Curcumin Attenuates Diabetic Neuropathic Pain by Downregulating TNF-α in a Rat Model

Li, Yue; Zhang, Yong; Liu, Debao; Liu, Haiying; Hou, Wugang; Dong, Yushu

doi:10.7150/ijms.5224

Cited by 73 publications

(51 citation statements)

References 22 publications

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“…As generally accepted, rats with fasting plasma glucose levels exceeding 300 mg/dL were considered diabetic while ranging from 90 to 130 mg/dL were considered normal [21]. As shown in Fig.…”

Section: Fasting Blood Glucose and Cardiac Function Evaluationsmentioning

confidence: 99%

Protein kinase RNA-like endoplasmic reticulum kinase (PERK)/calcineurin signaling is a novel pathway regulating intracellular calcium accumulation which might be involved in ventricular arrhythmias in diabetic cardiomyopathy

Liu

Cai

Zhu

et al. 2014

Cellular Signalling

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Section: Fasting Blood Glucose and Cardiac Function Evaluationsmentioning

confidence: 99%

Protein kinase RNA-like endoplasmic reticulum kinase (PERK)/calcineurin signaling is a novel pathway regulating intracellular calcium accumulation which might be involved in ventricular arrhythmias in diabetic cardiomyopathy

Liu

Cai

Zhu

et al. 2014

Cellular Signalling

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“…Activation of Schwann cells in turn promotes their secretion of proinflammatory cytokines, thereby producing a positive feedback mechanism that perpetuates injury 109,110 . Inflammatory cytokines such as IL-1, tumour necrosis factor (TNF) and IL-17 can be produced by many cell types, including Schwann cells, and these factors sensitize Aδ-fibres and C-fibres, triggering neuropathic pain [111][112][113] . Indeed, blocking the TNF signalling pathway with a recombinant human TNF receptorantibody fusion protein has been shown to be beneficial in animal models of diabetic neuro pathy, leading to recovery of nerve conduction velocity and increased expression of myelin basic protein 109 .…”

Section: Box 3 | Satellite Glial Cellsmentioning

confidence: 99%

Schwann cell interactions with axons and microvessels in diabetic neuropathy

et al. 2017

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The incidence of diabetes mellitus has increased dramatically over the past two to three decades. According to the International Diabetes Federation Diabetes Atlas, 415 million people worldwide had diabetes in 2015, and this number is expected to grow by 5% annually, predominantly as a result of increasing prevalence of type 2 diabetes. Furthermore, an estimated 100 million Europeans and 80 million Americans have impaired glucose tolerance or prediabetes. Few people die from acute diabetes in countries with comprehensive health care systems, but the disease is inflicting a huge medical, social and economic burden on society owing to the need for lifelong treatment of its systemic consequences and the insidious development of multi-organ damage.Peripheral neuropathy (BOXES 1,2) is a common but often neglected complication of long-term diabetes, and the lack of treatment options reflects an incomplete understanding of the pathogenic mechanisms. Hyperglycaemia is generally accepted as the primary pathogenic insult in type 1 and type 2 diabetic neuropathy, although roles are emerging for other factors, such as impaired insulin signalling, hypertension and dyslipidaemia (particularly for type 2 diabetes), which might precede overt hyperglycaemia 1 . Many preclinical studies, and occasional clinical studies, have indicated that diabetic neuropathy -like diabetic nephropathy and retinopathy -results from microvascular disease, with a focus on axonal degeneration as a consequence of ischaemia and/or hypoxia. This mechanism, however, is likely to be only one aspect of a more complex pathogenesis.The earliest descriptions of pathology in diabetic neuropathy indicated that Schwannopathy accompanied axonal degeneration. The majority of clinical and basic research in diabetic neuropathy since then has focused on the effects on neurons. However, accumulating data from research into the development and regeneration of the PNS has identified Schwann cells as equally indispensable components that maintain neuronal structure and function, nourish axons, and promote survival and growth upon injury. The early reports from 1979 that demonstrated morphological changes in Schwann cells in human diabetic neuropathy 2 are now supported by an increased awareness of molecular alterations in Schwann cells during diabetes 3 . Schwann cells express a wide range of receptors and, when they sense insults or danger signals, they upregulate synthesis and secretion of factors that stimulate neuroprotection, regrowth and remyelination, or factors that aggravate disease phenotypes 4 . The most recent studies have demonstrated that Schwann cells regulate many aspects of axonal function, so that disruption of their metabolism by diabetes results in the accumulation of neurotoxic intermediates and compromises production of neuronal support factors, contributing to axonal degeneration, endothelial dysfunction and diabetic neuropathy. Abstract | The prevalence of diabetes worldwide is at pandemic levels, with the number of patients increasing by 5% annu...

