4-Hydroperoxy-2-decenoic acid ethyl ester protects against 6-hydroxydopamine-induced cell death via activation of Nrf2-ARE and eIF2α-ATF4 pathways

Inoue, Yuki; Hara, Hirokazu; Mitsugi, Yukari; Yamaguchi, Eiji; Kamiya, Tetsuro; Itoh, Akichika; Adachi, Tetsuo

doi:10.1016/j.neuint.2017.08.011

Cited by 34 publications

(51 citation statements)

References 38 publications

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“…PD brains exhibit exceptionally high levels of autoxidation and enzymatic oxidation of dopamine resulting in high emission of reactive oxygen species (ROS). ROS stimulates mitochondrial dysfunction of respiratory chain complex I in the SNC resulting in activation of apoptotic signaling pathways, finally leading to neuronal cell death [ 12 , 13 ]. In addition, mitochondrial impairment—caused by mutations in certain genes such as α -synuclein, parkin, protein deglycase (DJ-1), and PTEN-induced kinase 1 (PINK1)—leads to further ROS production in dopaminergic neurons of the SNC resulting in several brain changes such as higher metabolic stress, increased synaptic aberrations, and low expression of neuroprotective factors, which all lead to a highly selective nigrostriatal dopaminergic degeneration [ 12 , 14 – 16 ].…”

Section: The Pathology Underlying Parkinson's Diseasementioning

confidence: 99%

“…Royal jelly is an acidic, pungent smelling, yellow-whitish, creamy substance excreted from the pharyngeal gland of young Apis mellifera bee workers [ 13 , 52 , 53 ]. RJ is a complex material ( Figure 2 ).…”

Section: Apitherapy As a Possible Complementary Treatment For Parkmentioning

confidence: 99%

“…Rotenone was used in one study to induce PD in rodents via inhibition of mitochondrial complex I of the mitochondrial respiratory chain, which was associated with high emission of mitochondrial ROS and induction of apoptosis via activation of caspase-3 [ 44 ]. 6-Hydroxydopamine (6-OHDA) has been used both in vivo and in vitro in 6 studies to induce PD [ 13 , 42 , 45 , 79 , 82 , 83 ]. It selectively provokes apoptosis of dopaminergic neurons via mechanisms that involve increasing the production of ROS, accelerating lipid peroxidation (production of malondialdehyde (MDA)), and evoking an imbalance between the antiapoptotic B cell lymphoma 2 (bcl-2) and the proapoptotic bcl-2-associated X protein (bax) [ 79 ].…”

Section: Animal Models Of Parkinson's Diseasementioning

confidence: 99%

“…PB conferred protection against cytotoxicity induced by MPP+ and 6-OHDA in vitro through upregulation of the expression of heme oxygenase-1 (HO-1) [ 85 , 86 ], superoxide dismutase (SOD), and γ -glutamylcysteine synthetase ( γ -GCS) [ 79 ]. An in vitro study involving application of 6-OHDA to human neuroblastoma SH-SY5Y cells to induce cell death as a model of PD showed that treatment with a derivative of RJ lipids known as 4-hydroperoxy-2-decenoic acid ethyl ester (HPO-DAEE) markedly stimulated the expression of antioxidant genes such as HO-1, γ -glutamylcysteine ligase ( γ -GCL), and NAD(P)H quinone dehydrogenase 1 (NQO1) [ 13 ].…”

Section: Mechanisms Of Action Of Propolis and Royal Jelly In Parkimentioning

confidence: 99%

“…Western blot analysis shows that the antioxidant effects of PB and HPO-DAEE in SH-SY5Y cells result from activation of 2 main signaling pathways: nuclear factor erythroid 2- (NRF2-) antioxidant response element (ARE), which is a main regulator of antioxidative responses, and eukaryotic initiation factor 2 α (eIF2 α ), an upstream effector of the activating transcription factor-4 (ATF4), which cooperates with NRF2 to modulate the expression of antioxidant genes [ 13 , 86 ]. Interestingly, the mechanism through which HPO-DAEE exerts its antioxidant effect involves slight emission of ROS upon HPO-DAEE treatment, which represents a sublethal stress that causes preconditioning of SH-SY5Y cells against subsequent severer oxidative stress induced by 6-OHDA.…”

Section: Mechanisms Of Action Of Propolis and Royal Jelly In Parkimentioning

confidence: 99%

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Apitherapy for Parkinson’s Disease: A Focus on the Effects of Propolis and Royal Jelly

