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DOI: 10.1055/s-0030-1264871
The protective effect of luteolin on amyloid β protein (25–35)-induced neurotoxicity in primary rat cortical neuron cells and possible mechanisms
It is well known that neurodegeneration of the amyloid β peptide (Aβ) plays a major part in the memory dysfunction observed in early stages of Alzheimer's disease which shows a significant extent of oxidative damage. The flower bud of Lonicera japonica Thunb. has been shown to possess antibacterial, antipyretic and anti-inflammatory effects. Luteolin, belongs to favonoid compounds, is a main active constituent of Lonicerae Flos. In modern pharmacological studies, Luteolin possesses DNA protective effect, anti-inflammatory, anti-oxidant, and is a free radical scavenger.


Fig.1: Chemical structure of Luteolin and protective effect of Luteolin
The present study was carried out to investigate the neuroprotective effect of Luteolin on amyloid β (25–35)-induced neuro-toxicity using cultured rat cortical cells. After exposure of primary cultures of rat cortical cells to 10µM Aβ (25–35) for 48h, it exhibited marked apoptotic death. Pretreatment with Luteolin (1, 10µM) significantly protected cortical cell cultures against Aβ (25–35)-induced toxicity. Luteolin (1, 10µM) showed a concentration-dependent inhibition on 10µM Aβ (25–35)-induced apoptotic neuronal death, as assessed by MTT assay. Furthermore, Luteolin reduced apoptotic characteristics by DAPI staining. For Western blot analysis, the results showed that protective effect of Luteolin on Aβ (25–35)-induced neurotoxicity was mediated by preventing of p-ERK, JNK, p-JNK, p-P38 and caspase 3 activations in rat primary cortical cells. Taken together, the results suggest that Luteolin prevents Aβ (25–35)-induced apoptotic neuronal death through inhibiting the protein level of JNK, ERK and p38 MAP kinases and caspase 3 activations.
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