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首页> 外文期刊>The journal of sexual medicine >Sonic Hedgehog Regulates Brain-Derived Neurotrophic Factor in Normal and Regenerating Cavernous Nerves
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Sonic Hedgehog Regulates Brain-Derived Neurotrophic Factor in Normal and Regenerating Cavernous Nerves

机译：声波刺猬调节正常和再生海绵状神经的脑源性神经营养因子。

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Introduction. The cavernous nerve (CN) is commonly injured during prostatectomy. Manipulation of the nerve microenvironment is critical to improve regeneration and develop novel erectile dysfunction therapies. Sonic hedgehog (SHH) treatment promotes CN regeneration. The mechanism of how this occurs is unknown. Brain-derived neurotrophic factor (BDNF) facilitates return of erectile function after CN injury and it has been suggested in cortical neurons and the sciatic nerve that BDNF may be a target of SHH. Aim. To determine if SHH promotes CN regeneration through a BDNF-dependent mechanism. Methods. Sprague Dawley rats underwent (i) bilateral CN crush (N=15); (ii) SHH treatment of pelvic ganglia (PG)/CN (N=10); (iii) SHH inhibition in PG/CN (N=14 rats); (iv) CN crush with SHH treatment of PG/CN (N=10 rats); (v) CN crush with SHH treatment and BDNF inhibition (N=14 rats); and (vi) CN injury and SHH treatment of the penis (N=23). Main Outcome Measures. BDNF and glial fibrillary acidic protein were quantified in PG/CN by Western, and a t-test was used to determine differences. Results. In normal rats SHH inhibition in the PG/CN decreased BDNF 34% and SHH treatment increased BDNF 36%. BDNF was increased 44% in response to SHH treatment of crushed CNs, and inhibition of BDNF in crushed CNs treated with SHH protein hampers regeneration. Conclusions. SHH regulates BDNF in the normal and regenerating PG/CN. BDNF is part of the mechanism of how SHH promotes regeneration, thus providing an opportunity to further manipulate the nerve microenvironment with combination therapy to enhance regeneration. ? 2012 International Society for Sexual Medicine.
机译：介绍。前列腺切除术通常会损伤海绵状神经（CN）。神经微环境的操纵对于改善再生和开发新的勃起功能障碍疗法至关重要。声波刺猬（SHH）处理可促进CN再生。发生这种情况的机制尚不清楚。脑源性神经营养因子（BDNF）促进CN损伤后勃起功能的恢复，并且已在皮质神经元和坐骨神经中提示BDNF可能是SHH的靶标。目标。确定SHH是否通过依赖BDNF的机制促进CN再生。方法。 Sprague Dawley大鼠（i）双侧CN压迫（N = 15）; （ii）SHH治疗骨盆神经节（PG）/ CN（N = 10）; （iii）PG / CN中SHH的抑制（N ＝ 14只大鼠）; （iv）用SHH处理PG / CN的CN压碎（N = 10只大鼠）; （v）用SHH处理和BDNF抑制作用的CN压迫（N = 14只大鼠）; （vi）阴茎的CN损伤和SHH治疗（N ＝ 23）。主要观察指标。通过Western定量分析PG / CN中的BDNF和神经胶质原纤维酸性蛋白，并使用t检验确定差异。结果。在正常大鼠中，PG / CN中的SHH抑制使BDNF降低34％，SHH治疗使BDNF升高36％。响应于SHH处理压碎的CNs，BDNF增加了44％，而用SHH蛋白处理的压碎CNs对BDNF的抑制会阻碍再生。结论。 SHH调节正常和再生PG / CN中的BDNF。 BDNF是SHH促进再生的机制的一部分，因此提供了通过联合疗法进一步操纵神经微环境以增强再生的机会。 ？ 2012年国际性医学学会。

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