Protective Effects of Jujubosides on 6-OHDA-Induced Neurotoxicity in SH-SY5Y and SK-N-SH Cells

Abstract

6-hydroxydopamine (6-OHDA) is used to induce oxidative damage in neuronal cells, which can serve as an experimental model of Parkinson’s disease (PD). Jujuboside A and B confer free radical scavenging effects but have never been examined for their neuroprotective effects, especially in PD; therefore, in this study, we aimed to investigate the feasibility of jujubosides as protectors of neurons against 6-OHDA and the underlying mechanisms. 6-OHDA-induced neurotoxicity in the human neuronal cell lines SH-SY5Y and SK-N-SH, was used to evaluate the protective effects of jujubosides. These findings indicated that jujuboside A and B were both capable of rescuing the 6-OHDA-induced loss of cell viability, activation of apoptosis, elevation of reactive oxygen species, and downregulation of the expression levels of superoxide dismutase, catalase, and glutathione peroxidase. In addition, jujuboside A and B can reverse a 6-OHDA-elevated Bax/Bcl-2 ratio, downregulate phosphorylated PI3K and AKT, and activate caspase-3, -7, and -9. These findings showed that jujubosides were capable of protecting both SH-SY5Y and SK-N-SH neuronal cells from 6-OHDA-induced toxicity via the rebalancing of the redox system, together with the resetting of the PI3K/AKT apoptotic signaling cascade. In conclusion, jujuboside may be a potential drug for PD prevention.

Resveratrol Karbon Noktalarının SH-SY5Y İnsan Nöroblastoma Hücrelerinde 6-OHDA Kaynaklı Nöronal Hücre Ölümü Üzerinde Koruyucu Etkileri

“…Caspase-3 is a considerable component of the cysteine protease family in the mitochondrial apoptotic pathway (24). In this report, when cells were subjected to 6-OHDA, the mRNA expression of caspase-3 was markedly enhanced beckoning the 6-OHDA-induced apoptosis in SH-SY5Y cells, confirming previous studies (24,25). In opposition, the RES C-Dots treatment at all concentrations down-regulated caspase-3 expression and showed antiapoptotic effects.…”

Multitarget Protective Effects of JUB on Aβ-Induced Neurotoxicity and the Mechanism Predication Using Network Pharmacology Analysis

“…Some nematodes still survived at 270 min (10 mM) and 210 min (20 mM) after 200 μM of JUB pretreatment (Figure A). ROS interacted with NO to form a more toxic molecule that attacked neuronal cells nonspecifically . ROS destroys cellular components such as lipoprotein receptor-related proteins, lipids, and DNA, causing Aβ to flow out of the brain through the blood–brain barrier and accumulate in the blood .…”

The Protection of EGCG Against 6-OHDA-Induced Oxidative Damage by Regulating PPARγ and Nrf2/HO-1 Signaling

“…There are several proposed mechanisms of the 6-OHDA neurotoxicity, including free radicals damage, mitochondrial dysfunction, and oxidative stress. 25 , 26 6-OHDA can alter the expression of iron-related proteins, resulting into perturbed iron homeostasis. 27 , 28 6-OHDA can also cause iron release from cytosolic ferritin and increase intracellular free iron concentration.…”