Mitochondrial-targeted metal-phenolic nanoparticles to attenuate intervertebral disc degeneration: Alleviating oxidative stress and mitochondrial dysfunction
As intervertebral discdegeneration(IVDD)proceeds, the dysfunctional mitochondria disrupt the viability of nucleus pulposuscells, initiatingthedegradationof theextracellularmatrix. To date, there is a lack of effective therapies targeting the mitochondria of nucleus pulposus cells. Here, we synthesized polygallicacid-manganese(PGA-Mn)nanoparticlesviaself-assembly polymerizationofgallicacidinanaqueousmediumandintroduceda mitochondrial targetingpeptide(TP04)ontothenanoparticlesusing aSchiffbaselinkage, resultinginPGA-Mn-TP04nanoparticles.With a size smaller than50nm, PGA-Mn-TP04possesses pH-buffering capacity, avoiding lysosomal confinementandselectivelyaccumulat ingwithinmitochondriathroughelectrostaticinteractions.Therapid electronexchangebetweenmanganeseionsandgallicacidenhances theredoxcapabilityofPGA-Mn-TP04, effectivelyreducingmitochondrialdamagecausedbymitochondrial reactiveoxygen species.Moreover,PGA-Mn-TP04restoresmitochondrial functionbyfacilitatingthefusionofmitochondriaandminimizing theirfission, therebysustaining thevitalityofnucleuspulposus cells. Intherat IVDDmodel,PGA-Mn-TP04maintained intervertebraldischeightandnucleuspulposustissuehydration. ItoffersanonoperativetreatmentapproachforIVDDand other skeletalmusclediseases resulting frommitochondrial dysfunction, presentinganalternative to traditional surgical interventions.
As intervertebral discdegeneration(IVDD)proceeds, the dysfunctional mitochondria disrupt the viability of nucleus pulposuscells, initiatingthedegradationof theextracellularmatrix. To date, there…
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