Effects of vitamin D administration on nociception and spinal cord pro-oxidant and antioxidant markers in a rat model of neuropathic pain

Santos, Marí Castro; Silva, T.C.B. da; Silva, F.B.O. da; Siebert, Cassiana; Kroth, Adarly; Silveira, Elza Maria Santos da; Wyse, Ângela T. S.; Partata, Wania Aparecida

doi:10.1590/1414-431x2021e11207

Cited by 9 publications

(5 citation statements)

References 37 publications

(91 reference statements)

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“…To detect the potential molecular pathways that was involved in the pathogenesis of PN, we applied a well-recognized IoN-CCI rat model as our in vivo investigation target. IoN-CCI rats underwent a mechanical injury will automatically develop a symptom of spontaneous neuropathic pain and accumulation of ROS in neuron tissue, as indicated by previous studies [32,33] . To determine the status of IoN-CCI rats in our experiment, we performed the Von Frey test to quantify the extent of neuropathic pain in rats.…”

Section: Post-translational Modification But Not Gene Expression Of R...mentioning

confidence: 72%

Accumulation of RIPK1 into mitochondria is requisite for oxidative stress-mediated necroptosis and proliferation in Rat Schwann cells

Wang¹,

Fu²,

Chai³

et al. 2022

Int. J. Med. Sci.

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The injury of Schwann cells is an important pathological feature of peripheral neuropathy. However, the explicit molecular mechanism and blocking method remains to be explored. In this study, we identified an pivotal executor of necroptosis-RIPK1, performed an unique function in response to oxidative stress-induced injury in Rat Schwann cells. We found that after oxidative stress-simulation by H2O2, RIPK1 was activated independent of genetic up-regulation, but through the post-translational modification, including its protein levels, phosphorylation of Serine 166 and Serine 321 sites and its general ubiquitination levels. Under a confocal microscopy, we found that RIPK1 was significantly accumulated into the mitochondria. And the phosphorylation, ubiquitination levels were also elevated in mitochondrial RIPK1, as indicated by immunoprecipitation. Through the administration of N-Acetyl-L-cysteine (NAC), a ROS inhibitor, we found that the phosphorylation, ubiquitination and mitochondrial location of RIPK1 was significantly suppressed. While administration of Necrostatin-1 (Nec-1) failed to influence the levels of ROS and mitochondrial membrane potential, revealing that RIPK1 served as the down-stream regulators of ROS. Lastly, pharmacological inhibition of RIPK1 by Nec-1 attenuated the levels of necroptosis, increased proliferation, as indicated by Annexin V/PI evaluation, CCK-8 detection, TEM scanning and EdU staining. Our results indicate a previous un-recognized post-translational change of RIPK1 in response to oxidative stress in Schwann cells.

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Section: Post-translational Modification But Not Gene Expression Of R...mentioning

confidence: 72%

Accumulation of RIPK1 into mitochondria is requisite for oxidative stress-mediated necroptosis and proliferation in Rat Schwann cells

Wang¹,

Fu²,

Chai³

et al. 2022

Int. J. Med. Sci.

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“…Herein, we observed elevated ROS and MDA levels, as well as reduced GSH and SOD levels, in the β-cells of T2DM mice in comparison with healthy mice, suggesting that OS was induced in T2DM. Serval animal studies have reported the anti-OS function of vitamin D 52 53 54 . Similar to previous findings 14 , the present study demonstrated inhibition of OS after 1,25(OH) 2 D 3 treatment in the β-cells of T2DM mice.…”

Section: Discussionmentioning

confidence: 99%

Vitamin D Alleviates Type 2 Diabetes Mellitus by Mitigating Oxidative Stress-Induced Pancreatic β-Cell Impairment

