首页> 外文期刊>Acta Pharmacologica Sinica >Protective effect of ginsenoside Rg1 against MPTP-induced apoptosis in mouse substantia nigra neurons
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Protective effect of ginsenoside Rg1 against MPTP-induced apoptosis in mouse substantia nigra neurons

机译:人参皂苷Rg1对MPTP诱导的小鼠黑质神经元凋亡的保护作用

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AIM: To explore the possible mechanism of the ginsenoside Rg1 in protecting substantia nigra neurons from 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP)-induced apoptosis in C57BL mice. METHODS: C57BL male mice were given with MPTP to prepare Parkinson's disease mouse model. Different doses of Rg1 (2.5, 5.0, and 10.0 mg/kg, respectively) were given 3 d prior to MPTP in the pretreatment groups. Niss1 staining, TH immunostaining, and TUNEL labeling were used to observe the damage and apoptosis of nigral neurons. The immunohistochemistry assay was used to detect the protein levels of Bcl-2, Bcl-xl, Bax, inducible nitric oxide synthase (iNOS), neuronal NOS (nNOS), and cleaved caspase-3. RESULTS: Compared with MPTP model group, pretreatment with Rg1 (5.0 and 10.0 mg/kg) was shown to increase the Niss1 staining neurons and TH-positive neurons (P<0.01), and to decrease the TUNEL-positive neurons in the substantia nigra zona compacta (P<0.01). Moreover, Rg1 elevated the levels of cleaved caspase-3, Bax, and iNOS, but reduced the levels of Bcl-2 and Bcl-xl (P<0.01). CONCLUSION: Rg1 has protective effect against MPTP-induced apoptosis and this effect may be attributed to enhancing Bcl-2 and Bcl-xl expression, reducing Bax and iNOS expression, and inhibiting activation of caspase-3.
机译:目的:探讨人参皂苷Rg1在保护黑质神经元免受1-甲基-4-苯基-1、2、3、6-四氢吡啶(MPTP)诱导的C57BL小鼠凋亡的可能机制。方法:对C57BL雄性小鼠进行MPTP制备帕金森氏病小鼠模型。在MPTP治疗前3天,分别给予不同剂量的Rg1(分别为2.5、5.0和10.0 mg / kg)。 Niss1染色,TH免疫染色和TUNEL标记用于观察黑质神经元的损伤和凋亡。免疫组织化学测定法用于检测Bcl-2,Bcl-xl,Bax,诱导型一氧化氮合酶(iNOS),神经元NOS(nNOS)和裂解的caspase-3的蛋白水平。结果:与MPTP模型组相比,Rg1(5.0和10.0 mg / kg)预处理可增加Niss1染色神经元和TH阳性神经元(P <0.01),并减少黑质中TUNEL阳性神经元致密带(P <0.01)。此外,Rg1升高了裂解的caspase-3,Bax和iNOS的水平,但降低了Bcl-2和Bcl-xl的水平(P <0.01)。结论:Rg1对MPTP诱导的细胞凋亡具有保护作用,其作用可能与增强Bcl-2和Bcl-xl的表达,降低Bax和iNOS的表达以及抑制caspase-3的活化有关。

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