HericiumErinaceus (HE) is a medicinal plant known to possess anticarcinogenic, antibiotic and antioxidant activities. It has been shown to have a protective effect against ischemia-injury-induced neuronal cell death in rats. As an extending study, here we examined inpheochromocytoma 12(PC12)cells, whether HE could exert a protective effect against oxidative stress and apoptosis induced by di(2-ethylhexyl)phthalate (DEHP), a plasticizer known to cause neurotoxicity. We demonstrate that pretreatment with HEsignificantly attenuated DEHP induced cell death. This protective effect may be attributed to its ability to reduce intracellular reactive oxygen species levels, preserving the activity of respiratory complexes and stabilizing the mitochondrial membrane potential. Additionally, HE pretreatment significantly modulated Nrf2 and Nrf2-dependent vitagenes expression, preventing the increase of pro-apoptoticand the decrease of anti-apoptotic markers. Collectively, our data provide evidence of new preventive nutritional strategy using HE against DEHP-induced apoptosis in PC12 cells.
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Titolo: | Hericium Erinaceus prevents DEHP-induced mitochondrial dysfunction and apoptosis in PC12 cells |
Autori: | |
Data di pubblicazione: | 2020 |
Rivista: | |
Abstract: | HericiumErinaceus (HE) is a medicinal plant known to possess anticarcinogenic, antibiotic and antioxidant activities. It has been shown to have a protective effect against ischemia-injury-induced neuronal cell death in rats. As an extending study, here we examined inpheochromocytoma 12(PC12)cells, whether HE could exert a protective effect against oxidative stress and apoptosis induced by di(2-ethylhexyl)phthalate (DEHP), a plasticizer known to cause neurotoxicity. We demonstrate that pretreatment with HEsignificantly attenuated DEHP induced cell death. This protective effect may be attributed to its ability to reduce intracellular reactive oxygen species levels, preserving the activity of respiratory complexes and stabilizing the mitochondrial membrane potential. Additionally, HE pretreatment significantly modulated Nrf2 and Nrf2-dependent vitagenes expression, preventing the increase of pro-apoptoticand the decrease of anti-apoptotic markers. Collectively, our data provide evidence of new preventive nutritional strategy using HE against DEHP-induced apoptosis in PC12 cells. |
Handle: | http://hdl.handle.net/11586/258986 |
Appare nelle tipologie: | 1.1 Articolo in rivista |