Diphenyl diselenide alleviates diabetic peripheral neuropathy in rats with streptozotocin-induced diabetes by modulating oxidative stress

2020 ◽  
Vol 182 ◽  
pp. 114221
Author(s):  
Xing Wang ◽  
Yi Huan ◽  
Caina Li ◽  
Hui Cao ◽  
Sujuan Sun ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Peripheral Neuropathy ◽  
Diabetic Peripheral Neuropathy ◽  
Diphenyl Diselenide ◽  
Streptozotocin Induced Diabetes

scholarly journals Long Non-coding RNA XIST Attenuates Diabetic Peripheral Neuropathy by Inducing Autophagy Through MicroRNA-30d-5p/sirtuin1 Axis

2021 ◽  
Vol 8 ◽  
Author(s):  
Bei-Yan Liu ◽  
Lin Li ◽  
Li-Wei Bai ◽  
Chang-Shui Xu
Keyword(s):  
Oxidative Stress ◽  
Peripheral Neuropathy ◽  
Schwann Cells ◽  
Diabetic Peripheral Neuropathy ◽  
Beclin 1 ◽  
Diabetic Mice ◽  
Non Coding Rna ◽  
Non Coding Rnas ◽  
Long Non Coding Rna

Diabetic peripheral neuropathy (DPN) is a prevalent diabetes mellitus (Feldman et al., 2017) complication and the primary reason for amputation. Meanwhile, long non-coding RNAs (lncRNAs) are a type of regulatory non-coding RNAs (ncRNAs) that broadly participate in DPN development. However, the correlation of lncRNA X-inactive specific transcript (XIST) with DPN remains unclear. In this study, we were interested in the role of XIST in the modulation of DPN progression. Significantly, our data showed that the expression of XIST and sirtuin1 (SIRT1) was inhibited, and the expression of microRNA-30d-5p (miR-30d-5p) was enhanced in the trigeminal sensory neurons of the diabetic mice compared with the normal mice. The levels of LC3II and Beclin-1 were inhibited in the diabetic mice. The treatment of high glucose (HG) reduced the XIST expression in Schwann cells. The apoptosis of Schwann cells was enhanced in the HG-treated cells, but the overexpression of XIST could block the effect in the cells. Moreover, the levels of LC3II and Beclin-1 were reduced in the HG-treated Schwann cells, while the overexpression of XIST was able to reverse this effect. The HG treatment promoted the production of oxidative stress, while the XIST overexpression could attenuate this result in the Schwann cells. Mechanically, XIST was able to sponge miR-30d-5p and miR-30d-5p-targeted SIRT1 in the Schwann cells. MiR-30d-5p inhibited autophagy and promoted oxidative stress in the HG-treated Schwann cells, and SIRT1 presented a reversed effect. MiR-30d-5p mimic or SIRT1 depletion could reverse XIST overexpression-mediated apoptosis and autophagy of the Schwann cells. Thus, we concluded that XIST attenuated DPN by inducing autophagy through miR-30d-5p/SIRT1 axis. XIST and miR-30d-5p may be applied as the potential targets for DPN therapy.

scholarly journals TSH Combined with TSHR Aggravates Diabetic Peripheral Neuropathy by Promoting Oxidative Stress and Apoptosis in Schwann Cells

2021 ◽  
Vol 2021 ◽  
pp. 1-23
Author(s):  
Jingwen Fan ◽  
Qi Pan ◽  
Qun Gao ◽  
Wenqing Li ◽  
Fei Xiao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Peripheral Neuropathy ◽  
Diabetic Peripheral Neuropathy ◽  
Cell Model ◽  
Cell Damage ◽  
Motor Nerve ◽  
Thyroid Stimulating Hormone ◽  
Motor Nerve Conduction Velocity ◽  
The Impact

