Oxidative Stress in Diabetic Peripheral Neuropathy: Pathway and Mechanism-Based Treatment

Lin, Qingxia; Li, Kezheng; Chen, Yinuo; Xie, Jin; Wu, Chunxue; Cui, Can; Deng, Binbin

doi:10.1007/s12035-023-03342-7

Cited by 15 publications

(11 citation statements)

References 160 publications

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“…OS plays a pivotal role in the pathogenesis of numerous neurological and psychiatric disorders. It seems to be a consensus that OS has been implicated in the pathogenesis of multiple disease states and may be a common pathogenic mechanism of many major psychiatric disorders [ 101 ], including AD [ 99 , 102 , 103 , 104 , 105 ], depression [ 101 , 103 , 106 , 107 , 108 ], ALS [ 109 , 110 , 111 , 112 , 113 ], peripheral nervous system diseases [ 114 , 115 , 116 ], etc. ROS attack proteins, oxidize the backbone and side chains, and then react with amino acid side chains to form carbonyl functional groups.…”

Section: Resultsmentioning

confidence: 99%

L-Carnitine in the Treatment of Psychiatric and Neurological Manifestations: A Systematic Review

Wang,

Pan,

Liu

et al. 2024

Nutrients

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L-carnitine (LC), a vital nutritional supplement, plays a crucial role in myocardial health and exhibits significant cardioprotective effects. LC, being the principal constituent of clinical-grade supplements, finds extensive application in the recovery and treatment of diverse cardiovascular and cerebrovascular disorders. However, controversies persist regarding the utilization of LC in nervous system diseases, with varying effects observed across numerous mental and neurological disorders. This article primarily aims to gather and analyze database information to comprehensively summarize the therapeutic potential of LC in patients suffering from nervous system diseases while providing valuable references for further research. Methods: A comprehensive search was conducted in PubMed, Web Of Science, Embase, Ovid Medline, Cochrane Library and Clinicaltrials.gov databases. The literature pertaining to the impact of LC supplementation on neurological or psychiatric disorders in patients was reviewed up until November 2023. No language or temporal restrictions were imposed on the search. Results: A total of 1479 articles were retrieved, and after the removal of duplicates through both automated and manual exclusion processes, 962 articles remained. Subsequently, a meticulous re-screening led to the identification of 60 relevant articles. Among these, there were 12 publications focusing on hepatic encephalopathy (HE), while neurodegenerative diseases (NDs) and peripheral nervous system diseases (PNSDs) were represented by 9 and 6 articles, respectively. Additionally, stroke was addressed in five publications, whereas Raynaud’s syndrome (RS) and cognitive disorder (CD) each had three dedicated studies. Furthermore, migraine, depression, and amyotrophic lateral sclerosis (ALS) each accounted for two publications. Lastly, one article was found for other symptoms under investigation. Conclusion: In summary, LC has demonstrated favorable therapeutic effects in the management of HE, Alzheimer’s disease (AD), carpal tunnel syndrome (CTS), CD, migraine, neurofibromatosis (NF), PNSDs, RS, and stroke. However, its efficacy appears to be relatively limited in conditions such as ALS, ataxia, attention deficit hyperactivity disorder (ADHD), depression, chronic fatigue syndrome (CFS), Down syndrome (DS), and sciatica.

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Section: Resultsmentioning

confidence: 99%

L-Carnitine in the Treatment of Psychiatric and Neurological Manifestations: A Systematic Review

Wang,

Pan,

Liu

et al. 2024

Nutrients

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“…Oxidative damage promotes nerve structural changes, such as axonal degeneration, segmental demyelination, and apoptosis of Schwann cells, leading to the subsequent damage and/or loss of myelinated and unmyelinated fibers in DPN. Oxidative stress could lead to the activation of the NF-κB pathway, and activation of the NF-κB inflammatory response attenuates Nrf2antioxidant signaling, which could also in turn aggravate oxidative stress [12]. Additionally, our past studies have found that inhibition of TNF-α restores nerve injury, including improvement of NCV, reduction of nerve fiber demyelination, lamellar and axonal structural disturbances, and increase of MBP expression in neural tissues [47].…”

