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Protective effect of fangchinoline on cyanide-induced neurotoxicity in cultured rat cerebellar granule cells

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Abstract

The present study was performed to examine the effect of fangchinoline, abis- benzylisoquin-oline alkaloid, which exhibits the characteristics of a Ca2+ channel blocker, on cyanide-induced neurotoxicity using cultured rat cerebellar granule neurons. NaCN produced a concentrationdependent reduction of cell viability, which was blocked by MK-801, an N-methyl-D-aspartate (NMDA) receptor antagonist, verapamil, L-type Ca2+ channel blocker, and L-NAME, a nitric oxide synthase inhibitor. Pretreatment with fangchinoline over a concentration range of 0.1 to 10μM significantly decreased the NaCN-induced neuronal cell death, glutamate release into medium, and elevation of [Ca2+]i and oxidants generation. These results suggest that fangchinoline may mitigate the harmful effects of cyanide-induced neuronal cell death by interfering with [Ca2+], influx, due to its function as a Ca2+ channel blocker, and then by inhibiting glutamate release and oxidants generation.

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Correspondence to Yeon Hee Seong.

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Cho, S.O., Seong, Y.H. Protective effect of fangchinoline on cyanide-induced neurotoxicity in cultured rat cerebellar granule cells. Arch Pharm Res 25, 349–356 (2002). https://doi.org/10.1007/BF02976638

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