Abstract
Hericium Erinaceus (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 in pheochromocytoma 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 demonstrated that pretreatment with HE significantly 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-apoptotic and 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.
Highlights
Phthalates are common plasticizers, used in a large variety of household and medical products to confer flexibility to many polyvinyl chlorides (PVC)–based plastics [1]
Here we examined in pheochromocytoma 12 (PC12) cells, whether Hericium Erinaceus (HE) could exert a protective effect against oxidative stress and apoptosis induced by di(2-ethylhexyl)phthalate (DEHP), a plasticizer known to cause neurotoxicity
Excessive reactive oxygen species (ROS) generation, membrane potential (MMP) disturbance, and modulation of pro and anti-apoptotic proteins play a key role in neuronal apoptosis, we tested by western blotting analysis the effect of DEHP on apoptotic protein expression in PC12 cells
Summary
Phthalates are common plasticizers, used in a large variety of household and medical products to confer flexibility to many polyvinyl chlorides (PVC)–based plastics [1]. After treatment with DEHP, an increase in the level of Nrf was observed, but pretreatment of cells with HE, modulated redox induced Nrf expression (Figure 5). Pretreatment of cells by HE for 2 h, significantly modulates expression of stress responsive vitagenes (Figures 3a,b and 4a,b). Excessive ROS generation, MMP disturbance, and modulation of pro and anti-apoptotic proteins play a key role in neuronal apoptosis, we tested by western blotting analysis the effect of DEHP on apoptotic protein expression in PC12 cells. DEHP treatment (NFieguurroed7eag,ebn).eTrahtiisveinddiuscotridonerws aasreasassoscoicaitaetdedwwithiththme oitvoecrheoxnpdrersiasiodnysoffupnrcotiaopnosp, taolttiecration of the protein, Baxr(eFsipgiurraeto7ray,bc)h,aainndcowmitphleaxdees,cMreaMsePidneacnretaiaspe,oapntodtRicOpSrointecirne,aBsecl[243(F].igEuxrcees7saiv,be).RAOlSl tgheenseeration, MMP effects weredpirsetuvrebnatendceb, yanpdremtroedautmlaetinotnwofitphroHaEn(dFaignutir-eap7oap,bt)o.tiWc pernoetexitnesxpalmayinaekdeyinrvoolelvinemneeunrtoonfal apoptosis, caspase 3 in tahpuospwtoesistepstaetdhwbayyws.eWsteesrnterbnlobtltointtginagnaanlyasliyssitshesheofwfeecdt othf aDtEDHEPHoPntraepatompteontticrepsruoltteeidninexpression in increased levPeCl o12f ccleelalsv.ed active caspase 3 (Figure 7a,b). Western blotting analysis showed that DEHP treatment resulted in increased level of cleaved active caspase 3 (Figure 7a,b). Our results indicate the involvement of the caspase-mediated apoptosis pathway
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