Section: Discussionmentioning

confidence: 99%

“…Many experimental and clinical studies have indicated that the underlying pathogenic mechanisms of DPN are inflammation and oxidative stressinduced sciatic nerve damage [9]. The accumulation of free radicals and reduced activity of antioxidant enzymes cause redox imbalance, which promotes oxidative damage in DPN [10][11][12]. Treatment of DPN rats with antioxidants has been found to slow the decrease in nerve conduction velocity [13].…”

Section: Diabetic Peripheral Neuropathy (Dpn)mentioning

confidence: 99%

Protective effect of alirocumab, a PCSK9 inhibitor, on the sciatic nerve of rats with diabetic peripheral neuropathy

Cui,

Feng,

Wang

et al. 2024

Endocr J

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Dyslipidemia has been considered a risk factor for diabetic peripheral neuropathy. Proprotein convertase subtilisinlike/Kexin 9 inhibitor (PCSK9) inhibitors are a new type of lipid-lowering drug currently in clinical use. The role of PCSK9 in diabetic peripheral neuropathy is still unclear. In this study, the effect of alirocumab, a PCSK9 inhibitor, on the sciatic nerve in rats with diabetic peripheral neuropathy and its underlying mechanisms were investigated. The diabetic peripheral neuropathy rat model was established by using a high-fat diet combined with streptozotocin injection, and experimental subjects were divided into normal, diabetic peripheral neuropathy, and alirocumab groups. The results showed that Alirocumab improved nerve conduction, morphological changes, and small fiber deficits in rats with DPN, possibly related to its amelioration of oxidative stress and the inflammatory response.

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“…Metabolic disturbances, oxidative stress, endothelial dysfunction, dysregulation of neurotrophic factors, activation of the polyol pathway and accumulation of advanced glycosylation products (AGEs) have all been reported to be closely related to the development of DPN [25][26][27]. Overproduction of reactive oxygen species (ROS) in mitochondria and cytoplasm combined with the deregulation of antioxidant defense systems, causes oxidative stress [28].…”

Section: Discussionmentioning

confidence: 99%

Hydrogen sulfide alleviates neural degeneration in streptozotocin-induced diabetic rats probably through reducing oxidative stress and aldose reductase expression

Shen#,

Hu#,

Zhang

et al. 2024

Preprint

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Background Diabetic peripheral neuropathy(DPN) is one of the most common complications of diabetes. In this study, we investigated the potential role of H2S as a novel therapy for DPN in diabetic rats. Method All the rats were divided into non-diabetic control group(n = 10), diabetic control group (n = 10) and H2S treated diabetic group (n = 10). A single dose of streptozotocin (60mg/kg) was applied to the rats for the diabetic models. Sodium bisulfide (50µmol/kg/d) was intraperitoneally injected daily for 2 weeks as H2S treatment. Biochemical assay, electromyogram, hematoxylin eosin (HE) staining, transmission electron microscopy, western blot and enzyme linked immunosorbent assay (ELISA) were then performed. Results H2S treatment did not affect the body weight, blood glucose levels or liver and kidney function in diabetic rats. Cell atrophy and axon degeneration of sciatic nerve and dorsal root ganglion (DRG) in diabetic rats were relieved after H2S treatment through observation of light microscopy and transmission electron microscopy. Furthermore, superoxide dismutase levels in serum and superoxide dismutase2 in sciatic nerve of diabetic rats were lower than non-diabetic rats, but restored obviously after H2S treatment. Serum and sciatic nerve homogenate malondialdehyde and aldose reductase expression were obviously higher in diabetic rats, but decreased significantly after H2S treatment. Finally, the sciatic nerve conduction velocity of diabetic rats improved after H2S treatment compared with diabetic control group, however without statistical significance. Conclusions Our study revealed that H2S alleviates neural degeneration in diabetic rats probably through reducing oxidative stress and downregulating aldose reductase expression.

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Oxidative Stress in Diabetic Peripheral Neuropathy: Pathway and Mechanism-Based Treatment

Cited by 15 publications

References 160 publications

L-Carnitine in the Treatment of Psychiatric and Neurological Manifestations: A Systematic Review

L-Carnitine in the Treatment of Psychiatric and Neurological Manifestations: A Systematic Review

Protective effect of alirocumab, a PCSK9 inhibitor, on the sciatic nerve of rats with diabetic peripheral neuropathy

Hydrogen sulfide alleviates neural degeneration in streptozotocin-induced diabetic rats probably through reducing oxidative stress and aldose reductase expression

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