Potential role of α-lipoic acid and Ginkgo biloba against silver nanoparticles-induced neuronal apoptosis and blood-brain barrier impairments in rats

Lebda, Mohamed A.; Sadek, Kadry M.; Tohamy, Hossam G.; Abouzed, Tarek K.; Shukry, Mustafa; Umezawa, Masakazu; El‐Sayed, Yasser S.

doi:10.1016/j.lfs.2018.10.011

Cited by 44 publications

(21 citation statements)

References 71 publications

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“…To evaluate the capacity of EGB761 to maintain the integrity of the hematoencephalic barrier, Lebda et al [37], administrated 50 mg/g of AgNPs (silver nanoparticles) in mice by intraperitoneal route, inducing neurotoxicity. After the administration of EGB761 (120 mg/kg), the authors observed that EGB761 was able to neutralize the adverse effects of AgNPs, stabilizing the integrity of the ▶ Table 2 Components of Ginkgo biloba and their respective actions related to oxidative stress.…”

Section: Wistar Ratsmentioning

confidence: 99%

Effects of Ginkgo biloba on Diseases Related to Oxidative Stress

et al. 2020

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ABSTR AC TGinkgo biloba (GB) is one of the most widely used phytotherapeutic products in the world, and its extract has beneficial properties for the treatment of several pathologies, such as diabetic cardiomyopathy, neurodegenerative diseases, cataracts, hearing loss, myocardial lesion, hippocampus neuronal lesions, morphometry testicular changes, and liver damage. This review aims to investigate the effects of GB on diseases related to oxidative stress. Databases such as MEDLINE/ PUBMED and EMBASE were consulted, and PRISMA guidelines were used to build the review. This plant has antioxidant properties since it regulates the expression of antioxidant enzymes positively and reduces reactive oxygen and nitrogen species, contributing to the reduction of lipid peroxidation. It also exhibits anti-inflammatory properties, inhibiting the expression of pro-inflammatory cytokines, such as IL-1, IL-6, and TNF-α. In animal models, the use of GB can show positive effects on brain damage, neurodegenerative diseases, myocardial injury, and renal and liver damage. In humans, the positive effects were shown in diabetes, metabolic syndrome, and ischemic colitis. These effects are due to the presence of compounds such as bilobalide, isoramnetina, quercetin, kaempferol, and ginkgolides A, B, and C. For these reasons, GB can be a lowcost alternative to the therapeutic approach of several pathologies since it acts in the prevention, treatment, and inhibition of several complications of common comorbidities.

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Section: Wistar Ratsmentioning

confidence: 99%

Effects of Ginkgo biloba on Diseases Related to Oxidative Stress

et al. 2020

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“…Researchers suggested that neurodegeneration after exposure to Ag NPs occurred through inflammatory effects [99]. Neurotoxicity and impaired BBB functions were also observed after intraperitoneal administration attributed to the change of level of trace element in serum and brain, reduction of antioxidant enzyme activity, apoptosis and induction of inflammatory processes and down regulated tight junction proteins expression [100]. Similarly, chronic, intragastrically exposure of rats to low doses of Ag NPs resulted in the presence of silver in various parts of the brain, including the hippocampus and impairment of hippocampal dependent memory and cognitive coordination processes [101].…”

Section: In Vivo Toxicity In Mammalsmentioning

confidence: 99%

Toxicity of metallic nanoparticles in the central nervous system

Sawicki

Czajka

Matysiak‐Kucharek

et al. 2019

Nanotechnology Reviews

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Metallic nanoparticles due to their small size and unique physico-chemical characteristics have found excellent applications in various branches of industry and medicine. Therefore, for many years a growing interest has been observed among the scientific community in the improvement of our understanding of the impact of nanoparticles on the living organisms, especially on humans. Considering the delicate structure of the central nervous systemit is one of the organs most vulnerable to the adverse effects of metallic nanoparticles. For that reason, it is important to identify the modes of exposure and understand the mechanisms of the effect of nanoparticles on neuronal tissue. In this review, an attempt is undertaken to present current knowledge about metallic nanoparticles neurotoxicity based on the selected scientific publications. The route of entry of nanoparticles is described, as well as their distribution, penetration through the cell membrane and the blood-brain barrier. In addition, a study on the neurotoxicity in vitro and in vivo is presented, as well as some of the mechanisms that may be responsible for the negative effects of metallic nanoparticles on the central nervous system. Graphical abstract: This review summarizes the current knowledge on the toxicity of metallic NPs in the brain and central nervous system of the higher vertebrates.

