Exp Clin Endocrinol Diabetes 2020; 128(01): 59-65
DOI: 10.1055/a-0919-4614
Article
© Georg Thieme Verlag KG Stuttgart · New York

Tanshinone II A Affects Diabetic Peripheral Neuropathic Pain via Spinal Dorsal Horn Neuronal Circuitry by Modulating Endoplasmic Reticulum Stress Pathways

Dawei Kong
1  Department of Neurosurgery, Peking University, China-Japan Friendship School of Clinical Medicine, Beijing, China
,
Zhuangli Guo
2  Department of Rehabilitation, The Affiliated Hospital of Qingdao University, Qingdao, China
,
Wenqiang Yang
1  Department of Neurosurgery, Peking University, China-Japan Friendship School of Clinical Medicine, Beijing, China
,
Qi Wang
1  Department of Neurosurgery, Peking University, China-Japan Friendship School of Clinical Medicine, Beijing, China
,
Yanbing Yu
1  Department of Neurosurgery, Peking University, China-Japan Friendship School of Clinical Medicine, Beijing, China
,
Li Zhang
1  Department of Neurosurgery, Peking University, China-Japan Friendship School of Clinical Medicine, Beijing, China
› Author Affiliations
Acknowledgements: This work was financed by the National Natural Science Foundation of China (No. 81673793, 81373796, 81173424).
Further Information

Publication History

received 10 April 2019
revised 10 April 2019

accepted 14 May 2019

Publication Date:
11 July 2019 (online)

Abstract

Diabetic peripheral neuropathic pain (DPNP) is a common manifestation of diabetic peripheral neuropathy (DPN). Although the pathogenesis of DPNP remains unclear, the disinhibition of spinal dorsal horn neuronal circuitry mediated by endoplasmic reticulum stress (ERS) is an important mechanism underlying neuropathic pain (NP). Tanshinone II A is mainly used to treat cardiovascular diseases but has also been shown to relieve various types of neuralgia, including DPNP. This study investigated the effects of tanshinone II A in DPNP model rats. We divided animals into two groups: 1) the model (diabetic) group and 2) the tanshinone II A-treatment group. Our results demonstrated that diabetic rats exhibited a decrease in the mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL), and that NMT is increased and TWL is prolonged in rats treated with tanshinone II A. Additionally, the levels of ERS-signaling pathway factors in the spinal dorsal horns of rats were lower in the tanshinone II A-treated group than in the diabetic group. Overall, our study demonstrated that the disinhibition of spinal dorsal horn neuronal circuitry mediated by endoplasmic reticulum stress underlies DPNP and is modulated by tanshinone II A treatment.