Abstract

Coreopsis lanceolata L. is a perennial plant of the family Asteraceae, and its flower is known to contain flavonoids with various bioactivities. We evaluated the effect of Coreopsis lanceolata L. flower (CLF) extracts on H2O2-induced oxidative stress (OS) in neuronal cells and mouse neurons. The flowering part of CL was used as CLF1 (70% ethanol extract) and CLF2 (water extract), and 10 types of phenolic compounds were quantified using high-performance liquid chromatography. To evaluate the neuroprotective effects of CLF, the antioxidant activities of the extracts were measured, and the expression levels of antioxidant enzymes and proteins related to OS-induced apoptosis in neuronal cells and mouse neurons treated with the extracts were investigated. In the in vitro study, CLF ameliorated H2O2-induced oxidative stress and induced the expression of antioxidant enzymes in PC12 cells. Furthermore, CLF1 enhanced the expression of the Bcl-xL protein but reduced the expression of Bax and the cleavage of caspase-3. In the same manner, CLF1 showed neuroprotective effects against OS in vivo. Pretreatment with CLF1 (200 mg/kg) increased the Bcl-2 protein and decreased Bax compared with the 1-methyl-4-phenylpyridinium ion (MPP+)-treated C57BL/6 mice model group. Our results suggest that the protective effects of CLF1 on MPP+-induced apoptosis may be due to its anti-apoptotic activity, through regulating the expression of the Bcl-2 family. CLF1 exerts neuroprotective effects against OS-induced apoptosis in PC12 cells in a Parkinson’s disease model mouse. This effect may be attributable to the upregulation of Bcl-2 protein expression, downregulation of Bax expression, and inhibition of caspase-3 activation. These data indicate that CLF may provide therapeutic value for the treatment of progressive neurodegenerative diseases.

Highlights

  • IntroductionMost human neurodegenerative diseases such as Alzheimer’s disease (AD) and Parkinson’s disease (PD) are related to biological aging processes [1,2]

  • We evaluated the effects of CLF1 on the apoptotic pathway in MPTP-treated mouse brains

  • The results show that CLF1 could protect neurons from MPTP-induced apoptosis by downregulating the apoptotic pathway

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Summary

Introduction

Most human neurodegenerative diseases such as Alzheimer’s disease (AD) and Parkinson’s disease (PD) are related to biological aging processes [1,2]. One of the aging processes is to stop the accumulation of and increase in oxidative damage. This has been linked to the prevention of neurodegenerative diseases. The increase in oxidative stress (OS), which reduces the activity of antioxidant enzymes, occurs when normal cells in the body are attacked by reactive oxygen species (ROS), including superoxides and hydrogen peroxide (H2 O2 ) [3]. Antioxidant mechanisms are associated with decreased intracellular

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