Rutin abrogates manganese—Induced striatal and hippocampal toxicity via inhibition of iron depletion, oxidative stress, inflammation and suppressing the NF-κB signaling pathway

Nkpaa, Kpobari W.; Onyeso, Godspower I.; Kponee, Kale

doi:10.1016/j.jtemb.2019.01.014

Cited by 42 publications

(20 citation statements)

References 38 publications

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“…These findings were almost the same as those reported earlier 17 . Rutin belongs to a group of plant bioflavonoid glycoside compounds called vitamin P and has a capacity for cytoprotection, antiinflammation, neuroprotection, and cardioprotection 1‐6 . Based on the previous study, it has been proposed that pretreatment of SH‐SY5Y neurons with 1, 5, and 10 μM of rutin for 30 minutes significantly reverses the cytotoxic effect induced by rotenone 29 .…”

Section: Discussionsupporting

confidence: 88%

“…17 Rutin belongs to a group of plant bioflavonoid glycoside compounds called vitamin P and has a capacity for cytoprotection, antiinflammation, neuroprotection, and cardioprotection. [1][2][3][4][5][6] Based on the previous study, it has been proposed that pretreatment of SH-SY5Y neurons with 1, 5, and 10 μM of rutin for 30 minutes significantly reverses the cytotoxic effect induced by rotenone. 29 In addition, pretreatment of RAW264.7 macrophages with 40 and 80 μM of rutin significantly reverse the nitric oxide production induced by LPS.…”

Section: Effects Of Rutin On Bisgma-inhibited Aoe Activities In Rawmentioning

confidence: 99%

“…Rutin, the chemical named 3,3′,4′,5,7‐pentahydroxyflavone‐3‐rhamnoglucoside, also called rutoside, sophorin, and phytomelin, is a flavonol compound found abundantly in Passiflora , buckwheat seeds, citrus fruits, vegetables, and tea. Rutin possesses numerous pharmacological and beneficial effects including antioxidative, cytoprotective, anti‐inflammatory, neuroprotective, cardioprotective, and anticarcinogenic activities 1‐6 . Bisphenol A‐glycidyl‐methacrylate (BisGMA), which synthesizes epoxy resin from methacrylic acid and diglycidyl ether of bisphenol‐A, is widely used in dentin restoration and as a bonding agent, a denture base material, a fissure sealant, and as bone cement 7,8 .…”

Section: Introductionmentioning

confidence: 99%

“…anti-inflammatory, neuroprotective, cardioprotective, and anticarcinogenic activities. [1][2][3][4][5][6] Bisphenol A-glycidyl-methacrylate (BisGMA), which synthesizes epoxy resin from methacrylic acid and diglycidyl ether of bisphenol-A, is widely used in dentin restoration and as a bonding agent, a denture base material, a fissure sealant, and as bone cement. 7,8 The characteristics of BisGMA-based polymeric resins include modulus, less shrinkage, lower diffusivity, and water insolubility.…”

mentioning

confidence: 99%

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Rutin‐protected BisGMA‐induced cytotoxicity, genotoxicity, and apoptosis in macrophages through the reduction of the mitochondrial apoptotic pathway and induction of antioxidant enzymes

Huang

Chang

et al. 2020

Environmental Toxicology

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Bisphenol-A-glycidyldimethacrylate (BisGMA) is a resin monomer frequently used in dentin restorative treatments. The leakage of BisGMA monomer from BisGMA-based polymeric resins can lead to cytotoxicity in macrophages. Rutin has various beneficial bioeffects, including antioxidation and antiinflammation. In this study, we found that pretreatment of RAW264.7 macrophages with rutin-inhibited cytotoxicity induced by BisGMA in a concentration-dependent manner. BisGMA-induced apoptosis, which was detected by levels of phosphatidylserine from the internal to the external membrane and formation of sub-G1, and genotoxicity, which was detected by cytokinesis-blocked micronucleus and single-cell gel electrophoresis assays, were inhibited by rutin in a concentration-dependent manner. Rutin suppressed the BisGMA-induced activation of caspase-3 and-9 rather than caspase-8. Rutin inhibited the activation of the mitochondrial apoptotic pathway, including cytochrome C release and mitochondria disruption, after macrophages were treated with Yin-Che Lu and Yu-Hsiang Kuan contributed equally to this work.

