Abstract
Most diabetic patients develop diabetic peripheral neuropathy (DPN). DPN is related to the increase of inflammatory cells in peripheral nerves, abnormal cytokine expression, oxidative stress, ischemia ,and pro-inflammatory changes in bone marrow. We summarized the progress of immune-inflammatory mechanism and treatment of DPN in recent years. Immune inflammatory mechanisms include TNF-α, HSPs, PARP, other inflammatory factors, and the effect of immune cells on DPN. Treatment includes tricyclic antidepressants and other drug therapy, immune and molecular therapy, and non-drug therapy such as exercise therapy, electrotherapy, acupuncture, and moxibustion. The pathogenesis of DPN is complex. In addition to strictly controlling blood glucose, its treatment should also start from other ways, explore more effective and specific treatment schemes for various causes of DPN, and find new targets for treatment will be the direction of developing DPN therapeutic drugs in the future.
Highlights
The prevalence of diabetes mellitus (DM) increased with age
Shi et al showed that compared with untreated diabetic peripheral neuropathy (DPN), recombinant human TNF-α receptor antibody fusion protein inhibited TNF-α in STZ induced diabetic rats, partially improving motor nerve conduction velocity (MCV) and sensory nerve conduction velocity (SCV), increasing the expression of myelin basic protein (MBP), and preventing myelin and neural structural abnormalities (Shi et al, 2013)
We found that in a high glucose environment, macrophages stimulated by LPS produced high levels of TNF-α and human macrophage chemoattractant protein-1 (MCP-1), but the effect of IL-6 was not so strong
Summary
The prevalence of diabetes mellitus (DM) increased with age. DM is present in 19.9% of 65–79-yearolds (Saeedi et al, 2019). Diabetic peripheral neuropathy (DPN) is one of the common chronic complication of diabetes mellitus. Its Clinical Syndrome can be dysfunction of peripheral neuropathy, influencing the quality of life in the dabetic patients. Studies have shown that blood glucose control can reduce the incidence of peripheral neuropathy in type 1 diabetes, it will increase the incidence of hypoglycemia, and aggressive blood glucose control can not reduce the incidence of peripheral neuropathy in type 2 diabetes (Group 1993; Boussageon et al, 2011; Callaghan et al, 2012a). Most studies on DPN were limited to metabolism, genetic mechanism, and the effect of hypoglycemic drugs (Ferland-Mccollough et al, 2016; Sztanek et al, 2016; De et al, 2017; Stino and Smith, 2017; Jamwal et al, 2018). Previous drug trials mainly focused on antioxidants (Ziegler et al, 1999; Ametov et al, 2003; Ziegler et al, 2006), aldose reductase inhibitors (Hotta et al, 2006; Bril et al, 2009; Ramirez and Borja, 2012), neurotrophic factors
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