Notoginsenoside R1 alleviates lipopolysaccharide-triggered PC-12 inflammatory damage via elevating microRNA-132
Background Delayed inflammatory response is closely associated with the severity of Spinal cord injury (SCI). Herein, the function and molecular mechanism of notoginsenoside R1 (NGR1) in the in vitro model of SCI inflammation injury were explored.Methods PC-12 neuronal cells were subjected with LPS...
| Main Authors: | , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Taylor & Francis Group
2019-12-01
|
| Series: | Artificial Cells, Nanomedicine, and Biotechnology |
| Subjects: | |
| Online Access: | https://www.tandfonline.com/doi/10.1080/21691401.2019.1610414 |
| _version_ | 1811302683134394368 |
|---|---|
| author | Yuanliang Sun Bing Liu Xiujun Zheng Dechun Wang |
| author_facet | Yuanliang Sun Bing Liu Xiujun Zheng Dechun Wang |
| author_sort | Yuanliang Sun |
| collection | DOAJ |
| description | Background Delayed inflammatory response is closely associated with the severity of Spinal cord injury (SCI). Herein, the function and molecular mechanism of notoginsenoside R1 (NGR1) in the in vitro model of SCI inflammation injury were explored.Methods PC-12 neuronal cells were subjected with LPS to construct a cell-based model of SCI inflammatory injury. NGR1 was applied in this cell model. miR-132 was silenced by transfection with miR-132 inhibitor. Cell viability and apoptosis were assessed, respectively. Then, the expression changes of pro-inflammatory cytokines and JNK pathway were examined.Results In this model, LPS was neurotoxic, with inhibiting PC-12 cell viability, inducing apoptosis, and enhancing concentrations of IL-6, IL-8 and TNF-α. However, NGR1 weakened the influence of LPS on PC-12 cells via elevating cell viability, decreasing apoptosis, decreasing pro-inflammatory cytokines expression, and suppressing activation of JNK signalling pathway. miR-132 was up-regulated by NGR1 treatment. Silence of miR-132 eliminated the influence of NGR1 on LPS-stimulated PC-12 cells.Conclusion NGR1 relieved PC-12 cells from LPS-triggered inflammatory damage via elevating miR-132 and hereafter suppressing JNK pathway. |
| first_indexed | 2024-04-13T07:32:31Z |
| format | Article |
| id | doaj.art-6175e1620fb74c9cb1ade19e43fd5fd4 |
| institution | Directory Open Access Journal |
| issn | 2169-1401 2169-141X |
| language | English |
| last_indexed | 2024-04-13T07:32:31Z |
| publishDate | 2019-12-01 |
| publisher | Taylor & Francis Group |
| record_format | Article |
| series | Artificial Cells, Nanomedicine, and Biotechnology |
| spelling | doaj.art-6175e1620fb74c9cb1ade19e43fd5fd42022-12-22T02:56:17ZengTaylor & Francis GroupArtificial Cells, Nanomedicine, and Biotechnology2169-14012169-141X2019-12-014711808181410.1080/21691401.2019.1610414Notoginsenoside R1 alleviates lipopolysaccharide-triggered PC-12 inflammatory damage via elevating microRNA-132Yuanliang Sun0Bing Liu1Xiujun Zheng2Dechun Wang3Department of Spine Surgery, The Affiliated Hospital of Qingdao University, Qingdao, ChinaDepartment of Critical Care Medicine, The Affiliated Hospital of Qingdao University, Qingdao, ChinaDepartment of Spine Surgery, The Affiliated Hospital of Qingdao University, Qingdao, ChinaDepartment of Spine Surgery, Qingdao Municipal Hospital, Qingdao, ChinaBackground Delayed inflammatory response is closely associated with the severity of Spinal cord injury (SCI). Herein, the function and molecular mechanism of notoginsenoside R1 (NGR1) in the in vitro model of SCI inflammation injury were explored.Methods PC-12 neuronal cells were subjected with LPS to construct a cell-based model of SCI inflammatory injury. NGR1 was applied in this cell model. miR-132 was silenced by transfection with miR-132 inhibitor. Cell viability and apoptosis were assessed, respectively. Then, the expression changes of pro-inflammatory cytokines and JNK pathway were examined.Results In this model, LPS was neurotoxic, with inhibiting PC-12 cell viability, inducing apoptosis, and enhancing concentrations of IL-6, IL-8 and TNF-α. However, NGR1 weakened the influence of LPS on PC-12 cells via elevating cell viability, decreasing apoptosis, decreasing pro-inflammatory cytokines expression, and suppressing activation of JNK signalling pathway. miR-132 was up-regulated by NGR1 treatment. Silence of miR-132 eliminated the influence of NGR1 on LPS-stimulated PC-12 cells.Conclusion NGR1 relieved PC-12 cells from LPS-triggered inflammatory damage via elevating miR-132 and hereafter suppressing JNK pathway.https://www.tandfonline.com/doi/10.1080/21691401.2019.1610414Notoginsenoside R1inflammation injuryspinal cord injury (SCI)lipopolysaccharideJNK pathway |
| spellingShingle | Yuanliang Sun Bing Liu Xiujun Zheng Dechun Wang Notoginsenoside R1 alleviates lipopolysaccharide-triggered PC-12 inflammatory damage via elevating microRNA-132 Artificial Cells, Nanomedicine, and Biotechnology Notoginsenoside R1 inflammation injury spinal cord injury (SCI) lipopolysaccharide JNK pathway |
| title | Notoginsenoside R1 alleviates lipopolysaccharide-triggered PC-12 inflammatory damage via elevating microRNA-132 |
| title_full | Notoginsenoside R1 alleviates lipopolysaccharide-triggered PC-12 inflammatory damage via elevating microRNA-132 |
| title_fullStr | Notoginsenoside R1 alleviates lipopolysaccharide-triggered PC-12 inflammatory damage via elevating microRNA-132 |
| title_full_unstemmed | Notoginsenoside R1 alleviates lipopolysaccharide-triggered PC-12 inflammatory damage via elevating microRNA-132 |
| title_short | Notoginsenoside R1 alleviates lipopolysaccharide-triggered PC-12 inflammatory damage via elevating microRNA-132 |
| title_sort | notoginsenoside r1 alleviates lipopolysaccharide triggered pc 12 inflammatory damage via elevating microrna 132 |
| topic | Notoginsenoside R1 inflammation injury spinal cord injury (SCI) lipopolysaccharide JNK pathway |
| url | https://www.tandfonline.com/doi/10.1080/21691401.2019.1610414 |
| work_keys_str_mv | AT yuanliangsun notoginsenosider1alleviateslipopolysaccharidetriggeredpc12inflammatorydamageviaelevatingmicrorna132 AT bingliu notoginsenosider1alleviateslipopolysaccharidetriggeredpc12inflammatorydamageviaelevatingmicrorna132 AT xiujunzheng notoginsenosider1alleviateslipopolysaccharidetriggeredpc12inflammatorydamageviaelevatingmicrorna132 AT dechunwang notoginsenosider1alleviateslipopolysaccharidetriggeredpc12inflammatorydamageviaelevatingmicrorna132 |