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“…In recent years, many researchers have explored the use of natural products for treating various ailments as they are inexpensive, readily available, and devoid of serious side effects. [29][30][31][32][33][34][35][36][37][38][39][40][41][42][43] To the best of our knowledge, this study is the first to examine the underlying mechanism(s) responsible for the prophylactic effect of PE on DOX-induced cardiotoxicity. The well-known cardiotoxicity of DOX has been associated with inflammation [8] and induction of oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Proanthocyanidin alleviates doxorubicin‐induced cardiac injury by inhibiting NF‐kB pathway and modulating oxidative stress, cell cycle, and fibrogenesis

Sadek

Mahmoud

Zeweil

et al. 2021

J Biochem & Molecular Tox

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This study investigated the potential mechanism(s) and the signaling pathway(s) underlying the prophylactic effect of proanthocyanidin extract (PE) against doxorubicin (DOX)‐induced cardiotoxicity in rats. A total of 32 male albino rats were randomly allocated into four groups. Control rats were orally administrated normal saline. Rats in the second group were orally administrated PE (50 mg/kg bw/once daily) for 4 weeks. Rats in the third group were intraperitoneally injected with DOX (10 mg/kg on Days 3, 9, 15, and 21 of the experiment). Rats in the fourth group were injected with DOX and PE simultaneously for 4 weeks. DOX significantly augmented the levels of serum heart damage biomarkers. In addition, histopathology indicated that DOX‐induced cardiac tissue injury upregulated the expression of fibrogenic factors, alpha smooth muscle actin (α‐SMA), transforming growth factor β1 (TGF‐ β1), and p16INK4A. Downregulation of cell proliferation markers, cyclin‐dependent kinase‐4 (CDK4), and retinoblastoma (Rb) was also observed. Furthermore, DOX‐induced oxidative and inflammatory stress resulted in increased cardiac malondialdehyde (MDA), protein carbonyl (PC), interleukin‐2 (IL‐2), interleukin‐6 (IL‐6), and tumor necrosis factor‐alpha (TNF‐α). Decreased cardiac glutathione (GSH) levels and enzyme activity of catalase (CAT), superoxide dismutase (SOD), and glutathione S‐transferase (GST) were observed. Treatment of DOX‐induced rat cardiotoxicity with PE normalized serum parameters for the aforementioned parameters and alleviated cardiac tissue structure. Furthermore, reduced cardiac tissue α‐SMA and TGF‐β1, and increased CDK4 and Rb protein expression, along with the amelioration of oxidative and inflammatory effects were observed. PE attenuates DOX‐induced cardiomyocyte inflammation possibly by attenuating the nuclear factor kappa‐B (NF‐ kB) signaling pathway. These results indicate that PE may be useful as a preventative agent against DOX‐induced cardiac toxicity.

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Potential role of α-lipoic acid and Ginkgo biloba against silver nanoparticles-induced neuronal apoptosis and blood-brain barrier impairments in rats

Cited by 44 publications

References 71 publications

Effects of Ginkgo biloba on Diseases Related to Oxidative Stress

Effects of Ginkgo biloba on Diseases Related to Oxidative Stress

Toxicity of metallic nanoparticles in the central nervous system

Proanthocyanidin alleviates doxorubicin‐induced cardiac injury by inhibiting NF‐kB pathway and modulating oxidative stress, cell cycle, and fibrogenesis

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