Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Liquiritin alleviates spinal cord injury through suppression of in@258;ammation, oxidative stress, and cell apoptosis in a rat model

Yongsheng Luo¹ , Shihai Chen², Ting Li³, Yonglin Guan¹, Yongming Liu¹, Binxiang Ma¹

¹Department of Spine Orthopedics; ²Department of Pediatric Orthopaedics, Gansu provincial hospital of traditional Chinese medicine, Lanzhou City, Gansu Province 730050; ³Department of Hematology, Donggang Hospital, Lanzhou University First Hospital, Lanzhou City, Gansu Province 730000, China.

For correspondence:- Yongsheng Luo Email: YongshengLuosde@163.com Tel:+869312687916

Accepted: 24 July 2019 Published: 28 August 2019

Citation: Luo Y, Chen S, Li T, Guan Y, Liu Y, Ma B. Liquiritin alleviates spinal cord injury through suppression of in@258;ammation, oxidative stress, and cell apoptosis in a rat model. Trop J Pharm Res 2019; 18(8):1683-1589 doi: 10.4314/tjpr.v18i8.17

© 2019 The authors.
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Abstract

Purpose: Liquiritin is an extract from Glycyrrhiza Radix, one of the oldest traditional Chinese herbal medicines, which is commonly used to treat various injuries and swellings. This study is aimed to determine whether liquiritin can protect spinal cord injuries (SCIs) from secondary injuries.

Methods: A rat SCI model was established. After liquiritin treatment, the neural-function of Rats was determined by Basso, Beattie and Bresnahan (BBB) scores, paw withdrawal threshold (PWT), and thermal withdrawal latency (PWL). The effects of anti-inflammation, anti-oxidation, and anti-apoptosis of liquiritin were also examined in the rats with SCI. Moreover, the activities of several signaling elements, such as, inflammation-associated nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), toll-like receptor 4 (TLR4), proliferative-related p38 mitogen-activated protein kinases (MAPK) and myeloid differentiation primary response 88 (MyD88) which was involved in the TLR4 signaling, were used for further investigation of the underlying molecular mechanisms.

Results: Liquiritin improved locomotor function recovery, alleviated allodynia and hyperalgesia, and decreased water content of spinal cord in SCI rats. Also, liquiritin reduced SCI–induced inflammatory responses by decreasing the levels of tumor necrosis factor alpha (TNF-α), interleukin 1 beta (IL-1β), and IL-6. Liquiritin inhibited SCI–induced oxidative stress by decreasing malondialdehyde (MDA) level and increasing the levels of uperoxide dismutase (SOD) (p < 0.05), glutathione (GSH) (p < 0.01), and GSH-PX (p < 0.001). In addition, liquiritin alleviated spinal cord injury (SCI) –induced apoptosis of neural cells by decreasing the expression of cleaved caspase-9, -3 and cleaved poly ADP-ribose polymerase (PARP). Finally, liquiritin decreased spinal cord injury (SCI) -induced up-regulation of TLR4/MyD88/NFR09;-κB and p38 MAPK signaling cascades.

Conclusion: Liquiritin exerts protective role in SCI by reducing excessive inflammation, suppressing oxidative stress, and inhibiting neural cell apoptosis in a rat model of SCI. Thus, the agent can potentially be used for the management of SCI

Keywords: Liquiritin, Spinal cord injury (SCI), In@258;ammation, Oxidative stress, Apoptosis