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.
journal_name
Exp Ther Medjournal_title
Experimental and therapeutic medicineauthors
Zheng X,Chen L,Du X,Cai J,Yu S,Wang H,Xu G,Luo Zdoi
10.3892/etm.2017.4334subject
Has Abstractpub_date
2017-06-01 00:00:00pages
2855-2861issue
6eissn
1792-0981issn
1792-1015pii
ETM-0-0-4334journal_volume
13pub_type
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