Chronic unpredictable stress exacerbates surgery-induced sickness behavior and neuroinflammatory responses via glucocorticoids secretion in adult rats.
<h4>Methods</h4>Sprague-Dawley adult male rats (12-14 weeks old) were exposed to 14-day CUS and then subjected to partial hepatectomy 24 h after the last stress session. The rats were pretreated with an antagonist of the glucocorticoids (GCs) receptor RU486 (30 mg/kg, i.p.) 1 h prior to...
Saved in:
| Main Authors: | , , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Public Library of Science (PLoS)
2017-01-01
|
| Series: | PLoS ONE |
| Online Access: | https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0183077&type=printable |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1850229080953192448 |
|---|---|
| author | Na Wang Hong Ma Zhe Li Yalei Gao Xuezhao Cao Yanhua Jiang Yongjian Zhou Sidan Liu |
| author_facet | Na Wang Hong Ma Zhe Li Yalei Gao Xuezhao Cao Yanhua Jiang Yongjian Zhou Sidan Liu |
| author_sort | Na Wang |
| collection | DOAJ |
| description | <h4>Methods</h4>Sprague-Dawley adult male rats (12-14 weeks old) were exposed to 14-day CUS and then subjected to partial hepatectomy 24 h after the last stress session. The rats were pretreated with an antagonist of the glucocorticoids (GCs) receptor RU486 (30 mg/kg, i.p.) 1 h prior to stress exposure. The behavioral changes were evaluated with open field test and elevated plus-maze test. The hippocampal cytokines interleukin (IL)-1β and IL-6 were measured on postoperative days 1, 3 and 7. Ionized calcium binding adaptor protein (Iba)-1, microglial M2 phenotype marker Arg1, brain derived neurotrophic factor (BDNF) and CD200 were also examined at each time point.<h4>Results</h4>CUS exacerbated surgery-induced sickness behavior. Exposure to CUS alone failed to alter the levels of pro-inflammatory cytokines in the brain. However, CUS exaggerated surgery-induced pro-inflammatory cytokines expression (e.g. IL-1β and IL-6) and upregulated the levels of Iba-1 on postoperative days 1 and 3. An additional significant decreased BDNF, CD200 and a lower level of Arg1 were also observed in the stressed rats following surgical procedure. Pretreatment with RU486 blunted the potentiating effects of CUS on surgery-induced sickness behavior and neuroinflammatory responses.<h4>Conclusion</h4>Chronic unpredictable stress enhanced surgery-induced sickness behavior and neuroinflammatory responses. Stress-induced GCs played a pivotal role in enhancing surgery-induced neuroinflammatory processes by modulation of microglia functions. |
| format | Article |
| id | doaj-art-b4c257a71d6a4c39acdb0f2d4e17f419 |
| institution | OA Journals |
| issn | 1932-6203 |
| language | English |
| publishDate | 2017-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj-art-b4c257a71d6a4c39acdb0f2d4e17f4192025-08-20T02:04:20ZengPublic Library of Science (PLoS)PLoS ONE1932-62032017-01-01128e018307710.1371/journal.pone.0183077Chronic unpredictable stress exacerbates surgery-induced sickness behavior and neuroinflammatory responses via glucocorticoids secretion in adult rats.Na WangHong MaZhe LiYalei GaoXuezhao CaoYanhua JiangYongjian ZhouSidan Liu<h4>Methods</h4>Sprague-Dawley adult male rats (12-14 weeks old) were exposed to 14-day CUS and then subjected to partial hepatectomy 24 h after the last stress session. The rats were pretreated with an antagonist of the glucocorticoids (GCs) receptor RU486 (30 mg/kg, i.p.) 1 h prior to stress exposure. The behavioral changes were evaluated with open field test and elevated plus-maze test. The hippocampal cytokines interleukin (IL)-1β and IL-6 were measured on postoperative days 1, 3 and 7. Ionized calcium binding adaptor protein (Iba)-1, microglial M2 phenotype marker Arg1, brain derived neurotrophic factor (BDNF) and CD200 were also examined at each time point.<h4>Results</h4>CUS exacerbated surgery-induced sickness behavior. Exposure to CUS alone failed to alter the levels of pro-inflammatory cytokines in the brain. However, CUS exaggerated surgery-induced pro-inflammatory cytokines expression (e.g. IL-1β and IL-6) and upregulated the levels of Iba-1 on postoperative days 1 and 3. An additional significant decreased BDNF, CD200 and a lower level of Arg1 were also observed in the stressed rats following surgical procedure. Pretreatment with RU486 blunted the potentiating effects of CUS on surgery-induced sickness behavior and neuroinflammatory responses.<h4>Conclusion</h4>Chronic unpredictable stress enhanced surgery-induced sickness behavior and neuroinflammatory responses. Stress-induced GCs played a pivotal role in enhancing surgery-induced neuroinflammatory processes by modulation of microglia functions.https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0183077&type=printable |
| spellingShingle | Na Wang Hong Ma Zhe Li Yalei Gao Xuezhao Cao Yanhua Jiang Yongjian Zhou Sidan Liu Chronic unpredictable stress exacerbates surgery-induced sickness behavior and neuroinflammatory responses via glucocorticoids secretion in adult rats. PLoS ONE |
| title | Chronic unpredictable stress exacerbates surgery-induced sickness behavior and neuroinflammatory responses via glucocorticoids secretion in adult rats. |
| title_full | Chronic unpredictable stress exacerbates surgery-induced sickness behavior and neuroinflammatory responses via glucocorticoids secretion in adult rats. |
| title_fullStr | Chronic unpredictable stress exacerbates surgery-induced sickness behavior and neuroinflammatory responses via glucocorticoids secretion in adult rats. |
| title_full_unstemmed | Chronic unpredictable stress exacerbates surgery-induced sickness behavior and neuroinflammatory responses via glucocorticoids secretion in adult rats. |
| title_short | Chronic unpredictable stress exacerbates surgery-induced sickness behavior and neuroinflammatory responses via glucocorticoids secretion in adult rats. |
| title_sort | chronic unpredictable stress exacerbates surgery induced sickness behavior and neuroinflammatory responses via glucocorticoids secretion in adult rats |
| url | https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0183077&type=printable |
| work_keys_str_mv | AT nawang chronicunpredictablestressexacerbatessurgeryinducedsicknessbehaviorandneuroinflammatoryresponsesviaglucocorticoidssecretioninadultrats AT hongma chronicunpredictablestressexacerbatessurgeryinducedsicknessbehaviorandneuroinflammatoryresponsesviaglucocorticoidssecretioninadultrats AT zheli chronicunpredictablestressexacerbatessurgeryinducedsicknessbehaviorandneuroinflammatoryresponsesviaglucocorticoidssecretioninadultrats AT yaleigao chronicunpredictablestressexacerbatessurgeryinducedsicknessbehaviorandneuroinflammatoryresponsesviaglucocorticoidssecretioninadultrats AT xuezhaocao chronicunpredictablestressexacerbatessurgeryinducedsicknessbehaviorandneuroinflammatoryresponsesviaglucocorticoidssecretioninadultrats AT yanhuajiang chronicunpredictablestressexacerbatessurgeryinducedsicknessbehaviorandneuroinflammatoryresponsesviaglucocorticoidssecretioninadultrats AT yongjianzhou chronicunpredictablestressexacerbatessurgeryinducedsicknessbehaviorandneuroinflammatoryresponsesviaglucocorticoidssecretioninadultrats AT sidanliu chronicunpredictablestressexacerbatessurgeryinducedsicknessbehaviorandneuroinflammatoryresponsesviaglucocorticoidssecretioninadultrats |