Ethanol Extracts from Toona sinensis Seeds Alleviates Diabetic Peripheral Neuropathy through Inhibiting Oxidative Stress and Regulating Growth Factor

Background: Diabetic Peripheral neuropathy (DPN) is a common complication of diabetes mellitus. Recentstudies have demonstrated the involvement of Nerve growth factor (NGF) in the occurrence of DPN. TheDiabetes Mellitus was caused reduced the number and disruption of the function of the NGF. External MuscleStimulation (EMS) might be induced the NGF synthesis. The study objective has to found the effect of EMSon the NGF.Methods: Study design was before and after treatment without control on subjects with DPN. The bloodsample was taken before and after an intervention, as well as the Diabetic Neuropathy symptom (DNSym) andscore (DNSc). The EMS treated all of the participants within three times a week for four weeks.Results: There were 35 subjects were participated. Paired t-test showed a significant increase in NGF serumlevels and decrease both DNSym and DNSc with the difference value 12.64 ± 16.09 (p=0.000), 1.23 ± 0.82(p=0.000), 1.20 ± 0.85 (p=0.000). There was a significant negative correlation between NGF serum level withthe DNS- INA (r= -0.56; p=0.001) and the DNE-INA (r= -0.48; p=0.007).Conclusion: EMS treatment can increase serum NGF level. EMS has a strong correlation with a decrease inthe value of the DNS-INA and DNE-INA.Keywords: Diabetic Peripheral neuropathy, External Muscle Stimulation, Nerve Growth Factor.

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

Frontiers in Molecular Biosciences ◽

10.3389/fmolb.2021.655157 ◽

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.

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Molecular Basis of Diabetic Peripheral Neuropathy: Role of Oxidative Stress

International Physiology ◽

10.21088/ip.2347.1506.3215.9 ◽

2015 ◽

Vol 3 (2) ◽

pp. 123-124

Author(s):

Nisha Rani Jamwal ◽

◽

Senthil P Kumar. ◽

Keyword(s):

Oxidative Stress ◽

Peripheral Neuropathy ◽

Diabetic Peripheral Neuropathy ◽

Molecular Basis

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

Biochemical Pharmacology ◽

10.1016/j.bcp.2020.114221 ◽

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

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

Oxidative Medicine and Cellular Longevity ◽

10.1155/2021/2482453 ◽

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.

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