We previously reported that Smilacis chinae rhizome inhibits amyloid b protein (25—35) (Ab (25—35))-induced
neurotoxicity in cultured rat cortical neurons. The present study evaluated the neuroprotective effect of
oxyresveratrol isolated from Smilacis chinae rhizome against Ab (25—35)-induced neurotoxicity on cultured rat
cortical neurons. Oxyresveratrol over the concentration range of 1—10mM significantly inhibited 10mM Ab (25—
35)-induced neuronal cell death, which was measured by a 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl-tetrazolium
bromide (MTT) assay and Hoechst 33342 staining. Oxyresveratrol (10mM) inhibited 10mM Ab (25—35)-induced
elevation of cytosolic calcium concentration ([Ca2]c), which was measured by a fluorescent dye, Fluo-4 AM.
Oxyresveratrol (1, 10mM) also inhibited glutamate release into medium and reactive oxygen species (ROS) generation
induced by 10mM Ab (25—35). These results suggest that oxyresveratrol prevents Ab (25—35)-induced
neuronal cell damage by interfering with the increase of [Ca2]c, and then by inhibiting glutamate release and
ROS generation. Furthermore, these effects of oxyresveratrol may be associated with the neuroprotective effect
of Smilacis chinae rhizome.
We previously reported that Smilacis chinae rhizome inhibits amyloid b protein (25—35) (Ab (25—35))-inducedneurotoxicity in cultured rat cortical neurons. The present study evaluated the neuroprotective effect ofoxyresveratrol isolated from Smilacis chinae rhizome against Ab (25—35)-induced neurotoxicity on cultured ratcortical neurons. Oxyresveratrol over the concentration range of 1—10mM significantly inhibited 10mM Ab (25—35)-induced neuronal cell death, which was measured by a 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl-tetrazoliumbromide (MTT) assay and Hoechst 33342 staining. Oxyresveratrol (10mM) inhibited 10mM Ab (25—35)-inducedelevation of cytosolic calcium concentration ([Ca2]c), which was measured by a fluorescent dye, Fluo-4 AM.Oxyresveratrol (1, 10mM) also inhibited glutamate release into medium and reactive oxygen species (ROS) generationinduced by 10mM Ab (25—35). These results suggest that oxyresveratrol prevents Ab (25—35)-inducedneuronal cell damage by interfering with the increase of [Ca2]c, and then by inhibiting glutamate release andROS generation. Furthermore, these effects of oxyresveratrol may be associated with the neuroprotective effectof Smilacis chinae rhizome.
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