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Exp Biol Med:针灸降压第一个分子证据被确认

来源:科技日报 2011-12-22 13:22

12月19日,美国乔治城大学医学中心在《实验生物学与医学》杂志网站发表了最新研究发现"Acupuncture at ST36 prevents chronic stress-induced increases in neuropeptide Y in rat ",研究结果表明针灸能极大地降低小鼠体内一种与慢性压力有关的蛋白质水平,为针灸降压提供了第一个分子证据。研究人员表示,如果该发现能在人类身上重复,针灸将成为一种可证实的治疗压力的方法,并有助于解释中医的含义,让更多人接受中医。

慢性压力会导致血压升高和心脏病。“长期以来,人们认为针灸能降低压力。世界卫生组织也表示,在治疗50多种包括慢性压力在内的身体机能失调类疾病中,针灸作为一种辅助性疗法是有效的。”该研究领导作者、乔治城大学护理与卫生研究院副教授、认证针灸师拉丹·埃西瓦瑞说,但至今还没有人提出相应的生物证据。

为此,埃西瓦瑞设计了专门的实验,通过检测血液中神经肽Y(NPY)的含量来验证针灸的效果。神经肽Y是由身体交感神经系统分泌的一种肽,这一系统与人类面对巨大压力时的“逃跑或战斗”反应有关,会导致血液流向除了心脏、肺部和大脑以外的其他身体部分。

研究人员选择了膝盖下面的足三里穴位作为针灸点,这里能缓解包括压力在内的多种症状。他们对4组小鼠进行了14天的实验:控制组不施压也不用针灸;对照组中的一组接受每天一小时的压力但不接受针灸,另一组接受压力并在靠近尾巴的地方接受“假”针灸;实验组接受压力并在腿部足三里处接受针灸,并用无痛低电荷的电针刺以确保每只小鼠得到相同的治疗剂量。

他们发现,实验组小鼠血液中的神经肽Y含量水平下降到了控制组的水平,而对照组的蛋白含量水平很高。在第二次实验中,他们对实验组停止针灸后,继续给它多施加了4天的压力,发现神经肽Y水平仍然很低。

“看起来这种疗法对抵抗压力有着保护性的效果。”埃西瓦瑞说,他们还将进一步用小鼠模型来研究针灸效果,以检验其他的关键经络。(生物谷Bioon.com)

Acupuncture at ST36 prevents chronic stress-induced increases in neuropeptide Y in rat

Ladan Eshkevari1, Rupert Egan2, Dylan Phillips3, Jason Tilan1, Elissa Carney2, Nabil Azzam4, Hakima Amri5 and Susan E Mulroney2

Chronic stress, as seen in post-traumatic stress disorder, can exacerbate existing diseases. Electroacupuncture (EA) has been proposed to treat chronic stress, although information on its efficacy or mechanism(s) of action is limited. While many factors contribute to the chronic stress response, the sympathetic peptide, neuropeptide Y (NPY), has been shown to be elevated in chronic stress and is hypothesized to contribute to the physiological stress response. Our objective was to determine if EA at acupuncture point stomach 36 (ST36) is effective in mitigating cold stress-induced increase in NPY in rats. Both pretreatment and concomitant treatment with EA ST36 effectively suppressed peripheral and central NPY after 14 d of cold stress (P < 0.05). The effect was specific, as NPY in Sham-EA rats was not different than observed in stress-only rats. Additionally, the effect of EA ST36 was long-lasting, as NPY levels remained suppressed despite early cessation of EA ST36, while exposure to cold stress was continued. In the paraventricular nucleus (PVN), it was notable that changes in NPY mirrored plasma NPY levels, and that the significant elevation in PVN Y1 receptor observed with stress was also prevented with EA ST36. The findings indicate that EA ST36 is effective in preventing one of the sympathetic pathways stimulated during chronic stress, and thus may be a useful adjunct therapy in stress-related disorders.

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