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首页> 外文期刊>Molecular medicine reports >Neuroprotective effect of tanshinone IIA weakens spastic cerebral palsy through inflammation, p38MAPK and VEGF in neonatal rats
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Neuroprotective effect of tanshinone IIA weakens spastic cerebral palsy through inflammation, p38MAPK and VEGF in neonatal rats

机译:丹参酮IIa的神经保护作用通过新生大鼠的炎症,p38mapk和Vegf减弱痉挛性脑瘫

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摘要

As one of main active ingredients of salvia miltiorrhizae, which is a traditional Chinese medicine, tanshinone IIA is the basis of its pharmacological activities. In the present study, the effect of tanshinone IIA on weakening spastic cerebral palsy (SCP) in neonatal rats was investigated. Radial arm water maze and holding tests were used to measure the alterations of spastic cerebral palsy, inflammation was measured using an ELISA kit, and western blot analysis was used to analyze the protein expression of p-p38 mitogen-activated protein kinase (MAPK) and vascular endothelial growth factor (VEGF). The central mechanisms involved in the mediation or modulation of inflammation, p-p38 MAPK and VEGF were also investigated. Treatment with tanshinone IIA effectively inhibited spastic cerebral palsy, and the activities of interleukin (IL)-1, IL-6, tumor necrosis factor-, monocyte chemoattractant protein 1, cyclooxygenase-2 and prostaglandin E2 in a neonatal rat model of SCP. Tanshinone IIA effectively suppressed the protein expression of inducible nitric oxide synthase (NOS), phosphorylated (p-) nuclear factor (NF)-B, p-p38MAPK and VEGF, and activated the phosphorylation of inhibitor of NF-B and the protein expression of neuronal NOS in the SCP rat model. These results suggested that the neuroprotective effect of tanshinone IIA weakened SCP through inflammation, p38MAPK and VEGF in the neonatal rats.
机译:作为丹参的主要活性成分之一,是一种中医,丹参酮IIA是其药理活动的基础。在本研究中,研究了丹参酮IIA对新生大鼠痉挛性脑瘫(SCP)疲软的影响。径向臂水迷宫和保持试验用于测量痉挛性脑瘫的改变,使用ELISA试剂盒测量炎症,并且使用Western印迹分析来分析P-P38丝裂原激活蛋白激酶(MAPK)的蛋白质表达和血管内皮生长因子(VEGF)。还研究了炎症的中枢或调节的中央机制,P-P38 MAPK和VEGF。用丹石IIA治疗有效地抑制了SCP新生大鼠模型中白细胞介素(IL)-1,IL-6,肿瘤坏死因子,单核细胞化学蛋白-2和前列腺素E2的运动蛋白(IL)-1,IL-6,肿瘤坏死因子,单核糖酶-2和前列腺素E2。丹参酮IIA有效地抑制了诱导型一氧化氮合酶(NOS),磷酸化(P-)核因子(NF)-B,P-P38MAPK和VEGF的蛋白质表达,并激活了NF-B抑制剂的磷酸化和蛋白质表达SCP大鼠模型中神经元NOS。这些结果表明,丹参酮IIA的神经保护作用通过新生大鼠炎症,P38MAPK和VEGF减弱了SCP。

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