Effect of Shikonin on Spinal Cord Injury in Rats Via Regulation of HMGB1/TLR4/NF-kB Signaling Pathway
Background/Aims: Shikonin, a compound extracted from Zicao, has been demonstrated to hold anti-bacterial, anti-inflammatory, and anti-tumor activities in various diseases and it has been shown to protect human organs from injuries. However, the effect of shikonin on the recovery of spinal cord injur...
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Cell Physiol Biochem Press GmbH & Co KG
2017-09-01
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Series: | Cellular Physiology and Biochemistry |
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Online Access: | http://www.karger.com/Article/FullText/480474 |
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author | Yihui Bi Yapeng Zhu Mingkai Zhang Keke Zhang Xingyi Hua Zheng Fang Jian Zhou Wenjie Dai Yixing Cui Jun Li Tao You |
author_facet | Yihui Bi Yapeng Zhu Mingkai Zhang Keke Zhang Xingyi Hua Zheng Fang Jian Zhou Wenjie Dai Yixing Cui Jun Li Tao You |
author_sort | Yihui Bi |
collection | DOAJ |
description | Background/Aims: Shikonin, a compound extracted from Zicao, has been demonstrated to hold anti-bacterial, anti-inflammatory, and anti-tumor activities in various diseases and it has been shown to protect human organs from injuries. However, the effect of shikonin on the recovery of spinal cord injury (SCI) remains unknown. This study was designed to estimate the potential therapeutic effect and underlying mechanism of shikonin on SCI in vivo. Methods: In the study, we used HE staining, ELISA assay, transfection assay, TUNEL assay, real time PCR and Western blot to detect the effects of shikonin on spinal cord injury in rats. Results: we showed that shikonin could promote the recovery of motor function and tissue repair after SCI treatment in rats SCI model. Moreover, we demonstrated that shikonin inhibited the spinal cord edema in SCI model of rats. According to further investigation, shikonin induced the reduction of inflammatory response through decreasing the expression levels of HMGB1, TLR4 and NF-κB after SCI injury. In addition, we also found that shikonin could suppress the apoptosis and expression of caspase-3 protein in SCI model of rats. Conclusion: Our results demonstrated that shikonin induced the recovery of tissue repair and motor function via inactivation of HMGB1/TLR4/NF-κB signaling pathway in SCI model of rats. Meanwhile, shikonin regulated the inflammation response in SCI by suppressing the HMGB1/TLR4/NF-κB signaling pathway. The described mechanism sheds novel light on molecular signaling pathway in spinal cord injury and secondary injury including inflammatory response. |
first_indexed | 2024-04-13T21:32:42Z |
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id | doaj.art-bcebf2bdb9504c8086a4ebd6889980da |
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issn | 1015-8987 1421-9778 |
language | English |
last_indexed | 2024-04-13T21:32:42Z |
publishDate | 2017-09-01 |
publisher | Cell Physiol Biochem Press GmbH & Co KG |
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series | Cellular Physiology and Biochemistry |
spelling | doaj.art-bcebf2bdb9504c8086a4ebd6889980da2022-12-22T02:29:06ZengCell Physiol Biochem Press GmbH & Co KGCellular Physiology and Biochemistry1015-89871421-97782017-09-0143248149110.1159/000480474480474Effect of Shikonin on Spinal Cord Injury in Rats Via Regulation of HMGB1/TLR4/NF-kB Signaling PathwayYihui BiYapeng ZhuMingkai ZhangKeke ZhangXingyi HuaZheng FangJian ZhouWenjie DaiYixing CuiJun LiTao YouBackground/Aims: Shikonin, a compound extracted from Zicao, has been demonstrated to hold anti-bacterial, anti-inflammatory, and anti-tumor activities in various diseases and it has been shown to protect human organs from injuries. However, the effect of shikonin on the recovery of spinal cord injury (SCI) remains unknown. This study was designed to estimate the potential therapeutic effect and underlying mechanism of shikonin on SCI in vivo. Methods: In the study, we used HE staining, ELISA assay, transfection assay, TUNEL assay, real time PCR and Western blot to detect the effects of shikonin on spinal cord injury in rats. Results: we showed that shikonin could promote the recovery of motor function and tissue repair after SCI treatment in rats SCI model. Moreover, we demonstrated that shikonin inhibited the spinal cord edema in SCI model of rats. According to further investigation, shikonin induced the reduction of inflammatory response through decreasing the expression levels of HMGB1, TLR4 and NF-κB after SCI injury. In addition, we also found that shikonin could suppress the apoptosis and expression of caspase-3 protein in SCI model of rats. Conclusion: Our results demonstrated that shikonin induced the recovery of tissue repair and motor function via inactivation of HMGB1/TLR4/NF-κB signaling pathway in SCI model of rats. Meanwhile, shikonin regulated the inflammation response in SCI by suppressing the HMGB1/TLR4/NF-κB signaling pathway. The described mechanism sheds novel light on molecular signaling pathway in spinal cord injury and secondary injury including inflammatory response.http://www.karger.com/Article/FullText/480474ShikoninSCIInflammation responseApoptosisHMGB1/TLR4/NF-κB signaling pathway |
spellingShingle | Yihui Bi Yapeng Zhu Mingkai Zhang Keke Zhang Xingyi Hua Zheng Fang Jian Zhou Wenjie Dai Yixing Cui Jun Li Tao You Effect of Shikonin on Spinal Cord Injury in Rats Via Regulation of HMGB1/TLR4/NF-kB Signaling Pathway Cellular Physiology and Biochemistry Shikonin SCI Inflammation response Apoptosis HMGB1/TLR4/NF-κB signaling pathway |
title | Effect of Shikonin on Spinal Cord Injury in Rats Via Regulation of HMGB1/TLR4/NF-kB Signaling Pathway |
title_full | Effect of Shikonin on Spinal Cord Injury in Rats Via Regulation of HMGB1/TLR4/NF-kB Signaling Pathway |
title_fullStr | Effect of Shikonin on Spinal Cord Injury in Rats Via Regulation of HMGB1/TLR4/NF-kB Signaling Pathway |
title_full_unstemmed | Effect of Shikonin on Spinal Cord Injury in Rats Via Regulation of HMGB1/TLR4/NF-kB Signaling Pathway |
title_short | Effect of Shikonin on Spinal Cord Injury in Rats Via Regulation of HMGB1/TLR4/NF-kB Signaling Pathway |
title_sort | effect of shikonin on spinal cord injury in rats via regulation of hmgb1 tlr4 nf kb signaling pathway |
topic | Shikonin SCI Inflammation response Apoptosis HMGB1/TLR4/NF-κB signaling pathway |
url | http://www.karger.com/Article/FullText/480474 |
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