Objective: To explore the anti-apoptotic effects of Piper bitle leaf extract (PLE) on 6-OHDA induced cellular injury in human neuroblastoma cell SH-SY5Y. To analyse the neuroprotective effects of PLE in Parkinson’s disease C. elegans model

Background: The molecular pathogenesis leading to neurodegeneration of dopaminergic neurons in PD is largely unknown. There is a need of an effective therapy to control the progression of proteinopathies. PLE attenuates 6-OHDA induced apoptotic events by regulating various signalling cascades in SH-SY5Y cells, and PLE ameliorates the α-synuclein accumulation, DAergic neurodegeneration, restore the lipid content and increase the lifespan of C. elegans treated with 6-OHDA.

Methods: SH-SY5Y: Cell viability, LDH release, nuclear condensation, detection of apoptosis, mitochondrial membrane potential, cell cycle and western blot analysis. C.elegans : α-synuclein aggregation, lipid deposition, DAergic neurodegeneration and lifespan analysis. 

Results: The results revealed that pre-treatment with PLE in SH-SY5Y cells prior to 6-OHDA exposure improves the cell viability, decrease the LDH release, reverse mitochondrial transmembrane abnormalities, restore the Bax/Bcl2 ratio, and cytochrome c release. Meanwhile, PLE inhibits the phosphorylation of MAPKs (p38, JNK and ERK) pathway and p53 activation. Moreover, PLE could increase the expression of PI3K/Akt. In addition, PLE could significantly decrease the α-synuclein aggregation; attenuates the DAergic neurodegeneration; ameliorate the lipid content in NL5901 worms; increased the lifespan and decreased the lipofuscin in 6-OHDA treated N2 wild type worms.

Conclusions: Findings demonstrated that PLE exerts its neuroprotective effect by anti-oxidative and anti-apoptotic ability. Moreover, PLE has a potent anti-parkinsonism effects and this effect was driven by the inhibition of neurotoxicity, apoptotic cascade events, and ROS-mediated activation of downstream signalling pathways, MAPKs and PI3K/Akt. Studies were strongly proves that PLE exhibits strong ameliorative futures against α-synuclein accumulation, DAergic neurodegeneration and physiological impairments induced by 6-OHDA. Taken together, we believe that PLE was a potent candidate for the prevention of neurodegeneration in the patients with PD.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/piper-betle-l-attenuates-6-ohda-induced-apoptosis-in-sh-sy5y-cells-and-neuronal-injury-in-caenorhabditis-elegans-parkinsons-model/