Effect of Chuankezhi Injection on TLR4/NF-B/NLRP3 Pathway in Mice with Acute Lung Injury

WANG Kai; LIU Xiao-hong

doi:10.13422/j.cnki.syfjx.2017220143

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Effect of Chuankezhi Injection on TLR4/NF-B/NLRP3 Pathway in Mice with Acute Lung Injury

更新时间：2024-01-04

- Effect of Chuankezhi Injection on TLR4/NF-B/NLRP3 Pathway in Mice with Acute Lung Injury
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 23, Issue 22, Pages: 143-148(2017)
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- DOI：10.13422/j.cnki.syfjx.2017220143
  CLC： R285.5
- Published：2017
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WANG Kai, LIU Xiao-hong. Effect of Chuankezhi Injection on TLR4/NF-B/NLRP3 Pathway in Mice with Acute Lung Injury[J]. Chinese journal of experimental traditional medical formulae, 2017, 23(22): 143-148.
DOI：

WANG Kai, LIU Xiao-hong. Effect of Chuankezhi Injection on TLR4/NF-B/NLRP3 Pathway in Mice with Acute Lung Injury[J]. Chinese journal of experimental traditional medical formulae, 2017, 23(22): 143-148. DOI： 10.13422/j.cnki.syfjx.2017220143.

摘要

目的：研究喘可治注射液对脂多糖（LPS）诱导的小鼠急性肺损伤（ALI）的防治效果及作用机制。方法：SPF级雌性C57BL/6J小鼠48只，随机分为正常组、模型组、地塞米松组、喘可治组，每组12只。喘可治组每只小鼠腹腔注射0.2 mL ·d-1，1次/d，连续7 d；地塞米松组造模前3 d按1 mg ·kg-1腹腔注射，1次/d，连续3 d；模型组注射等剂量的生理盐水，正常组不作处理。除正常组外，第8天腹腔注射LPS 0.1 mL（0.5 g ·L-1），乙醚吸入麻醉后，各小鼠滴鼻LPS 25 μL（0.5 g ·L-1），制作ALI模型。24 h后取材检测。酶联免疫吸附法（ELISA）检测小鼠血清肿瘤坏死因子-α（TNF-α），白细胞介素-1β（IL-1β），IL-18的含量；免疫组织化学染色检测核转录因子-κB （NF-κB）p65的蛋白表达；蛋白免疫印迹法（Western blot）检测肺组织p65，Toll样受体4（TLR4），Nod样受体蛋白3 （NLRP3），半胱氨酸天冬氨酸蛋白酶-1 （Caspase）-1蛋白表达；实时荧光定量PCR（Real-time PCR）检测肺组织p65和TLR4的mRNA表达。结果：与正常组比较，模型组小鼠血清TNF-α，IL-1β，IL-18含量升高（P<0.01），肺组织p65，TLR4，NLRP3，Caspase-1蛋白表达升高，p65和TLR4 mRNA的表达升高（P<0.05）；与模型组比较，喘可治组小鼠血清TNF-α，IL-1β，IL-18含量降低（P<0.01），肺组织p65，TLR4，NLRP3，Caspase-1蛋白表达降低，p65和TLR4 mRNA的表达降低（P<0.05）。结论：喘可治注射液能有效改善LPS诱导的急性肺损伤小鼠肺组织的损伤程度，其机制可能通过抑制TLR4/NF-κB/NLRP3信号通路进而对肺组织起到保护作用。

Abstract

Objective: To study the effect of Chuankezhi injection on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice and its mechanism. Method: The 48 SPF grade female C57BL/6J mice were randomly divided into normal group

model group

dexamethasone group

and Chuankezhi group

a total of 4 groups

12 mice in each group. Each mouse was intraperitoneally injected with 0.2 mL · d-1 in Chuankezhi group

once a day for 7 days. The mice in the dexamethasone group were injected intraperitoneally at 1 mg · kg-1 per day for 3 days before modeling. The mice in model group were injected with equal dose of normal saline while the normal group had no treatment. Except in the normal group

LPS 0.1 mL (0.5 g · L-1) was injected intraperitoneally on the 8 day

and the mice received 25 μL (0.5 g · L-1) by nasal drops after ether inhalation for anesthesia to establish ALI models. Detection was conducted after 24 h. The expression levels of tumor necrosis factor (TNF)-α

interleukin (IL)-1β and IL-18 were detected by enzyme-linked immunosorbent assay (ELISA). The expression level of nuclear factor-kappa B (NF-κB) p65 protein was detected by immunohistochemistry. Western blot was used to detect the expression levels of p65

Toll-like receptor4 (TLR4)

Nod-like receptor protein 3 (NLRP3) and cysteine aspartate protease-1 (Caspase-1) protein in lung tissues

and Real-time polymerase chain reaction (Real-time PCR) was used to detect the expression of p65 and TLR4 mRNA in lung tissues. Result: As compared with the normal group

the levels of TNF-α

IL-1β and IL-18 in serum in the model group were increased (P<0.01); the expression of p65

TLR4

NLRP3 and Caspase-1 were increased; p65 and TLR4 mRNA were increased (P<0.05). As compared with the model group

the levels of TNF-α

IL-1β and IL-18 in serum in Chuankezhi group were significantly decreased (P<0.01)

and the levels of p65

TLR4

NLRP3 and Caspase-1 protein and expression levels of p65 and TLR4 mRNA were also decreased (P<0.05). Conclusion: Chuankezhi injection can effectively improve the injury of lung tissues induced by LPS in mice with acute lung injury. The mechanism may be associated with inhibiting TLR4/NF-κB/NLRP3 signaling pathway to protect the lung tissues.

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