• ISSN 1674-8301
  • CN 32-1810/R
Volume 36 Issue 3
May  2022
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Min Shi, Xiangcheng Zhang, Ridong Zhang, Hong Zhang, Dalong Zhu, Xiao Han. Glycyrrhizic acid promotes sciatic nerves recovery in type 1 diabetic rats and protects Schwann cells from high glucose-induced cytotoxicity[J]. The Journal of Biomedical Research, 2022, 36(3): 181-194. doi: 10.7555/JBR.36.20210198
Citation: Min Shi, Xiangcheng Zhang, Ridong Zhang, Hong Zhang, Dalong Zhu, Xiao Han. Glycyrrhizic acid promotes sciatic nerves recovery in type 1 diabetic rats and protects Schwann cells from high glucose-induced cytotoxicity[J]. The Journal of Biomedical Research, 2022, 36(3): 181-194. doi: 10.7555/JBR.36.20210198

Glycyrrhizic acid promotes sciatic nerves recovery in type 1 diabetic rats and protects Schwann cells from high glucose-induced cytotoxicity

doi: 10.7555/JBR.36.20210198
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  • Corresponding author: Hong Zhang, Department of Endocrinology, the Affiliated Huai'an No. 1 People's Hospital of Nanjing Medical University, 6 West Beijing Road, Huai'an, Jiangsu 223300, China. Tel: +86-517-80872128, E-mail: zhh79318@163.com; Dalong Zhu, Department of Endocrinology, Nanjing Drum Tower Hospital Clinical College of Nanjing Medical University, 321 Zhongshan Road, Nanjing, Jiangsu 210008, China. Tel: +86-25-83304616, E-mail: zhudldr@gmail.com; Xiao Han, Key Laboratory of Human Functional Genomics of Jiangsu Province, Department of Biochemistry and Molecular Biology, Nanjing Medical University, 101 Longmian Avenue, Nanjing, Jiangsu 211166, China. Tel: +86-25-86869426, E-mail: hanxiao@njmu.edu.cn
  • Received: 2021-11-24
  • Revised: 2022-03-08
  • Accepted: 2022-03-16
  • Published: 2022-05-15
  • Issue Date: 2022-05-28
  • The present study aims to investigate the therapeutic effect and mechanism of glycyrrhizic acid (GA) in diabetic peripheral neuropathy (DPN). GA significantly mitigated nerve conduction velocity (NCV) deficit and morphological abnormality and reduced high-mobility group box-1 (HMGB1) expression in the sciatic nerves of diabetic rats independent of blood glucose and body weight. Notably, GA alleviated the increase of HMGB1 and the decrease of cell viability in high glucose-stimulated RSC96 cells. Furthermore, GA obviously reduced the concentration of inflammatory cytokines in the sciatic nerves of diabetic rats and supernatants of high glucose-exposed RSC96 cells, then restored the decreased expression levels of nerve growth factor (NGF) and neuritin-1, and the increased expression levels of cleaved caspase-3 and neuron-specific enolase. Additionally, GA markedly inhibited receptor for advanced glycation end products (RAGE) expression, p38MAPK phosphorylation, and the nuclear translocation of NF-κBp65 in diabetic rats and high glucose-exposed RSC96 cells. The promotional effect of high glucose in RSC96 cells was diminished following Hmgb1 siRNA treatment. Our findings indicate that GA may exert neuroprotection on DPN by suppressing HMGB1, which lead to extenuation of inflammation response, balance of NGF, neuritin-1 and caspase-3, as well as inactivation of RAGE/p38MAPK/NF-κBp65 signaling pathway.


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