白肉灵芝水提物对神经元损伤的保护作用及其机制

Protective effect and mechanism of the aqueous extracts of Ganoderma leucocontextum on neurons injury

【目的】探讨白肉灵芝水提物(Ganoderma leucocontextum aqueous extracts,GLAE)对脂多糖(LPS)所致神经元损伤的保护作用及机制.【方法】将50只健康大鼠分成对照组、模型组、GLAE低剂量组、GLAE中剂量组和GLAE高剂量组,用LPS建立大鼠大脑皮层神经元炎症损伤模型,给予不同剂量的(0、50、100、200 mg/kg)的GLAE干预,ELISA法检测大脑额叶皮层肿瘤坏死因子α(tumor necrosis factor-α,TNF-α)、白细胞介素1(interleukin-1β,IL-1β)、脑源性神经生长因子(brain derived neurotrophic factor,BDNF)和β-神经生长因子(β-nerve growth factor,β-NGF)含量,Western-blot和PCR法检测大脑额叶皮层原肌球蛋白受体激酶B(tropomyosin receptor kinase B,TrkB)、原肌球蛋白受体激酶A(tropomyosin receptor kinase A,TrkA)、BDNF、NGF蛋白及mRNA表达,免疫组织化学法检测大脑额叶皮层NGF蛋白的表达.【结果】与模型组比较,GLAE干预后,大脑额叶皮层TNF-α和IL-1β的含量显著降低(P<0.01,P<0.05),BDNF和β-NGF的含量显著增高(P<0.01,P<0.05),TrkB、TrkA、BDNF、NGF蛋白及mRNA的表达水平显著上升(P<0.01,P<0.05).【结论】GLAE对LPS所致的神经元损伤有一定的保护作用,其机制可能与抑制炎症因子水平、促进大脑皮层神经元生长有关.

【Objective】To investigate the protective effect and mechanism of the aqueous extracts of Ganoderma leucocontextum(GLAE)on lipopolysaccharide-induced neurons injury.【Method】Fifty rats were divided into five groups:control group,model group,GLAE low-dose group,GLAE middle-dose group and GLAE high-dose group.The inflammatory model of cerebral neuron was induced by LPS,and then treated continuously with different doses(0,50,100,200 mg/kg)of GLAE.The contents of tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β),brain derived neurotrophic factor(BDNF)andβ-nerve growth factor(β-NGF)in cerebral subcortex were detected by ELISA,and the expressions of tropomyosin receptor kinase B(TrkB),tropomyosin receptor kinase A(TrkA),BDNF and NGF protein and mRNA in cerebral subcortex were detected by Western blot and PCR,respectively.Immunohistochemistry was used to analyze the expression of NGF protein.【Result】Compared to model group,administration of GLAE could significantly decrease the contents of TNF-αand IL-1β,and improve the contents of BDNF andβ-NGF in cerebral subcortex(P<0.01,P<0.05).The levels of TrkB,TrkA,BDNF,NGF protein and mRNA were increased in cerebral subcortex(P<0.01,P<0.05).【Conclusion】GLAE has a certain protective effect on LPS induced cerebral neuron injury,and its mechanism might be depend on inhibiting inflammatory response and promoting the growth of cerebral cortical neurons.