RESUMO
As more and more people worldwide begin using Chinese herbs, authentication of these herbs becomes an increasingly critical, international problem. Mistakes, misidentification, or willful deception can cause illness and even death. Questionable authenticity with regard to Chinese herbs arises for a number of historical, geographical and nomenclatural reasons, which will be described in this paper. The current situation in the Hong Kong market and some suggestions for alleviating the problem are also discussed.
Assuntos
Medicamentos de Ervas Chinesas/economia , Medicamentos de Ervas Chinesas/normas , Marketing , Farmacognosia/métodos , Hong Kong , HumanosRESUMO
BACKGROUND: Previously we showed that atrial natriuretic peptide (ANP) increases cGMP production in PC12 (sympathetic-neuron-like) cells, cGMP elevations increase survival of hippocampal neurons during glutamate toxicity and ANP-induced cGMP elevations prolongs survival of stressed PC12 cells, all suggesting cGMP mediates anti-apoptotic/pro-survival effects in neural cells. AIM: The objective was to use a new technology, capillary electrophoresis-laser-induced-fluorescence-detector (CE-LIF) to accurately measure nitric oxide (NO)-induced stimulation and ANP/cGMP-induced inhibition of apoptotic DNA fragmentation in PC12 and NG108-15 (cholinergic-neuron-like) cells. METHODS: Apoptotic DNA fragmentation was quantified by CE-LIF. RESULTS: Sodium nitroprusside (SNP, 0.1-1.0 mM, 24 hours), NO donor, increased apoptotic DNA fragmentation in NG108-15 cells, but not PC12 cells (both with serum). In serum-deprived PC12 cells, ANP at 1, 10 and 100 nM inhibited apoptotic DNA fragmentation by 75.8%, 84.7%, and 94.1%, respectively. CONCLUSIONS: The data show that NO at higher levels induces apoptosis in NG108-15 cells, but not PC12 cells, indicating differences in susceptibility to NO-induced toxicity, and that ANP-induced cGMP elevation is a potent and effective inhibitor of apoptosis in PC12 cells. The data suggest that NO-induced cGMP elevations in certain neural cells (e.g. PC12 cells) provide a protective (anti-apoptotic) mechanism that counter-balances the pro-apoptotic actions of NO, thus helping to limit damage caused by NO.