Abstract
Objective To investigate the role of phosphatase and tensin homologue deleted on chromosome 10(PTEN)protein in the spinal cord neurons in diabetic neuropathic pain(DNP)in rats. Methods Male Sprague-Dawley rats, aged 2 months, weighing 180-200 g, were studied.Diabetes mellitus was induced by single intraperitoneal injection of streptozotocin(STZ)60 mg/kg.Sixteen rats with DNP were randomly divided into 2 groups(n=8 each)using a random number table: DNP group and DNP+ PTEN inhibitor bpv(pic)group(DPN-bpv group). Another 16 rats were equally and randomly divided into either control group(group C)or bpv group.In DNP-bpv and bpv groups, bpv(pic)0.2 mg/kg was injected intraperitoneally once a day within 14-28 days after injection of STZ.Before STZ injection(T1), and at 2, 7, 14, 2l and 28 days after STZ injection(T2-6), the mechanical paw withdrawal threshold(MWT)was measured.After measurement of MWT, the rats were sacrificed, and the lumbar segments of the spinal cord(L4, 5)were removed for determination of PTEN protein activity(by ELISA)and Akt(s473)phosphorylation(by Western blot). Results Compared with group C, the MWT was significantly decreased at T4-6, and the PTEN protein activity and Akt(s473)phosphorylation were significantly increased in DNP and DNP-bpv groups(P<0.05 or 0.01). Compared with group DNP, the MWT was significantly increased at T6, and the PTEN protein activity and Akt(s473)phosphorylation were significantly decreased in group DNP-bpv(P<0.05). Conclusion PTEN protein in the spinal cord neurons is involved in the maintenance of DNP in rats. Key words: Chromosomes, human, pair 10; Genes, tumor suppressor; Spinal cord; Neuralgia; Diabetes mellitus
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