Neuroprotective Effects of Coreopsis lanceolata Flower Extract against Oxidative Stress-Induced Apoptosis in Neuronal Cells and Mice

• Published in: Antioxidants Vol. 10; no. 6; p. 951
• Main Authors: Kim, Hyung Don, Lee, Ji Yeon, Park, Jeong-Yong, Kim, Dong Hwi, Kang, Min Hye, Seong, Hyun-A, Seo, Kyung Hye, Ji, Yun-Jeong
• Format: Journal Article
• Language: English
• Published: Basel MDPI AG 12-06-2021; MDPI
• Subjects: Acids; Alzheimer's disease; Antioxidants; Apoptosis; BAX protein; Bcl-2 protein; Bcl-x protein; Caspase-3; Coreopsis lanceolata; Coreopsis lanceolate; Enzymes; Ethanol; Flavonoids; Flowering; High-performance liquid chromatography; Hydrogen peroxide; Movement disorders; MPP; MPTP; Neurodegenerative diseases; Neuroprotection; neuroprotective; Nitric oxide; Oxidative stress; Parkinson's disease; PC12 cells; Penicillin; Phenolic compounds; Phenols; Pheochromocytoma cells; Reagents; St Louis Missouri; Canada; United States > US
• ISSN: 2076-3921; 2076-3921
• DOI: 10.3390/antiox10060951

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.