首页> 美国卫生研究院文献>Evidence-based Complementary and Alternative Medicine : eCAM >Electroacupuncture Zusanli (ST36) on Release of Nitric Oxide in the Gracile Nucleus and Improvement of Sensory Neuropathies in Zucker Diabetic Fatty Rats
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Electroacupuncture Zusanli (ST36) on Release of Nitric Oxide in the Gracile Nucleus and Improvement of Sensory Neuropathies in Zucker Diabetic Fatty Rats

机译:电针祖三里(ST36)对祖克氏糖尿病大鼠脂肪核中一氧化氮释放及感觉神经病的改善作用

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摘要

The purpose of these studies was to examine the effects of electroacupuncture (EA) Zusanli (ST36) on release of nitric oxide (NO) in the gracile nucleus (GN) and determine if functional neuropathic changes were modified by EA ST36-induced NO in the nucleus in Zucker diabetic fatty (ZDF) rats. The foot withdrawal responses to mechanical, thermal and cold stimuli were measured before and after EA stimulation. A microdialysis probe was implanted in the GN and dialysate samples were collected 20 min before, during and after EA ST36. Total nitrate and nitrite (NOx ) concentrations in the samples were quantified by using chemiluminescence. The baseline dialysate NOx concentrations in the GN were decreased in ZDF rats compared to lean control (LC) rats (P < .05). In ZDF rats, dialysate NOx releases in the GN were markedly increased during EA ST36, whereas in LC rats, the releases were moderately enhanced at 20–40 min after EA ST36. The withdrawal latencies to mechanical, cold and thermal stimuli were significantly improved 20 min after EA ST36 both in LC and ZDF rats, but not altered by non-acupoint stimulation. The withdrawal latencies to EA ST36 were further potentiated by 3-morpholinyl-sydnoneimine and inhibited by NG-Propyl-l-arginine infused into the GN in ZDF rats (P < .05). These results show that EA ST36 increases NO release in the GN, and NO in the nucleus modifies withdrawal latencies to mechanical, cold, and thermal nociception stimuli. Data suggest that EA ST36 induces NO release in the GN, which contributes to improvement of sensory neuropathies in rats.
机译:这些研究的目的是检查电针(EA)足三里(ST36)对细纹状核(GN)中一氧化氮(NO)释放的影响,并确定EA ST36诱导的NO中是否改变了功能性神经病变。 Zucker糖尿病性脂肪(ZDF)大鼠的细胞核。在EA刺激之前和之后,测量足部对机械,热和冷刺激的退缩反应。将微透析探针植入GN中,并在EA ST36之前,期间和之后20分钟收集透析液样品。使用化学发光法定量样品中的总硝酸盐和亚硝酸盐(NOx -)浓度。与瘦对照(LC)大鼠相比,ZDF大鼠的GN中基线透析液NOx -浓度降低(P <.05)。在ZDF大鼠中,EA ST36期间GN中透析液NOx -的释放显着增加,而LC大鼠中,EA ST36之后20–40µmin释放量有所增加。 EA ST36对LC和ZDF大鼠的机械刺激,冷刺激和热刺激的撤回潜伏期均显着改善,但未因非穴位刺激而改变。 Z吗啡大鼠在GN中注入3-吗啉基-亚砜亚胺进一步增强了对EA ST36的戒断潜伏期,并被N G -丙基-1-精氨酸抑制(P <.05)。这些结果表明,EA ST36增加了GN中的NO释放,而细胞核中的NO改变了机械,冷和热伤害感受刺激的戒断潜伏期。数据表明,EA ST36诱导GN中NO的释放,这有助于改善大鼠的感觉神经病。

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