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  • Title: [Effects of salvianolic acid B on beta-amyloid peptide neurotoxicity of primary cultured fetal rat cortical neurons].
    Author: Feng Z, Zhang JT.
    Journal: Yao Xue Xue Bao; 2000 Dec; 35(12):881-5. PubMed ID: 12567906.
    Abstract:
    AIM: To study the roles of nitric oxide (NO) and nitric oxide synthase (NOS) on the glutamate (Glu) and beta-amyloid peptide [beta-AP (1-40)] mediated neurotoxicity in primary cultured fetal rat cortical neuron and the neuroprotective effects of salvianolic acid B (Sal B) against the beta-AP (1-40) and its mechanism of action. METHODS: With application of specific agonist and antagonist of NOS, establishment of the sodium nitroprusside (SNP), Glu and beta-AP (1-40) neurotoxicity model, the cell viability, lactate dehydrogenase (LDH) efflux and NO release were detected by using morphological observation, MTT stain, spectrophotometric measurement and Griess method, respectively, in primary cultured fetal rat cortical neurons. RESULTS: Glu and beta-AP (1-40) were shown to increase the NO release of the neuron. Furthermore, nNOS was found to play an important role in the neurotoxicity of glutamate, iNOS may probably be involved in the neurotoxicity of beta-AP (1-40). Sal B (0.01, 0.10, 1.00 microgram.L(-1)) was shown to increase the cell viability, decrease the LDH release rate and inhibit NO release in a dose-dependent manner. CONCLUSION: These results suggest that the neurotoxicity of Glu and beta-AP(1-40) may be partly mediated through different types of NOS. Sal B was found to prevent the beta-AP(1-40) toxicity by directly or indirectly decreasing NO release.
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