect of Astragaloside Ⅳ on Autophagy and Pyroptosis in Mice Bleomycin-induced Idiopathic Pulmonary Fibrosis

WANG Peng-fei; LIN Chang; LIU Yang; HUANG Mu-han; HAN Jia; OU Jiang-qin; DING Qian; XU Chang-jun; YANG Chang-fu

doi:10.13422/j.cnki.syfjx.20181036

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Effect of Astragaloside Ⅳ on Autophagy and Pyroptosis in Mice Bleomycin-induced Idiopathic Pulmonary Fibrosis

更新时间：2024-01-04

- Effect of Astragaloside Ⅳ on Autophagy and Pyroptosis in Mice Bleomycin-induced Idiopathic Pulmonary Fibrosis
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 24, Issue 10, Pages: 144-149(2018)
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- DOI：10.13422/j.cnki.syfjx.20181036
  CLC： R285.5
- Published：2018
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WANG Peng-fei, LIN Chang, LIU Yang, et al. Effect of Astragaloside Ⅳ on Autophagy and Pyroptosis in Mice Bleomycin-induced Idiopathic Pulmonary Fibrosis[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(10): 144-149.
DOI：

WANG Peng-fei, LIN Chang, LIU Yang, et al. Effect of Astragaloside Ⅳ on Autophagy and Pyroptosis in Mice Bleomycin-induced Idiopathic Pulmonary Fibrosis[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(10): 144-149. DOI： 10.13422/j.cnki.syfjx.20181036.

摘要

目的：探究黄芪甲苷对特发性肺纤维化（idiopathic pulmonary fibrosis，IPF）小鼠自噬和焦亡的影响及其作用机制，为黄芪抗肺纤维化的研究治疗提供新思路。方法：C57bl/6小鼠随机分为4组，分别为假手术组、模型组、黄芪甲苷组和地塞米松组。小鼠模型行气管切开术，滴注博来霉素（BLM）诱导成模。黄芪甲苷组和地塞米松组每天分别灌胃黄芪甲苷（50 mg·kg-1）和地塞米松（0.125 mg·kg-1），假手术组和模型组每天予等量生理盐水。小鼠于14 d取材，通过组织病理学染色评估黄芪甲苷对IPF诱导的肺损伤的治疗作用，通过蛋白质免疫印迹法（Western blot）检测肺组织中，LC3Ⅱ，白细胞介素-1β（IL-1β），IL-18和半胱氨酸天冬氨酸酶-1（Caspase-1）的水平以评估炎症反应程度和焦亡水平的表达水平。以苏木素-伊红（HE）和马松（Masson）三色染色观察肺组织形态和胶原纤维的表达水平。免疫组化（IHC）及Western blot分析自噬和焦亡标记蛋白表达水平。结果：与假手术组比较，模型组肺组织炎症反应明显、胶原蛋白显著增加（P<0.05），与模型组比较，黄芪甲苷组明显抑制肺组织炎症反应，下调胶原蛋白表达（P<0.05）。IHC和Western blot检测结果均显示，黄芪甲苷能显著提高LC3Ⅱ蛋白表达（P<0.05）同时抑制p62蛋白积累（P<0.05），降低Caspase-1，IL-1β和IL-18蛋白表达（P<0.05，P<0.01）的表达水平。结论：黄芪甲苷治疗显着改善了BLM诱导的小鼠肺纤维化，其作用机制可能与抑制焦亡并增强自噬有关。研究表明黄芪甲苷在抑制肺纤维化方面具有的治疗潜力。

Abstract

Objective: To explore the regulatory effect of astragaloside Ⅳ on autophagy and pyroptosis in mice lung tissue with idiopathic pulmonary fibrosis (IPF) and its mechanism

in order to provide new ideas for the study of astragalus' effect against lung fibrosis. Method: C57bl/6 mice induced by intratracheal instillation of bleomycin (BLM) were randomly divided into 4 groups:sham-operated group

model group

astragaloside Ⅳ group and dexamethasone group. astragaloside Ⅳ and dexamethasone groups were given respectively astragaloside Ⅳ (50 mg·kg-1) and dexamethasone (0.125 mg·kg-1) each day

while physiological saline was given in sham surgery and model groups each day. At the 14th day

lung tissues were collected for the analysis of the effect of astragaloside Ⅳ on morphology

collagen

autophagy and pyroptosis protein expression by hematoxylin-eosin (HE)

Masson

immunohistochemistry (IHC) and Western blot. Result: Astragaloside Ⅳ significantly inhibited the inflammatory reaction of lung tissues and down-regulated the expression of collagen (P<0.01). The results of IHC and Western blot showed that astragaloside Ⅳ significantly increased the expression of LC3Ⅱ/β-actin (P<0.05)

inhibited the accumulation of p62 (P<0.05)

and decreased the expression of Caspase-1 (P<0.01)

IL-1β (P<0.05) and IL-18 (P<0.05). Conclusion: Astragaloside Ⅳ group shows alleviationof pulmonary fibrosis. The mechanism may be related to the inhibition of pyroptosis and theincrease of autophagy. The study shows the therapeutic potential of Astragaloside Ⅳ in inhibiting pulmonary fibrosis.

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