Subclinical hypothyroidism (SCH) is associated with diabetic peripheral neuropathy (DPN); however, the mechanism underlying this association remains unknown. This study is aimed at examining neurofunctional and histopathological alterations in a type 2 diabetes (T2DM) mouse model of SCH and investigating the impact of thyroid-stimulating hormone (TSH) in an in vitro DPN cell model established using RSC96 cells under high glucose (HG) and palmitic acid (PA) stimulation. Our results indicated that T2DM, in combination with SCH, aggravated abnormal glucose and lipid metabolism in T2DM and dramatically destroyed the peripheral nervous system by increasing paw withdrawal latency, decreasing motor nerve conduction velocity, and exacerbating ultrastructural deterioration of the damaged sciatic nerve caused by diabetes. Furthermore, the results of our in vitro experiments showed that TSH intensified HG/PA-induced RSC96 cell damage by inducing oxidative stress, mitochondrial dysfunction, and apoptosis. More importantly, TSHR knockout or inhibition of PA-induced TSHR palmitoylation could alleviate the apoptosis induced by TSH. Overall, in this study, the novel mechanisms by which TSH, as an independent risk factor for DPN progression, aggravating Schwann cell apoptosis and demyelination, are elucidated. These findings indicate that TSHR could be a potential target for both the prevention and treatment of DPN and, possibly, other microvascular diseases, and have implication in the clinical management of patients with DPN.

Protective effect of gliclazide on diabetic peripheral neuropathy through Drp-1 mediated-oxidative stress and apoptosis

2012 ◽  
Vol 523 (1) ◽  
pp. 45-49 ◽  
Author(s):  
Yuan-bo Wu ◽  
Li-li Shi ◽  
Yuan-jie Wu ◽  
Wen-hua Xu ◽  
Li Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Peripheral Neuropathy ◽  
Protective Effect ◽  
Diabetic Peripheral Neuropathy

scholarly journals DW14006 as a direct AMPKα activator ameliorates diabetic peripheral neuropathy in mice

2020 ◽  
Author(s):  
Ada Admin ◽  
Xu Xu ◽  
Wei Wang ◽  
Zhengyu Wang ◽  
Jianlu Lv ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Peripheral Neuropathy ◽  
Diabetic Peripheral Neuropathy ◽  
Diabetic Mice ◽  
Adeno Associated Virus ◽  
Multiple Risk Factors ◽  
Underlying Mechanisms ◽  
Amp Activated Protein Kinase

<a>Diabetic peripheral neuropathy</a> (DPN) is a long-term complication of diabetes with a complicated pathogenesis. <a></a><a>AMP-activated protein kinase (</a><a></a><a>AMPK) </a>senses oxidative stress <a></a><a>and </a><a>mitochondrial function</a> playing a central role in the regulation of DPN. Here, we reported that DW14006 <a></a><a></a><a></a><a>(</a><a>2-(3-(7-chloro-6-(2'-hydroxy-[1,1'-biphenyl]-4-yl)-2-oxo-1,2-dihydroquinolin-3-yl)phenyl)acetic acid)</a> as a direct AMPKα activator efficiently ameliorated <a>DPN in both</a><a> streptozotocin</a> (STZ)-induced type 1 and BKS <i>db/<a></a><a></a><a>db</a></i> type 2 diabetic mice. <a></a><a></a><a>DW14006 administration highly enhanced neurite outgrowth of dorsal root </a><a>ganglion</a> (DRG) neuron and <a></a><a>improved neurological function</a> in diabetic mice. <a></a><a></a><a>The underlying mechanisms have been intensively investigated. DW14006 treatment improved mitochondrial </a><a></a><a>bioenergetics</a> profiles and <a></a><a>restrained </a>oxidative stress and inflammation in <a>diabetic mice</a> by targeting AMPKa, which has been verified by assay against the STZ-induced diabetic mice injected with <a></a><a>adeno associated virus AAV</a>8-AMPKa-RNAi. <a></a>To our knowledge, our work might be the first report on the amelioration of direct AMPKa activator on DPN by counteracting <a>multiple risk factors</a> including <a>mitochondrial dysfunction, oxidative stress and inflammation</a>, and DW14006 has been highlighted as a potential leading compound in the treatment of DPN.

scholarly journals Epalrestat protects against diabetic peripheral neuropathy by alleviating oxidative stress and inhibiting polyol pathway

2016 ◽  
Vol 11 (2) ◽  
pp. 345 ◽  
Author(s):  
Hong-ying Yang ◽  
Qing-rong Li ◽  
Zhuo Wang ◽  
Wei Zhou ◽  
Shou-rui Fan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Peripheral Neuropathy ◽  
Diabetic Peripheral Neuropathy ◽  
Polyol Pathway
Sign in / Sign up

Export Citation Format

Share Document