Neuroprotective effects of Brazilian green propolis on oxytosis/ferroptosis in mouse hippocampal HT22 cells

Takashima, Madoka; Ichihara, Kenji; Hirata, Yoko

doi:10.1016/j.fct.2019.110669

Cited by 48 publications

(21 citation statements)

References 37 publications

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“…More, PD is known as manifest Lewy body dementia because severe cognitive alterations develop, especially during late stages of the disease [ 19 ]. Research shows that propolis and RJ possess a capacity to improve cognitive performance [ 71 ] and alleviate depressive symptoms through mitigation of oxidative stress [ 117 ] and activation of signaling pathways that promote the production of various neurotrophic factors such as BDNF [ 118 ], GDNF [ 102 ], and NGF [ 119 , 120 ]. Altogether, according to these scenarios, propolis and RJ may represent a multidimensional treatment, which may promote the quality of life among PD patients.…”

Section: Discussionmentioning

confidence: 99%

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: Discussionmentioning

confidence: 99%

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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“…These are collected from plants by bees and mixed with their salivary secretions, resulting in a yellowish substance used in the construction, maintenance, and protection of hives, limiting the growth of bacteria and fungi [ 42 , 43 ]. Research on animal models and human cells has suggested the beneficial effects of propolis on coronary heart diseases and risk factors associated with cardiovascular diseases as well as on acute and chronic brain processes [ 44 , 45 , 46 , 47 , 48 , 49 , 50 , 51 ]. As disease-modifying approaches remain a crucial goal in PD, we aimed to examine whether propolis can alleviate heart rate parameters and nigrostriatal dopaminergic loss in the 6-OHDA model of PD.…”

Section: Introductionmentioning

confidence: 99%

Propolis as a Potential Disease-Modifying Strategy in Parkinson’s disease: Cardioprotective and Neuroprotective Effects in the 6-OHDA Rat Model

et al. 2020

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Patients with Parkinson’s disease (PD) manifest nonmotor and motor symptoms. Autonomic cardiovascular dysregulation is a common nonmotor manifestation associated with increased morbimortality. Conventional clinical treatment alleviates motor signs but does not change disease progression and fails in handling nonmotor features. Nutrition is a key modifiable determinant of chronic disease. This study aimed to assess the effects of propolis on cardiological features, heart rate (HR) and heart rate variability (HRV) and on nigrostriatal dopaminergic damage, detected by tyrosine hydroxylase (TH) immunoreactivity, in the 6-hydroxydopamine (6-OHDA) rat model of PD. Male Wistar rats were injected bilaterally with 6-OHDA or saline into the striatum and were treated with propolis or water for 40 days. Autonomic function was assessed by time domain parameters (standard deviation of all normal-to-normal intervals (SDNN) and square root of the mean of the squared differences between adjacent normal RR intervals (RMSSD)) of HRV calculated from electrocardiogram recordings. Reductions in HR (p = 1.47 × 10−19), SDNN (p = 3.42 × 10−10) and RMSSD (p = 8.2 × 10−6) detected in parkinsonian rats were reverted by propolis. Propolis attenuated neuronal loss in the substantia nigra (p = 5.66 × 10−15) and reduced striatal fiber degeneration (p = 7.4 × 10−5) in 6-OHDA-injured rats, which also showed significant weight gain (p = 1.07 × 10−5) in comparison to 6-OHDA-lesioned counterparts. Propolis confers cardioprotection and neuroprotection in the 6-OHDA rat model of PD.

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“…Here, we demonstrated that sodium chlorate weakened the protective effect of an iron chelator, deferoxamine, on erastin-induced cell death. Both Ca 2+ and Fe 2+ are involved intimately in glutamate-and erastin-induced cell death in HT22 cells [33], suggesting that reduced sulfation by the treatment with sodium chlorate enhances diffusion of divalent cations and exacerbates glutamate-and erastin-induced oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Reduced Sulfation Enhanced Oxytosis and Ferroptosis in Mouse Hippocampal HT22 Cells

et al. 2020

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Sulfation is a common modification of extracellular glycans, tyrosine residues on proteins, and steroid hormones, and is important in a wide variety of signaling pathways. We investigated the role of sulfation on endogenous oxidative stress, such as glutamate-induced oxytosis and erastin-induced ferroptosis, using mouse hippocampal HT22 cells. Sodium chlorate competitively inhibits the formation of 3′-phosphoadenosine 5′-phosphosulfate, the high energy sulfate donor in cellular sulfation reactions. The treatment of HT22 cells with sodium chlorate decreased sulfation of heparan sulfate proteoglycans and chondroitin sulfate proteoglycans. Sodium chlorate and β-d-xyloside, which prevents proteoglycan glycosaminoglycan chain attachment, exacerbated both glutamate- and erastin-induced cell death, suggesting that extracellular matrix influenced oxytosis and ferroptosis. Moreover, sodium chlorate enhanced the generation of reactive oxygen species and influx of extracellular Ca2+ in the process of oxytosis and ferroptosis. Interestingly, sodium chlorate did not affect antioxidant glutathione levels. Western blot analysis revealed that sodium chlorate enhanced erastin-induced c-Jun N-terminal kinase phosphorylation, which is preferentially activated by cell stress-inducing signals. Collectively, our findings indicate that sulfation is an important modification for neuroprotection against oxytosis and ferroptosis in neuronal hippocampal cells.

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Neuroprotective effects of Brazilian green propolis on oxytosis/ferroptosis in mouse hippocampal HT22 cells

Cited by 48 publications

References 37 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

Propolis as a Potential Disease-Modifying Strategy in Parkinson’s disease: Cardioprotective and Neuroprotective Effects in the 6-OHDA Rat Model

Reduced Sulfation Enhanced Oxytosis and Ferroptosis in Mouse Hippocampal HT22 Cells

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