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1.
Heliyon ; 9(3): e14126, 2023 Mar.
Article in English | MEDLINE | ID: mdl-36923841

ABSTRACT

Kidney has a crucial role in immunity, so any toxicity occurs for the kidney will result in reduced immunity. The aim of this study is to improve the immune response of insufficient kidneys through immune-related genes. Diethyl Nitrosamine has been used to cause kidney damage in animal models, vitamin C and curcumin have been used to treat impaired kidney. Renal function (urea, uric acid and creatinine) and oxidative stress parameters (superoxide dismutase, malondialdehyde and glutathione peroxidase) will be evaluated in this research work. Molecular docking also will be performed to investigate the role of vitamin C and curcumin in targeting immune response proteins. Also, Complementary component 3, Lipocalin-2, Toll-like receptor 2,Toll-like receptor 4, Kidney injury molecule-1, Interleukin 6, Interleukin-10, Tumor necrosis factor and p38 mitogen-activated protein kinases will be investigated. The obtained results showed that vitamin C and curcumin have good effects in the treatment of impaired kidneys, this was also observed in renal function and oxidative stress parameters, expression levels of proteins and histopathological examinations.

2.
Biomed Res Int ; 2022: 8962149, 2022.
Article in English | MEDLINE | ID: mdl-35528172

ABSTRACT

This study examined the protective effect of quercetin against high-altitude-induced brain damage in rats. A molecular docking study was performed to investigate the potential effect of quercetin in reducing brain damages through its ability to target the oxidative stress enzymes. Biomarker assessment screening assays were also performed then followed by in vivo studies. Three groups of rats were divided into the control group, an untreated animal model group with induced brain damage, and finally, the quercetin treated group that received quercetin dose equal to 20 mg/kg of their body weights. Molecular docking studies and biomarker assessment screening assays proved the potential effect of quercetin to affect the level of representative biomarkers glutathione (GSH), glutathione reductase (GR), glutathione-S-transferase (GST), glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase (CAT), and malondialdehyde (MDA). Additionally, the protective effect of quercetin against high altitude, low pressure, and low oxygen was also investigated by exploring the brain histopathology of experimental rats. Brain damage was observed in the untreated animal model group. After treatment with quercetin, the cerebral edema in the brain tissues was improved significantly, confirming the protective effects of quercetin. Therefore, quercetin can be used as a natural food additive to protect from the highaltitude-induced brain damage.


Subject(s)
Brain Injuries , Quercetin , Animals , Antioxidants/pharmacology , Brain/metabolism , Brain Injuries/drug therapy , Catalase/metabolism , Glutathione/metabolism , Glutathione Peroxidase/metabolism , Glutathione Transferase/metabolism , Molecular Docking Simulation , Oxidative Stress , Quercetin/pharmacology , Rats , Rats, Wistar , Superoxide Dismutase/metabolism
3.
Biomarkers ; 27(2): 138-150, 2022 Mar.
Article in English | MEDLINE | ID: mdl-34927500

ABSTRACT

INTRODUCTION: Bladder cancer is still of unknown initiation and progression, it is difficult to treat the patient once bladder cancer have a distant metastasis. MATERIALS AND METHODS: In the present study, propolis extract was evaluated against bladder cancer cells (T24). Two independent pathways were investigated, apoptosis and angiogenesis, Bax, Bcl-2, P53, and caspase-3 for apoptosis, vascular endothelial growth factor receptor and protein kinase A as angiogenesis potential targets. OBJECTIVES: Molecular docking studies will be conducted for the major known constituents of Egyptian propolis into apoptotic and angiogenic protein targets, to give better insights to the possible binding mode and interactions and investigate the ability of propolis constituents to target both apoptotic and angiogenic pathways. RESULTS: Propolis showed anti-proliferative activity against T24 cancer cell line, the IC50 value was 6.36 µg/ml. Also significant effects of propolis on Bax, Bcl-2, P53, and caspase-3 were observed. DISCUSSION: These obtained results proved the ability of propolis to induce cell death. Also it has revealed noticeable effects on protein kinase A and vascular endothelial growth factor receptor. CONCLUSION: The obtained results can encourage us to say that propolis extract can induce a programmed cell death in human bladder cancer cells, and also affect angiogenesis.


Subject(s)
Antineoplastic Agents , Propolis , Urinary Bladder Neoplasms , Antineoplastic Agents/pharmacology , Apoptosis , Cell Line, Tumor , Cell Proliferation , Early Detection of Cancer , Humans , Molecular Docking Simulation , Propolis/pharmacology , Propolis/therapeutic use , Urinary Bladder Neoplasms/drug therapy , Urinary Bladder Neoplasms/pathology , Vascular Endothelial Growth Factor A
4.
J Biol Chem ; 286(34): 29771-9, 2011 Aug 26.
Article in English | MEDLINE | ID: mdl-21757737

ABSTRACT

Many enteric pathogens, including enterotoxigenic Escherichia coli (ETEC), produce one or more serine proteases that are secreted via the autotransporter (or type V) bacterial secretion pathway. These molecules have collectively been referred to as SPATE proteins (serine protease autotransporter of the Enterobacteriaceae). EatA, an autotransporter previously identified in ETEC, possesses a functional serine protease motif within its secreted amino-terminal passenger domain. Although this protein is expressed by many ETEC strains and is highly immunogenic, its precise function is unknown. Here, we demonstrate that EatA degrades a recently characterized adhesin, EtpA, resulting in modulation of bacterial adhesion and accelerated delivery of the heat-labile toxin, a principal ETEC virulence determinant. Antibodies raised against the passenger domain of EatA impair ETEC delivery of labile toxin to epithelial cells suggesting that EatA may be an effective target for vaccine development.


Subject(s)
Bacterial Secretion Systems/physiology , Carrier Proteins/metabolism , Enterotoxigenic Escherichia coli/metabolism , Enterotoxigenic Escherichia coli/pathogenicity , Enterotoxins/metabolism , Escherichia coli Proteins/metabolism , Animals , Bacterial Adhesion/physiology , Bacterial Toxins/genetics , Carrier Proteins/genetics , Enterotoxigenic Escherichia coli/genetics , Enterotoxins/genetics , Escherichia coli Proteins/genetics , Escherichia coli Vaccines/genetics , Escherichia coli Vaccines/metabolism , Mice , Peptide Hydrolases , Protein Transport/physiology
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