党参多糖介导Nrf2通路对缺氧缺血性脑损伤的抗氧化和神经保护作用

目的研究党参多糖对缺氧缺血性脑损伤的抗氧化和神经保护作用及其机制。方法采用Rice法建立HIBI模型。假手术组和模型组灌胃给予生理盐水,模型加药组灌胃给予党参多糖。分别进行神经功能学评分,观察脑积水量,脑组织病理学改变,神经元细胞凋亡情况,脑组织脂质过氧化物水平,抗氧化和神经保护相关蛋白表达水平。结果党参多糖能显著改善模型大鼠神经功能、脑水肿(P<0.01)和病理改变,降低细胞凋亡率(P<0.01)和Bax表达(P<0.01),降低LDH和MDA含量(P<0.01);同时,上调Bcl-2表达(P<0.01)和SOD活性(P<0.01),增加bFGF、BDNF、PSD95、SYP、Nrf2和HO-1表达(P<0.01)。结论党参多糖对缺氧缺血性脑损伤具有抗氧化和神经保护作用,可能与介导Nrf2信号通路相关。

Antioxidant and neuroprotective effects of Codonopsis pilosula polysaccharides on hypoxic-ischemic brain injury induced by Nrf2 pathway

Objective　To study the antioxidant and neuroprotective effects of Codonopsis pilosula polysaccharides (CPP) and its possible mechanism.　Methods　Rice method was used to establish HIBI rat model. Normal saline was given to the sham group and the HIBI group, and corresponding doses of CPP solution were given to the drug groups. The neurological function, cerebral water content of rats, histopathologic changes, apoptosis in the rat hippocampus, the level of lipid peroxide, the expression of antioxidant and neuroprotective proteins were evaluated.　Results　Compared with the model group, the neurological function, cerebral water content and the pathological injury of brain tissue were significantly reduced (P<0.01). The apoptosis rate, expression of Bax, content of LDH and MDA also decreased significantly (P<0.01). Expression of Bcl-2 and activity of SOD were up-regulated (P<0.01). In addition, the expressions of bFGF, BDNF, PSD95, SYP, Nrf2 and HO-1 were significantly up-regulated (P<0.01). Conclusion　CPP has antioxidant and neuroprotective effects on hypoxic-ischemic brain injury, and its function may be related to mediating Nrf2 signal pathway.