Liu,

Zhang,

Shi

et al. 2023

Exp Clin Endocrinol Diabetes

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Objective Type 2 diabetes mellitus (T2DM) is a common metabolic disorder with rising incidence worldwide. This study explored the anti-T2DM role of vitamin D, thereby providing novel therapeutic strategies. Methods C57BL/6 J mice and MIN6 cells were used to induce in vivo T2DM and damaged β-cell models, respectively. Body weights, fasting blood glucose, and fasting insulin were measured in mice. Oral glucose tolerance test (OGTT) and insulin tolerance test (ITT) were conducted on mice. Lipid indices (TG, TC, LDL-C, and HDL-C) were detected in mouse serum. Hematoxylin-eosin staining was used to evaluate pancreatic tissue injury. ELISA was used to assess insulin and oxidative stress (OS) markers (MDA, GSH, and SOD) in mice and MIN6 cells. Production of ROS was detected in islet β-cells and MIN6 cells. Cell viability and apoptosis were evaluated using CCK-8 and flow cytometry, respectively. QRT-PCR and western blotting were used to detect pro-inflammatory factors (TNF-α and IL-6) and endoplasmic reticulum stress (ERS) markers (CHOP and GRP78), respectively. Results Vitamin D reduced body weights, fasting blood glucose, and insulin and ameliorated glucose tolerance and insulin sensitivity in T2DM mice. Besides, vitamin D decreased serum TG, TC, LDL-C, and increased HDL-C in T2DM mice. Vitamin D inhibited pancreatic histopathological injury, cell apoptosis, OS, and β-cell decline in T2DM mice. Moreover, vitamin D alleviated cell death, insufficient insulin secretion, inflammation, OS, and ERS in damaged MIN6 cells. Notably, N-acetyl-L-cysteine (an OS inhibitor) enhanced these effects of vitamin D. Conclusions Vitamin D relieved T2DM symptoms by alleviating OS-induced β-cell impairment.

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“…[27] Deney hayvanları üzerinde yapılan bir çalışmada, D vitamininin omurilikteki prooksidan ve antioksidanları modüle ederek antinosisepsiyona neden olabileceği bildirilmiştir. [28] Bununla birlikte D vitamini-nöropatik ağrı ilişkisini açığa çıkarmaya yönelik çalışmalar çoğunlukla diyabetik nöropati ile ilgilidir. Bu çalışmalardan birinde, Anju ve ark.…”

Section: Discussionunclassified

Investigation of neuropathic pain in women with low vitamin D levels

Çırakoğlu¹

2022

bogazicitip

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Objectives: Besides the known metabolic effects of vitamin D, its role in modulation of pain is controversial. In our study, we aimed to investigate the possible relationship between demographic data and some biochemical values of blood who has in female patients with low vitamin D levels and neuropathic pain. Methods:The data of the patients who applied to the Physical Medicine and Rehabilitation Polyclinic between January 2017 and January 2018 were evaluated retrospectively. Seventy-nine female patients with low vitamin D levels who met the inclusion criteria were included in the study. The painDETECT pain questionnaire was used to evaluate the presence of neuropathic pain. According to this questionnaire, the patients were divided into three groups as no neuropathic pain, suspicious, and present.Results: Neuropathic pain component was detected by the painDETECT questionnaire in 15 (19%) of the female patients with low vitamin D levels. There was no statistically significant difference between neuropathic pain groups and age, education levels, number of births, body mass index as well as plasma values of vitamin D, alkaline phosphatase, parathyroid hormone, and calcium in female patients with low vitamin D levels. Conclusion:In this retrospective study, we observed similar biochemical data in patients with different degrees of neuropathic pain and low vitamin D levels. We think that it can be prospectively investigated whether vitamin D supplementation will make a difference in treatment the patients with low vitamin D levels and neuropathic pain.

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Effects of vitamin D administration on nociception and spinal cord pro-oxidant and antioxidant markers in a rat model of neuropathic pain

Cited by 9 publications

References 37 publications

Accumulation of RIPK1 into mitochondria is requisite for oxidative stress-mediated necroptosis and proliferation in Rat Schwann cells

Accumulation of RIPK1 into mitochondria is requisite for oxidative stress-mediated necroptosis and proliferation in Rat Schwann cells

Vitamin D Alleviates Type 2 Diabetes Mellitus by Mitigating Oxidative Stress-Induced Pancreatic β-Cell Impairment

Investigation of neuropathic pain in women with low vitamin D levels

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