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Abstract
Here, we investigated whether hirsutenone, a compound isolated from Alnus japonica, was able to attenuate oxidative stress-induced death in transformed retinal ganglion (RGC-5) cells. Hirsutenone effectively protected RGC-5 cells from oxidative insult induced by, l-buthionine-(S,R)-sulfoximine (BSO) plus glutamate in a concentration-dependent manner, as demonstrated by propidium iodide (PI)/Hoechst 33342 double staining, flow cytometry, and MTT assays. Moreover, hirsutenone inhibited the increase in apoptotic protein expression resulting from BSO plus glutamate. Hirsutenone also effectively inhibited sodium nitroprusside (SNP)-induced lipid peroxidation in rat brain homogenates. To investigate the effects of hirsutenone in vivo, we used N-methyl-d-aspartate (NMDA) as a negative insult on the retinas of rats. NMDA affects the thinning of the inner plexiform layer (IPL) and causes an increase in the number of terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL)-positive ganglion cells in the ganglion cell layer (GCL). Hirsutenone treatment led to a reduction in NMDA-induced IPL and TUNEL staining of the GCL. In conclusion, hirsutenone isolated from A. japonica may act as neuroprotective agent for conditions such as glaucoma.
Published Version
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