Protective effects of Althaea officinalis L. extract in 6-hydroxydopamine-induced hemi-Parkinsonism model: behavioral, biochemical and histochemical evidence

Purpose: To investigation the protective effects of hesperetin against 6-hydroxydopamine (6-OHDA)- induced neurotoxicity. Methods: SH-SY5Y cells were incubated with 6-OHDA to create an in vitro model of neurotoxicity. This model was used to test the neuroprotective effects of hesperetin. Cell viability was assessed by MTT and lactate dehydrogenase (LDH) release assays. Flow cytometry and western blot were used to quantify apoptosis. Oxidative stress was evaluated by determining intracellular glutathione (GSH), malondialdehyde (MDA), superoxide dismutase (SOD), and reactive oxygen species (ROS). Results: In SH-SY5Y cells, treatment with 6-OHDA decreased cell viability and promoted LDH release. However, exogenous hesperetin protected against 6-OHDA-mediated toxicity. Similarly, although incubation with 6-OHDA induced apoptosis and increased cleaved caspase-3 and -9 levels, treatment with hesperetin protected against these effects. Treatment with 6-OHDA also led to significant oxidative stress, as indicated by reduced GSH and SOD levels and increased MDA and ROS levels in SH-SY5Y cells. However, these changes were reversed by pre-treatment with hesperetin. Of interest, hesperetin led to changes in 6-OHDA-induced expression of NRF2, heme oxygenase-1 (HO-1), glutamate-cysteine ligase (GCL) catalytic subunit (GCLC), and GCL modulatory (GCLM). Conclusion: Hesperetin protects against cell toxicity, apoptosis, and oxidative stress via activation of NRF2 pathway in a 6-OHDA-induced model of neurotoxicity. Future studies should investigate the use of hesperetin as a potential therapeutic approach for prevention or management of Parkinson’s disease. Keywords: Hesperetin, 6-OHDA, Neurotoxicity, NRF2, Parkinson’s disease

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Chinese Medicine PaBing-II Protects Human iPSC Derived Dopaminergic Neurons from Oxygen Stress

10.21203/rs.3.rs-179866/v1 ◽

2021 ◽

Author(s):

Shouhai Wu ◽

Tongxiang Lin ◽

Yang Xu

Keyword(s):

Oxidative Stress ◽

Chinese Medicine ◽

Pluripotent Stem Cells ◽

Dopaminergic Neurons ◽

Protective Effects ◽

Midbrain Dopaminergic Neurons ◽

Induced Pluripotent ◽

6 Hydroxydopamine ◽

Human Ipsc

Abstract BackgroundPaBing-II Formula (PB-II) is a traditional Chinese medicine developed to treat Parkinson's disease (PD). However, due to the complexity of PB-II and the difficulty of culturing human dopaminergic neurons (DAn) in vitro, the mechanism of PB-II to treat PD remains unclear. MethodsWe established the human induced pluripotent stem cells (iPSCs) and derived DAn from hiPSCs to study the protective effects of PB-II on DAn after oxidative stress, which plays an important role in PD pathogenesis. ResultsWe found that serum derived from rats that had ingested PB-II significantly protect hiPSC-derived DAn from reactive oxygen species (ROS). In addition, PB-II dependent serum can activate nuclear erythroid-derived factor 2 (Nrf2) responses, which are required for the neutralization of ROS. In addition, PB-II can activate the Nrf2/ARE signal pathway of midbrain dopaminergic neurons of PD rats induced with 6-hydroxydopamine (6-OHDA) injury, rescue DAn cells, and improve the symptoms of PD rats. ConclusionsPB-II significantly protects the DA neurons from oxidative stress by activating the Nrf2 pathway.

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Protective effects of 6‐gingerol on 6‐hydroxydopamine‐induced apoptosis in PC12 cells through modulation of SAPK/JNK and survivin activation

Journal of Biochemical and Molecular Toxicology ◽

10.1002/jbt.22956 ◽

2021 ◽

Author(s):

Farzaneh‐Sadat Rezazadeh‐Shojaee ◽

Elham Ramazani ◽

Jamal Kasaian ◽

Zahra Tayarani‐Najaran

Keyword(s):

Pc12 Cells ◽

Protective Effects ◽

Induced Apoptosis ◽

6 Hydroxydopamine

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Mitochondrial Ferritin Deletion Exacerbatesβ-Amyloid-Induced Neurotoxicity in Mice

Oxidative Medicine and Cellular Longevity ◽

10.1155/2017/1020357 ◽

2017 ◽

Vol 2017 ◽

pp. 1-10 ◽

Cited By ~ 16

Author(s):

Peina Wang ◽

Qiong Wu ◽

Wenyue Wu ◽

Haiyan Li ◽

Yuetong Guo ◽

...

Keyword(s):

Knockout Mice ◽

Memory Impairment ◽

Caspase 3 ◽

Disease Model ◽

Neurological Impairment ◽

Protective Effects ◽

Wild Type ◽

Iron Storage ◽

6 Hydroxydopamine ◽

Iron Storage Protein

Mitochondrial ferritin (FtMt) is a mitochondrial iron storage protein which protects mitochondria from iron-induced oxidative damage. Our previous studies indicate that FtMt attenuatesβ-amyloid- and 6-hydroxydopamine-induced neurotoxicity in SH-SY5Y cells. To explore the protective effects of FtMt onβ-amyloid-induced memory impairment and neuronal apoptosis and the mechanisms involved, 10-month-old wild-type andFtmtknockout mice were infused intracerebroventricularly (ICV) with Aβ25–35to establish an Alzheimer’s disease model. Knockout ofFtmtsignificantly exacerbated Aβ25–35-induced learning and memory impairment. The Bcl-2/Bax ratio in mouse hippocampi was decreased and the levels of cleaved caspase-3 and PARP were increased. The number of neuronal cells undergoing apoptosis in the hippocampus was also increased inFtmtknockout mice. In addition, the levels of L-ferritin and FPN1 in the hippocampus were raised, and the expression of TfR1 was decreased. Increased MDA levels were also detected inFtmtknockout mice treated with Aβ25–35. In conclusion, this study demonstrated that the neurological impairment induced by Aβ25–35was exacerbated inFtmtknockout mice and that this may relate to increased levels of oxidative stress.

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