School of Chinese Medicine, China Medical University, Taichung, Taiwan.
Evid Based Complement Alternat Med. 2011;2011:380809. doi: 10.1093/ecam/neq079. Epub 2011 Jun 15.
Dilong, also known as earthworm, has been widely used in traditional Chinese medicine (TCM) for thousands of years. Schwann cell migration and proliferation are critical for the regeneration of injured nerves and Schwann cells provide an essentially supportive role for neuron regeneration. However, the molecular mechanisms of migration and proliferation induced by dilongs in Schwann cells remain unclear. Here, we discuss the molecular mechanisms that includes (i) migration signaling, MAPKs (mitogen-activated protein kinases), mediated PAs and MMP2/9 pathway; (ii) survival and proliferative signaling, IGF-I (insulin-like growth factor-I)-mediated PI3K/Akt pathways and (iii) cell cycle regulation. Dilong stimulate RSC96 cell proliferation and migration. It can induce phosphorylation of ERK1/2 and p38, but not JNK, and activate the downstream signaling expression of PAs (plasminogen activators) and MMPs (matrix metalloproteinases) in a time-dependent manner. In addition, Dilong stimulated ERK1/2 and p38 phosphorylation was attenuated by pretreatment with chemical inhibitors (U0126 and SB203580), and small interfering ERK1/2 and p38 RNA, resulting in migration and uPA-related signal pathway inhibition. Dilong also induces the phosphorylation of IGF-I-mediated PI3K/Akt pathway, activates protein expression of PCNA (proliferating cell nuclear antigen) and cell cycle regulatory proteins (cyclin D1, cyclin E and cyclin A) in a time-dependent manner. In addition, it accelerates G(1)-phase progression with earlier S-phase entry and significant numbers of cells entered the S-phase. The siRNA-mediated knockdown of PI3K that significantly reduces PI3K protein expression levels, resulting in Bcl(2) survival factor reduction, revealing a marked blockage of G(1) to S transition in proliferating cells. These results reveal the unknown RSC96 cell migration and proliferation mechanism induced by dilong, which find use as a new medicine for nerve regeneration.
地龙,又称蚯蚓,在传统中药(TCM)中已有数千年的应用历史。施万细胞的迁移和增殖对于受损神经的再生至关重要,而施万细胞为神经元的再生提供了基本的支持作用。然而,地龙诱导施万细胞迁移和增殖的分子机制尚不清楚。在这里,我们讨论了包括(i)迁移信号、MAPKs(丝裂原活化蛋白激酶)介导的 PAs 和 MMP2/9 通路;(ii)存活和增殖信号、IGF-I(胰岛素样生长因子-I)介导的 PI3K/Akt 通路;(iii)细胞周期调控在内的分子机制。地龙刺激 RSC96 细胞的增殖和迁移。它可以诱导 ERK1/2 和 p38 的磷酸化,但不诱导 JNK 的磷酸化,并在时间依赖性方式下激活 PAs(纤溶酶原激活物)和 MMPs(基质金属蛋白酶)的下游信号表达。此外,地龙刺激 ERK1/2 和 p38 磷酸化被化学抑制剂(U0126 和 SB203580)预处理以及小干扰 ERK1/2 和 p38 RNA 减弱,导致迁移和 uPA 相关信号通路的抑制。地龙还诱导 IGF-I 介导的 PI3K/Akt 通路的磷酸化,在时间依赖性方式下激活 PCNA(增殖细胞核抗原)和细胞周期调控蛋白(cyclin D1、cyclin E 和 cyclin A)的蛋白表达。此外,它加速了 G1 期的进展,更早地进入 S 期,大量细胞进入 S 期。siRNA 介导的 PI3K 敲低显著降低了 PI3K 蛋白表达水平,导致 Bcl(2)存活因子减少,从而在增殖细胞中明显阻断 G1 期向 S 期的转变。这些结果揭示了地龙诱导的 RSC96 细胞迁移和增殖的未知机制,为神经再生提供了一种新的药物。