Abstract
Increased endoplasmic reticulum (ER) stress is known to be one of the causes of hypothalamic neuronal damage, as well as a cause of metabolic disorders such as obesity and diabetes. Recent evidence has suggested that Undaria pinnatifida (UP), an edible brown algae, has antioxidant activity. However, the neuroprotective effect of UP has yet to be examined. In this study, to investigate the neuroprotective effect of UP on ER stress-induced neuronal damage in mouse hypothalamic neurons, mice immortal hypothalamic neurons (GT1-7) were incubated with extract of UP. ER stress was induced by treating with tunicamycin. Tunicamycin induced apoptotic cell death was compared with the vehicle treatment through excessive ER stress. However UP protected GT1-7 cells from cell death, occurring after treatment with tunicamycin by reducing ER stress. Treatment with UP resulted in reduced increment of ATF6 and CHOP, and recovered the decrease of phosphorylation of Akt/mTOR by tunicamycin and the increment of autophagy. These results show that UP protects GT1-7 cells from ER stress induced cell death through the Akt/mTOR pathway. The current study suggests that UP may have a beneficial effect on cerebral neuronal degeneration in metabolic diseases with elevated ER stress.
Highlights
The endoplasmic reticulum (ER) provides a unique environment for the synthesis, folding, and maturation of secreted and transmembrane proteins
Undaria pinnatifida (UP) Has a Protective Effect in Tunicamycin-Induced Cell Death 2.1
Iμnga/mddLi)tiofonr, n2o4 ehfferectssulotnedceilnl vaitatebniluitaytiowneoref toubnsiecarvmeydciant-itnhdeuccoendcceenltlrdaetiaotnhs(FoifguUrPe 1uBs)e.dIninadtdhietiocun,rrneonet fsfetuctdsyon(Fcieglul rveia1bCil)i.tyTwheesre roebssuelrtvs erdaisaetdthtehecopnocsesnibtirlaityiotnhsaot fUUPPhuasseadbiennethfiecicaul rerfefencttsatugadiyns(tFitguunricea1mCy).ciTnh-iensdeurceesdulctselrladiseeadththine GpoTs1s-i7bicleitlyls.that UP has a beneficial effect against tunicamycin-induced cell death in GT1-7 cells
Summary
The endoplasmic reticulum (ER) provides a unique environment for the synthesis, folding, and maturation of secreted and transmembrane proteins. To counteract ER stress, the cell activates the unfolded protein response (UPR) to restore cellular homeostasis by clearing the misfolded protein within the ER lumen. Under severe and prolonged ER stress, when homeostasis cannot be restored, UPR activates unique pathways that lead to cell death through apoptosis [2]. Disruption of these physiological functions by ER stress has been implicated in a wide variety of human diseases, including Alzheimer’s disease, Parkinson’s disease, neuronal damage by ischemia, prion dMiosleecauslees,2c0y15s,t2ic0, pfiabgreo–spiasg,eobesity, and diabetes mellitus [1,3]. Hypothalamic ER stress has been suggested to cause feeding behavior disorder and glucose dysregulation as for obesity and dsuiagbgeetsetse[d4–t7o]. Hypothalamic ER stress has been suggested to cause feeding behavior disorder and glucose dysregulation as for obesity and dsuiagbgeetsetse[d4–t7o]. cause feeding behavior disorder and glucose dysregulation as for obesity and diabeTthees [e4d–i7b]l.e brown algae Undaria pinnatifida (UP) is widely distributed in Northeast Asia (China, JapanT,haeneddiKbloerebaro).wFnucaolgidaeanU, nadacrliaaspsinonfatfiuficdoase(U-ePn)riicshwedidesluylfdaitsetdribpuotleydsaicncNhaorritdheesa, sdt Aersiviaed(Cfhrionma, UJaPpahna,sabnedenKorerepao)r.teFductooidhaanv,eavcalraisosusofbifoulcoogsiec-aelnarcicthiveidtiessu, lifnatceluddpinoglyasanctic-htuarmidoer,s,adnetir-iovxeiddaftriovme, aUnPti-hinaflsabmemenatroerpyo, rtaendti-tvoirhaal,veanvdaraionutis-abnigoilooggeicnailc apcrtoivpietiretsie, sin[c8l,u9d].inRgecaennttil-ytu, mUoPr, wanasti-sohxoidwantivteo, aatntrtia-cint fdlaemvemloaptomreyn, tanatni-dvicroaml, panledxiatnytio-fanngeiuorgoennsic[1p0r,o1p1]e.rtHieosw[8e,9v]e.rR, encoensttulyd, yUPtowealuscsihdoawtenthtoe adttirreacctt edfefevcetloopfmUePnt oanndEcRomstprelesxsitaynodf EneRursotrnesss[-1i0n,d11u]c.eHdocwelelvedre,antho sitnudhyyptootehlaulcaimdaicte ntheue rdoinrescthaefsfebceteonf rUepPoortnedE.RThsetrreesfosrea,nsdinEceRhsytpreosths-ainladmuicceEdRcsetlrlesdsehatahd bineehnywpoidthelaylacmonicsidneeruerdonass ahnaaspbpereonacrhetpoowrtaerdd. pTrheevreenfotiroen, sionfceobheyspitoythaanladmdiicaEbRetsetsr,eswsehawdebreeeinntweridesetleydcoinnswidheerethdearsUanPaaplpsorohaacsh taowpraortdecptriveveeenftfieocnt forfomobEesRitsytraenssd-inddiaubceetdesn, ewureonwaelrceelilndteeraetsht.edInitnhiws shteutdhye,rwUePdeamlsoonhsatrsataedprtohteecstuipvepreefsfseicotnferoffmectEoRf estthreasnso-ilnedxutrcaecdt noefuUrPonoanl cEeRll sdtereasths-.inInduthciesdstcuedllyd, ewaethdoenmGonTs1t-r7atceedllsth, eansdupapttreemsspiotendetfofecetxaomf eitnheatnhoel mexetcrahcatnoisfmUPbyonwEhRicshtrUesPs-hinads uancetid-acpeollpdteoatitchaocntiGviTty1-a7gcaeilnlss,taEnRdsattrteesms.pted to examine the mechanism by which UP has anti-apoptotic activity against ER stress
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