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“…After some phenotypic changes, they release various proinflammatory cytokines, including interleukin 1β (IL-1β) and tumour necrosis factor α (TNF-α), which have been implicated directly in the induction of neuropathic pain (26). In confirmation of these theories, some proinflammatory cytokines are expressed in the dorsal horn of the spinal cord which is thought to contribute to the pathogenesis of diabetic neuropathic pain (11).…”

Section: Discussionmentioning

confidence: 69%

“…Diabetic pain is one of the most common symptoms of diabetic neuropathy and is characterized by spontaneous pain and hyperalgesia (9,10). Its under-lied mechanism is complicated (11). It is one of the major complaints of diabetic patients affecting their quality of life.…”

Section: Introductionmentioning

confidence: 99%

Effect of Hydroethanolic Extract of Rubus fruticosus on Neuropathic Pain in Wistar Diabetic Rats

Gomar

Hosseini

Mirazi

et al. 2015

Caspian.J.Neurol.Sci

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Background: Diabetes mellitus is the most common metabolic disorder with many complications such as neuropathic pain which relief from it is a dilemma. Objectives: To investigate the effect of hydroethanolic extract of Rubus fruticosus on neuropathic pain in diabetic rats. Materials and Methods:In this experimental case -control study, forty eight male Wistar rats (250±20 g) were divided randomly to non-diabetic and diabetic groups. Streptozotocin (60 mg/kg, intra-peritoneal) was used to induce experimental diabetes. Each group was divided into three groups: receiving orally normal saline, 100 and 200 mg/kg doses of Rubus fruticosus extract for 30 days. At the end; the rats were subjected to Tail-Flick test. The data were analyzed by one-way and two-way ANOVA followed by Tukey's test in SPSS 21. Results: In a paired comparison, all diabetic groups had shorter latency of tailflicking time (p < 0.01) and lower pain tolerance threshold. Also among diabetic rats, significant differences existed between saline group and group receiving the extract at a dose of 100 mg/Kg (p < 0.01), between saline group and the group receiving the extract at a dose of 200 mg/Kg (p < 0.001) and also between the groups receiving extract at two different doses (p < 0.001). But, only diabetic group receiving the extract at a dose of 200 mg/Kg showed positive significant difference with non-diabetic control group (p < 0.01). Conclusions:The hydroethanolic extract of Rubus fruticosus can heighten the pain tolerance threshold and reduce the neuropathic pain induced by diabetes mellitus.

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Curcumin Attenuates Diabetic Neuropathic Pain by Downregulating TNF-α in a Rat Model

Cited by 73 publications

References 22 publications

Protein kinase RNA-like endoplasmic reticulum kinase (PERK)/calcineurin signaling is a novel pathway regulating intracellular calcium accumulation which might be involved in ventricular arrhythmias in diabetic cardiomyopathy

Protein kinase RNA-like endoplasmic reticulum kinase (PERK)/calcineurin signaling is a novel pathway regulating intracellular calcium accumulation which might be involved in ventricular arrhythmias in diabetic cardiomyopathy

Schwann cell interactions with axons and microvessels in diabetic neuropathy

Effect of Hydroethanolic Extract of Rubus fruticosus on Neuropathic Pain in Wistar Diabetic Rats

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