Background: Nowadays, as technology and medical treatment improvements contribute to extending the lives of human beings, it also causes many diseases like noninfectious chronic and neurodegenerative with an aging population. Alzheimer’s disease (AD) is one of the most common neurodegenerative diseases. It almost always occurs in older adults whose age is above 65 years old. AD is clinically characterized by a progressive loss of cognitive abilities. Pathologically, it is defined by the appearance of senile plaques-extracellular insoluble, congophilic protein aggregates composed of amyloid β (Aβ), resulting in oxidative stress, mitochondrial disorders, synaptic atrophy, leading to function degradation of the brain. The scientific name of adlay is Coix lacryma-jobi L., which is an annual botanical.
Methods: This research uses the adlay hull, as a test sample in the experiment. The 95% ethanol extract of adlay hull (AHEE) was partitioned by ethyl acetate (AHEAE), n-butanol (AHBUE) and water (AHWE) subsequently, and the test of extracts by LPSinduce a RAW264.7 inflammatory response and Aβ25-35-induces dPC12 cells which cause neurotoxicity as an experimental model, respectively. Investigate the inflammatory and anti-apoptosis related protein expression.
Results: The results shown that the AHEE, AHEAE and AHWE exert antiinflammatory effects, AHWE also have anti-apoptosis effects. Through mouse macrophages inflammatory protein expression experiments, as well as inhibition of iNOS expression, resulted in inhibited nitrite production. In this study, we investigated the protective effects of AHWE against the Aβ25-35-induced neurotoxicity in dPC12 cells and explored the underlying mechanism. The results showed that pretreatment with AHWE significantly attenuated cell death and the elevated Bax/Bcl-2 ratio evoked by Aβ25-35. Moreover, AHWE significantly inhibited Aβ25-35 and enhanced the protein levels of Akt in dPC12 cells. These observations unambiguously suggested that the protective effect of AHWE against Aβ25-35-induced apoptosis in dPC12 cells was associated with the enhancement of the PI3K/Akt signaling pathway.
Conclusion: The results showed that adlay hull extracts have the anti-oxidant, antiinflammatory, anti-apoptotic and neuroprotective property. These results suggest that adlay hull extracts may have a preventive therapeutic potential in the management of AD.