ArticleExperimental and therapeutic medicine2017
Effects of hyperbaric factors on lidocaine-induced apoptosis in spinal neurons and the role of p38 mitogen-activated protein kinase in rats with diabetic neuropathic pain.
Article in Experimental and therapeutic medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Neonatal sevoflurane anesthesia can also affect rat medulla spinalis.Asian biomedicine : research, reviews and news · 2025Article
- Novel drugs affecting diabetic peripheral neuropathy.Iranian journal of basic medical sciences · 2024Review
- Protective role of lidocaine against cerebral ischemia-reperfusion injury: AnExperimental and therapeutic medicine · 2022Article
- Amitriptyline Protects Against Lidocaine-induced Neurotoxicity in SH-SY5Y Cells via Inhibition of BDNF-mediated Autophagy.Neurotoxicity research · 2021Article
- Koumine Decreases Astrocyte-Mediated Neuroinflammation and Enhances Autophagy, Contributing to Neuropathic Pain From Chronic Constriction Injury in Rats.Frontiers in pharmacology · 2018Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
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Abstract
The application of lidocaine can lead to nerve damage. Evidence suggests that patients with diabetic neuropathy are at a higher risk for neurotoxicity. In the present study, the successful induction of diabetic neuropathic pain (DNP) in rats via a high-sugar, high-fat diet and intraperitoneal injection of 1% streptozotocin was verified and pronounced tactile allodynia was observed. It was found that intrathecal injections of hyperbaric lidocaine produced motor blocks of longer durations in the DNP model rats than in nondiabetic rats, or in DNP model rats injected with isobaric lidocaine. Histology of the lumbar 4-5 spinal cord revealed a significant difference in neuropathology between the DNP and nondiabetic rats. Moreover, edematous neurons and TUNEL-positive cells were observed in the hyperbaric lidocaine group. It was also found that the inhibition of p38 mitogen-activated protein kinase (p38MAPK) played a neuroprotective role in response to hyperbaric lidocaine-induced apoptosis in DNP rats, which indicates that p38MAPK plays a key role in the regulation of hyperbaric lidocaine-induced apoptosis in DNP rats. These findings suggest that hyperbaric lidocaine can promote spinal cord neuronal apoptosis in rats with DNP. Furthermore, p38MAPK might play a key role in the regulation of hyperbaric lidocaine-induced apoptosis in rats with DNP.
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