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首页> 外文期刊>Drug Design, Development and Therapy >Tanshinone IIA Promotes Axonal Regeneration in Rats with Focal Cerebral Ischemia Through the Inhibition of Nogo-A/NgR1/RhoA/ROCKII/MLC Signaling
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Tanshinone IIA Promotes Axonal Regeneration in Rats with Focal Cerebral Ischemia Through the Inhibition of Nogo-A/NgR1/RhoA/ROCKII/MLC Signaling

机译：丹参酮IIA通过抑制Nogo-A / NGR1 / RoON / Roci / MLC信号传导，促进局灶性脑缺血的大鼠轴突再生

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Purpose: The aim of this study was to evaluate the neuroprotective effect of tanshinone IIA (TSA) on focal cerebral ischemia in rats and to investigate whether it was associated with Nogo-A/NgR1/RhoA/Rho-associated protein kinase 2 (ROCKII)/myosin light chain (MLC) signaling. Methods: In this study, focal cerebral ischemia animal model was used. Neurological deficit scores and infarction volume were investigated to evaluate the neuroprotection of TSA. Hematoxylin-eosin staining, Nissl staining, and immunofluorescence staining were conducted to detect ischemic changes in brain tissue and changes in neurofilament protein 200 (NF200) and growth-associated protein-43 (GAP-43) expression, respectively. Western blotting and qRT-PCR analyses were used to detect the expression levels of NF200, GAP-43 and Nogo-A/NgR1/RhoA/ROCKII/MLC pathway-related signaling molecules. Results: TSA treatment can improve the survival rate of rats, reduce the neurological score and infarct volume, and reduce neuron damage. In addition, TSA also increased axon length and enhanced expression of NF200 and GAP-43. Importantly, TSA significantly attenuated the expression of Nogo-A, NgR1, RhoA, ROCKII, and p-MLC, and thus inhibiting the activation of this signaling pathway. Conclusion: TSA promoted axonal regeneration by inhibiting the Nogo-A/NgR1/RhoA/ROCKII/MLC signaling pathway, thereby exerting neuroprotective effects in cerebral ischemia rats, which provided support for the clinical application of TSA in stroke treatment.
机译：目的：本研究的目的是评估丹参酮IIA（TSA）对大鼠局灶性脑缺血的神经保护作用，并研究其是否与Nogo-A / NGR1 / RHOA / RHO相关蛋白激酶2（Rockii）相关/ myosin轻链（MLC）信号传导。方法：在本研究中，使用了局灶性脑缺血动物模型。研究了神经缺陷分数和梗死体积，以评估TSA的神经保护作用。进行血清氧基 - 曙红染色，NISL染色和免疫荧光染色以检测脑组织的缺血变化，分别检测脑组织的缺血性变化和神经丝蛋白200（NF200）和生长相关蛋白-33（GAP-43）表达的变化。用于检测NF200，GAP-43和Nogo-A / NGR1 / ROOA / ROCKII / MLC途径相关信号分子的表达水平。结果：TSA治疗可以提高大鼠的存活率，降低神经系统评分和梗塞体积，降低神经元损伤。此外，TSA还增加了轴突长度和NF200和GAP-43的增强表达。重要的是，TSA显着减弱了Nogo-A，NGR1，RhOA，RockII和P-MLC的表达，从而抑制该信号通路的激活。结论：TSA通过抑制Nogo-A / NGR1 / RoCOA / Rocia / MLC信号通路促进轴突再生，从而施加脑缺血大鼠中的神经保护作用，这为临床应用提供了TSA在中风处理中的临床应用。

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