金欣口服液对RSV感染大鼠I型干扰素及SOCS1/3表达的影响

张沛; 夏正坤; 高春林

doi:10.13422/j.cnki.syfjx.2016140139

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金欣口服液对RSV感染大鼠I型干扰素及SOCS1/3表达的影响

药理 | 更新时间：2024-01-04

- 金欣口服液对RSV感染大鼠I型干扰素及SOCS1/3表达的影响
- Effect of Jinxin Oral Liquid on Expression of I-IFN and SOCS1/3 in RSV Infected Rats
- 中国实验方剂学杂志 2016年22卷第14期页码：139-144
- 作者机构：
- 作者简介：
- 基金信息：
  
  国家级重点学科南京中医药大学儿科开放课题（EZK2012022）;南京军区南京总医院自然科学基金项目（2012011）
- DOI：10.13422/j.cnki.syfjx.2016140139
  中图分类号： R285.5
- 纸质出版日期：2016
- 稿件说明：
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张沛, 夏正坤, 高春林. 金欣口服液对RSV感染大鼠I型干扰素及SOCS1/3表达的影响[J]. 中国实验方剂学杂志, 2016,22(14):139-144.

ZHANG Pei, XIA Zheng-kun, GAO Chun-lin. Effect of Jinxin Oral Liquid on Expression of I-IFN and SOCS1/3 in RSV Infected Rats[J]. Chinese journal of experimental traditional medical formulae, 2016, 22(14): 139-144.
张沛, 夏正坤, 高春林. 金欣口服液对RSV感染大鼠I型干扰素及SOCS1/3表达的影响[J]. 中国实验方剂学杂志, 2016,22(14):139-144. DOI： 10.13422/j.cnki.syfjx.2016140139.

ZHANG Pei, XIA Zheng-kun, GAO Chun-lin. Effect of Jinxin Oral Liquid on Expression of I-IFN and SOCS1/3 in RSV Infected Rats[J]. Chinese journal of experimental traditional medical formulae, 2016, 22(14): 139-144. DOI： 10.13422/j.cnki.syfjx.2016140139.

摘要

目的：通过研究金欣口服液对呼吸道合胞病毒（respiratory syncytial virus，RSV）感染大鼠肺组织细胞因子信号抑制因子1/3（suppressor of cytokine signaling1/3，SOCS1/3）蛋白的干预作用，探讨其抗RSV感染的可能机制。方法：SD大鼠70只，随机分为正常组，感染模型组，金欣口服液低、中、高剂量组（3.3，9.9，29.7g·kg-1），预防组（提前2dig金欣口服液中剂量），利巴韦林组（24.5g·kg-1），每组10只，除正常组外，滴鼻感染24h造模，给药组每天给药2次，连续给药3d。采用酶联免疫吸附测定（ELISA）法检测RSV感染大鼠体内I型干扰素IFN-α和IFN-β含量，逆转录-聚合酶链式反应（RT-PCR）法检测RSV感染大鼠肺组织SOCS1，SOCS3mRNA表达量的变化，苏木素-伊红（HE）染色观察大鼠肺组织病理学变化。结果：与正常组比较，模型组RSV感染大鼠体内IFN-α和IFN-β含量明显升高，大鼠肺组织SOCS1，SOCS3mRNA表达量明显升高（P<0.05，P<0.01），模型组大鼠肺组织病变较为明显；预防组和金欣口服液中剂量组IFN-α的表达量高于模型组（P<0.05），预防组、金欣口服液中剂量组、利巴韦林组IFN-β的表达量高于模型组（P<0.01），金欣口服液高剂量组IFN-β的表达量高于模型组（P<0.05），金欣口服液中、高剂量组SOCS1表达量低于模型组（P<0.05），金欣口服液高剂量组和利巴韦林组SOCS3表达量高于模型组（P<0.05），金欣口服液中剂量组SOCS3表达量高于模型组（P<0.01）。结论：金欣口服液可上调RSV感染大鼠体内I型干扰素的表达，并通过抑制SOCS1/3的表达，发挥抗病毒作用，推测其为金欣口服液抗RSV感染的机制之一。

Abstract

Objective: To investigate the intervention effect of Jinxin oral liquid (JOL) on the expression of suppressor of cytokine signaling1/3 (SOCS1/3) protein in lung tissues of respiratory syncytial virus(RSV) infected rats

and the possible mechanism of anti-RSV infection. Method: Totally 70 SD rats were randomly divided into the normal group

the infection model group

JOL low

medium and high dose groups (3.3

9.9

29.7 g · kg-1)

the prevention group (given JOL 2 d in advance

ig)

the ribavirin group (24.5 g · kg-1)

with 10 rats in each group. Except for the normal group

the remaining groups were intranasally infected for 24 h

and treatment groups were give drugs for consecutively three days. The enzyme-linked immunosorbent assay (ELISA) was adopted to detect contents of type I-interferons IFN-α and IFN-β in RSV infected rats in vivo. The reverse transcriptase polymerase chain reaction (RT-PCR) was used to detect the changes in SOCS1 and SOCS3 mRNA expressions in lung tissues of RSV infected rats. The hematoxylin eosin (HE) staining was applied to observe pathological changes in rat lung tissues. Result: Compared with the normal group

the model group showed significant increases in IFN-α and IFN-β contents in RSV infected rats

and SOCS1 and SOCS3 mRNA expressions in lung tissues of RSV infected rats (P<0.05

P<0.01)

and the model group showed more obvious pathological changes in rats lung tissues. The IFN-α expressions of prevention group and JOL middle dose group were higher than model group (P<0.05)

the IFN-β expressions of prevention group

JOL middle dose group and ribavirin group were higher than model group (P<0.01); The IFN-β expression of JOL high dose group was higher than model group(P<0.05)

the SOCS1 expressions of JOL middle dose group and JOL high dose group were lower than model group(P<0.05)

the SOCS3 expressions of JOL middle dose group and ribavirin group were lower than model group(P<0.05) and the SOCS3 expression of JOL middle dose group was lower than model group (P<0.01). Conclusion: JOL can up-regulate the expression of I-IFN in RSV infected rats and down-regulate the expression of SOCS1/3

thus inhibiting virus infection. The SOCS1/3 may be one of JOL's mechanisms in anti-RSV infection.

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