清燥救肺汤对Lewis肺癌小鼠EGFR,NF-B,ICAM-1表达及JAK1,STAT1蛋白磷酸化的影响

谢雄; 谢斌; 饶斌; 刘红宁

doi:10.13422/j.cnki.syfjx.2016240140

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清燥救肺汤对Lewis肺癌小鼠EGFR,NF-B,ICAM-1表达及JAK1,STAT1蛋白磷酸化的影响

药理 | 更新时间：2024-01-04

- 清燥救肺汤对Lewis肺癌小鼠EGFR,NF-B,ICAM-1表达及JAK1,STAT1蛋白磷酸化的影响
- Effect of Qingzao Jiufei Tang Expression on EGFR,NF-B,ICAM-1 and Protein Phosphorylation of JAK1 and STAT1 of Lewis Lung Cancer in Rats
- 中国实验方剂学杂志 2016年22卷第24期页码：140-144
- 作者机构：
- 作者简介：
- 基金信息：
  
  国家自然科学基金项目（81260523）;江西省教育厅科技项目（GJJ150833）;江西省研究生创新基金项目（YC2015-S351）
- DOI：10.13422/j.cnki.syfjx.2016240140
  中图分类号： R285.5
- 纸质出版日期：2016
- 稿件说明：
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谢雄, 谢斌, 饶斌, 等. 清燥救肺汤对Lewis肺癌小鼠EGFR,NF-B,ICAM-1表达及JAK1,STAT1蛋白磷酸化的影响[J]. 中国实验方剂学杂志, 2016,22(24):140-144.

XIE Xiong, XIE Bin, RAO Bin, et al. Effect of Qingzao Jiufei Tang Expression on EGFR,NF-B,ICAM-1 and Protein Phosphorylation of JAK1 and STAT1 of Lewis Lung Cancer in Rats[J]. Chinese journal of experimental traditional medical formulae, 2016, 22(24): 140-144.
谢雄, 谢斌, 饶斌, 等. 清燥救肺汤对Lewis肺癌小鼠EGFR,NF-B,ICAM-1表达及JAK1,STAT1蛋白磷酸化的影响[J]. 中国实验方剂学杂志, 2016,22(24):140-144. DOI： 10.13422/j.cnki.syfjx.2016240140.

XIE Xiong, XIE Bin, RAO Bin, et al. Effect of Qingzao Jiufei Tang Expression on EGFR,NF-B,ICAM-1 and Protein Phosphorylation of JAK1 and STAT1 of Lewis Lung Cancer in Rats[J]. Chinese journal of experimental traditional medical formulae, 2016, 22(24): 140-144. DOI： 10.13422/j.cnki.syfjx.2016240140.

摘要

目的：观察清燥救肺汤对荷Lewis小鼠肺癌瘤重、瘤指数、检测核转录因子-κB（NF-κB），细胞间黏附分子-1（ICAM-1），两面神激酶1（JAK1），表皮生长因子（EGFR）表达及信号传导及转录激活因子1（STAT1）蛋白磷酸化的影响。方法：雄性C57BL/6J小鼠50只，随机分为模型组，化疗[50 mg·kg-1·（2 d）-1]组，清燥救肺汤高、中、低剂量（15.2，7.6，3.8 g·kg-1·d-1）组，每组10只。右腋下注射细胞建立荷Lewis肺癌小鼠模型，清燥救肺汤组以相应剂量造模前2周开始灌胃给药，环磷酰胺（CTX）组以CTX相应剂量腹腔注射给药，隔日1次，模型组以等体积生理盐水灌胃给药，2周后处死各组小鼠并取瘤组织，称定质量计算瘤指数，免疫组化法检测NF-κB蛋白表达，实时荧光定量PCR法检测ICAM-1 mRNA表达，蛋白免疫印迹法（Western blot）检测EGFR，pJAK1及pSTAT1蛋白表达。结果：与模型组比较，清燥救肺汤高、中剂量组及CTX组瘤重、瘤指数显著降低（P<0.01），清燥救肺汤高、中剂量组及CTX组NF-κB蛋白表达，EGFR蛋白表达明显降低（P<0.05，P<0.01），清燥救肺汤高、中剂量组ICAM-1 mRNA，pJAK1蛋白表达明显降低（P<0.05，P<0.01），清燥救肺汤高、中、低剂量组pSTAT1蛋白磷酸化显著降低（P<0.01），高、中剂量组效果优于CTX组（P<0.01）。结论：清燥救肺汤能显著抑制荷Lewis小鼠肺癌细胞增殖，其机制可能与降低NF-κB，ICAM-1，pJAK1，EGFR表达及抑制STAT1蛋白磷酸化有关。

Abstract

Objective: To observe the effect of Qingzao Jiufei Tang(QJT) on tumor weight

tumor index

nuclear transcription factor kappa B (NF-κB)

intercellular cell adhesion molecule-1 (ICAM-1)

janus kinase 1(JAK1)

epidermal growth factor receptor (EGFR) and signal transducers and activators of transcription 1 (STAT1) protein phosphorylation of Lewis lung cancer mice. Method: Totally 50 male C57BL/6J mice were randomly divided into model group

chemotherapy group[50 mg·kg-1·(2 d)-1]

and high

medium and low-dose QJT groups (15.2

7.6

3.8 g·kg-1·d-1)

with 10 in each group. The animal model was induced through the axillary injection with Lewis cells in the right arm of mice. QJT groups were intragastrically administered with medicines two weeks before modeling

chemotherapy group was intragastrically administered with cyclophosvnamide(CTX) at the corresponding dose

once every other day

and model group was intragastrically administered with the same volume of saline. At 2 weeks after modeling

the mice were put to death to weigh the tumor index

detect the expression of NF-κB by immunohistochemical method

the expression of ICAM-1 by Real-time PCR method

and JAK1

pEGFR and pSTAT1 by Western blot method. Result: Tumor weight and tumor index of high and medium-dose QJT groups and CTX group were significantly decreased

compared with the model group

with significant differences(P<0.01). CTX group

and high and medium-dose QJT groups showed significant decreases in the expression of NF-κB and EGFR protein expression (P<0.05

P<0.01)

high and medium-dose QJT groups showed significant decrease in the expressions of ICAM-1 and pJAK1 (P<0.05

P<0.01)

high

medium and low-dose QJT groups showed significant decrease in phosphorylation of STAT1

compared with the model group

with significant differences (P<0.01)

high and medium-dose QJT groups were superior to CTX group (P<0.01). Conclusion: QJT can significantly inhibit the proliferation of Lewis lung cancer cells. It may inhibit lung cancer by reducing the protein expressions of NF-κB

ICAM-1

pJAK1

EGFR

phosphorylation of STAT1 protein.

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