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Section: Discussionsupporting

confidence: 88%

Section: Effects Of Rutin On Bisgma-inhibited Aoe Activities In Rawmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

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Rutin‐protected BisGMA‐induced cytotoxicity, genotoxicity, and apoptosis in macrophages through the reduction of the mitochondrial apoptotic pathway and induction of antioxidant enzymes

Huang

Chang

et al. 2020

Environmental Toxicology

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“…In turn, Mn-induced apoptosis was shown to mediate alterations in spatial learning and memory deficits in metal-exposed animals (30 mg/kg Mn p.o. for 35 days) [ 136 ].…”

Section: Mn-induced Alterations In Subcellular and Multicellular Biologymentioning

confidence: 99%

Molecular Targets of Manganese-Induced Neurotoxicity: A Five-Year Update

Tinkov

Paoliello

Mazilina

et al. 2021

IJMS

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Understanding of the immediate mechanisms of Mn-induced neurotoxicity is rapidly evolving. We seek to provide a summary of recent findings in the field, with an emphasis to clarify existing gaps and future research directions. We provide, here, a brief review of pertinent discoveries related to Mn-induced neurotoxicity research from the last five years. Significant progress was achieved in understanding the role of Mn transporters, such as SLC39A14, SLC39A8, and SLC30A10, in the regulation of systemic and brain manganese handling. Genetic analysis identified multiple metabolic pathways that could be considered as Mn neurotoxicity targets, including oxidative stress, endoplasmic reticulum stress, apoptosis, neuroinflammation, cell signaling pathways, and interference with neurotransmitter metabolism, to name a few. Recent findings have also demonstrated the impact of Mn exposure on transcriptional regulation of these pathways. There is a significant role of autophagy as a protective mechanism against cytotoxic Mn neurotoxicity, yet also a role for Mn to induce autophagic flux itself and autophagic dysfunction under conditions of decreased Mn bioavailability. This ambivalent role may be at the crossroad of mitochondrial dysfunction, endoplasmic reticulum stress, and apoptosis. Yet very recent evidence suggests Mn can have toxic impacts below the no observed adverse effect of Mn-induced mitochondrial dysfunction. The impact of Mn exposure on supramolecular complexes SNARE and NLRP3 inflammasome greatly contributes to Mn-induced synaptic dysfunction and neuroinflammation, respectively. The aforementioned effects might be at least partially mediated by the impact of Mn on α-synuclein accumulation. In addition to Mn-induced synaptic dysfunction, impaired neurotransmission is shown to be mediated by the effects of Mn on neurotransmitter systems and their complex interplay. Although multiple novel mechanisms have been highlighted, additional studies are required to identify the critical targets of Mn-induced neurotoxicity.

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The study of single‐cell dynamics contributes to the evaluation of food‐derived antioxidant capacity

Xiang

Qing

et al. 2023

eFood

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Exploring potential food‐derived bioactive substances that relieve oxidative stress is considered an important goal for antioxidant research. We first used the long‐pair electron index and orbital fingerprint to predict the molecular interactions in a range of polyphenols and polypeptides. We found Rutin and peptide PW5 had the highest LPE index values. Subsequently, by D‐galactose (D‐gal)‐induced oxidative NIH3T3 cell model, we proved both Rutin and PW5 could effectively protect cells against D‐gal‐induced damage, through enhancement in cell proliferation and reduction in β‐galactosidase activity. Although Rutin displayed better performance than PW5 in the oxidative stress model, we confirmed Rutin stimulated obvious changes in the morphology and motility of normal NIH3T3 cells based on the real‐time dynamic images. Taken together, combined computational and typical model experiment methods, proved useful in efficiently screening food‐derived antioxidants. Moreover, the analytical results of cell morphology and movement may provide novel insights for the safety evaluation of antioxidants.

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Rutin abrogates manganese—Induced striatal and hippocampal toxicity via inhibition of iron depletion, oxidative stress, inflammation and suppressing the NF-κB signaling pathway

Cited by 42 publications

References 38 publications

Rutin‐protected BisGMA‐induced cytotoxicity, genotoxicity, and apoptosis in macrophages through the reduction of the mitochondrial apoptotic pathway and induction of antioxidant enzymes

Rutin‐protected BisGMA‐induced cytotoxicity, genotoxicity, and apoptosis in macrophages through the reduction of the mitochondrial apoptotic pathway and induction of antioxidant enzymes

Molecular Targets of Manganese-Induced Neurotoxicity: A Five-Year Update

The study of single‐cell dynamics contributes to the evaluation of food‐derived antioxidant capacity

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