Ali

2020

Oxidative Medicine and Cellular Longevity

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The vast increase of world’s aging populations is associated with increased risk of age-related neurodegenerative diseases such as Parkinson’s disease (PD). PD is a widespread disorder characterized by progressive loss of dopaminergic neurons in the substantia nigra, which encompasses a wide range of debilitating motor, emotional, cognitive, and physical symptoms. PD threatens the quality of life of millions of patients and their families. Additionally, public welfare and healthcare systems are burdened with its high cost of care. Available treatments provide only a symptomatic relief and produce a trail of noxious side effects, which increase noncompliance. Hence, researchers have recently focused on the use of nutraceuticals as safe adjunctive treatments of PD to limit its progress and associated damages in affected groups. Propolis is a common product of the beehive, which possesses a large number of therapeutic properties. Royal jelly (RJ) is a bee product that is fed to bee queens during their entire life, and it contributes to their high physical fitness, fertility, and long lifespan. Evidence suggests that propolis and RJ can promote health by preventing the occurrence of age-related debilitating diseases. Therefore, they have been used to treat various serious disorders such as diabetes mellitus, cardiovascular diseases, and cancer. Some evolving studies used these bee products to treat PD in animal models. However, a clear understanding of the collective effect of propolis and RJ as well as their mechanism of action in PD is lacking. This review evaluates the available literature for the effects of propolis and RJ on PD. Whenever possible, it elaborates on the underlying mechanisms through which they function in this disorder and offers insights for fruitful use of bee products in future clinical trials.

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Section: The Pathology Underlying Parkinson's Diseasementioning

confidence: 99%

Section: Apitherapy As a Possible Complementary Treatment For Parkmentioning

confidence: 99%

Section: Animal Models Of Parkinson's Diseasementioning

confidence: 99%

Section: Mechanisms Of Action Of Propolis and Royal Jelly In Parkimentioning

confidence: 99%

Section: Mechanisms Of Action Of Propolis and Royal Jelly In Parkimentioning

confidence: 99%

See 3 more Smart Citations

Apitherapy for Parkinson’s Disease: A Focus on the Effects of Propolis and Royal Jelly

Ali

2020

Oxidative Medicine and Cellular Longevity

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Dose‐Dependent Effects of Royal Jelly on Estrogen‐ and Progesterone‐Induced Mammary Gland Hyperplasia in Rats

Liu

Wang

et al. 2022

Molecular Nutrition Food Res

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Scope: Royal jelly (RJ) has a wide range of biological functions, its effect on hyperplasia of the mammary gland (HMG) in mammals is unclear. This study aims to investigate the effect of RJ on HMG and the dose-response relationship of RJ in the treatment of HMG. Methods and Results: HMG rats are induced by intramuscular injection of estrogen (E2) and progesterone, and are treated with different doses of RJ (100, 200, 400, and 800 mg kg -1 d -1 ). As a result, RJ improves the expansion of acinar and breast tissue ducts, particularly at 100 and 800 mg kg -1 d -1 . These two doses also inhibit serum E2 and prolactin (PRL) secretion and increase serum progesterone secretion and the expression of estrogen receptor (ER)-𝜷 in the breast tissue. In addition, 800 mg kg -1 d -1 decrease and increase the mRNA expression of, respectively, hypothalamic gonadotropin-releasing hormone (GnRH) and pituitary GnRH receptors (GnRH-R). The lowest dosage (100 mg kg -1 d -1 ) increases GnRH-R mRNA expression as well. However, the effects of 200 and 400 mg kg -1 d -1 RJ on the reproductive parameters of HMG are not significant, implying a dose-dependent effect. Conclusion: RJ regulates endocrine dyscrasia in HMG rats and improves the breast tissue structure, indicating its potential in the prevention and treatment on HMG.

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Bee honey protects astrocytes against oxidative stress: A preliminary in vitro investigation

Ali

2019

Neuropsychopharm Rep

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Aim: Bee honey is widely used as a bioactive food to improve general health and produce therapeutic benefits in various physical disorders. It also improves cognitive and mood-related behaviors and symptoms in mice and humans. Still, its direct effect on brain cells is unclear. Here, we examined the effect of whole honey on the survival of astrocytes exposed to oxidative stress.Methods: Cultured cortical astrocytes were treated with honey (0.1%, 0.3%, 0.5%, 0.6%, 0.7%, 0.8%, 0.9%, 1%, 3%, and 5% [v/v]) for 24 hours followed by H 2 O 2 (100 μmol/L) for 3 hours. Cellular viability was assessed with MTT assay.Results: Honey prevented cellular death in a dose-dependent manner compared with H 2 O 2-treated cells. Honey at 1% concentration had the most significant effect (P = .015).

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4-Hydroperoxy-2-decenoic acid ethyl ester protects against 6-hydroxydopamine-induced cell death via activation of Nrf2-ARE and eIF2α-ATF4 pathways

Cited by 34 publications

References 38 publications

Apitherapy for Parkinson’s Disease: A Focus on the Effects of Propolis and Royal Jelly

Apitherapy for Parkinson’s Disease: A Focus on the Effects of Propolis and Royal Jelly

Dose‐Dependent Effects of Royal Jelly on Estrogen‐ and Progesterone‐Induced Mammary Gland Hyperplasia in Rats

Bee honey protects astrocytes against oxidative stress: A preliminary in vitro investigation

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