Vitamin C alleviates LPS-induced cognitive impairment in mice by suppressing neuroinflammation and oxidative stress

Aging is a neurodegenerative disease that leads to cognitive impairment, and an increase in oxidative stress as a major cause is an important factor. It has been reported that aging-related cognitive impairment is associated with increased oxidative damage in several brain regions during aging. As a powerful antioxidant, vitamin C plays an important role in preventing oxidative stress, but due to its unstable chemical properties, it is easily oxidized and thus the activity of antioxidants is reduced. In order to overcome this easily oxidized vulnerability, we developed NXP032 (vitamin C/DNA aptamer complex) that can enhance the antioxidant efficacy of vitamin C using an aptamer. We developed NXP032 (vitamin C/DNA Aptamin C320 complex) that can enhance the antioxidant efficacy of vitamin C using an aptamer. In the present study, we evaluated the neuroprotective effects of NXP032 on aging-induced cognitive decline, oxidative stress, and neuronal damage in 17-month-old female mice. NXP032 was orally administered at 200 mg/kg of ascorbic acid and 4 mg/kg of DNA aptamer daily for eight weeks. Before the sacrifice, a cognitive behavioral test was performed. Administration of NXP032 alleviated cognitive impairment, neuronal damage, microglia activity, and oxidative stress due to aging. We found that although aging decreases the Nrf2-ARE pathway, NXP032 administration activates the Nrf2-ARE pathway to increase the expression of SOD-1 and GSTO1/2. The results suggest that the new aptamer complex NXP032 may be a therapeutic intervention to alleviate aging-induced cognitive impairment and oxidative stress.

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Modulation of Age-Related Biochemical Changes and Oxidative Stress by Vitamin C and Glutathione Supplementation in Old Rats

Annals of Nutrition and Metabolism ◽

10.1159/000065402 ◽

2002 ◽

Vol 46 (5) ◽

pp. 165-168 ◽

Cited By ~ 11

Author(s):

M.A. Amer

Keyword(s):

Oxidative Stress ◽

Vitamin C ◽

Biochemical Changes ◽

Age Related ◽

Old Rats ◽

And Oxidative Stress

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Relationship between atherogenic index and oxidative stress among patients presented with coronary artery disease in a tertiary care hospital

International Journal of Research in Pharmaceutical Sciences ◽

10.26452/ijrps.v11ispl4.4560 ◽

2020 ◽

Vol 11 (SPL4) ◽

pp. 2807-2813

Author(s):

Resmi C R ◽

Kedari G S R ◽

Deepa P K

Keyword(s):

Oxidative Stress ◽

Vitamin E ◽

Vitamin C ◽

Density Lipoprotein ◽

Atherogenic Index ◽

Enzymatic Antioxidants ◽

Oxidative Stress Markers ◽

Stress Markers ◽

Lipid Parameters ◽

And Oxidative Stress

CAD is recognized as a multifactorial disease that is influenced by environmental and genetic factors. This study aimed to evaluate the levels of lipid parameters, oxidative stress and antioxidant markers in subjects with CAD compared to their age & sex matched controls and to analyze the relationship between atherogenic Index and oxidative stress among them 62 clinically proved CAD patients and 62 healthy age and sex matched subjects without CAD were selected for this study. 5 ml of fasting venous blood was collected from all the subjects and investigations such as FPG, lipid profile, oxidative markers Malondialdehyde (MDA), F2 isoprostanes (F2iso) and antioxidants glutathione S-transferase (GST), superoxide dismutase (SOD), vitamin-C, vitamin-E were performed. This study showed that levels of lipid parameters total cholesterol (TC), triglycerides (TG), low density lipoprotein cholesterol (LDL-c) and AI were significantly higher whereas high density lipoprotein cholesterol (HDL-c) were significantly low in CAD patients compared to normal controls. Oxidative stress markers MDA and F2 Isoprostanes level were significantly high, whereas enzymatic antioxidants GST and SOD and non-enzymatic antioxidants Vitamin-C and Vitamin-E levels were significantly low in CAD patients. Oxidative stress markers were found to significantly influence the AI. Results of this study showed that oxidative stress markers F2iso and MDA and antioxidants GST, VIT-C and VIT-E are found to influence the atherogenic index significantly.

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Rapamycin attenuated zinc-induced tau phosphorylation and oxidative stress in animal model: Involvement of dual mTOR/p70S6K and Nrf2/HO-1 pathways

10.1101/2021.09.24.461637 ◽

2021 ◽

Author(s):

Chencen Lai ◽

Qian Chen ◽

Yuanting Ding ◽

Songbai Su ◽

Heng Liu ◽

...

Keyword(s):

Oxidative Stress ◽

Cognitive Impairment ◽

Morris Water Maze ◽

Zinc Sulfate ◽

Water Maze ◽

Tau Phosphorylation ◽

Alzheimers Disease ◽

Tau Pathology ◽

Biochemical Assays ◽

And Oxidative Stress

Alzheimers disease is pathologically featured by abnormal accumulation of amyloid-beta plaque, neurofibrillary tangles, oxidative stress, neuroinflammation, and neurodegeneration. Metal dysregulation including excessive zinc released by presynaptic neurons plays an important role in tau pathology and oxidase activation. The activities of mammalian target of rapamycin (mTOR)/ ribosomal S6 protein kinase (p70S6K) are elevated in the brains of patients with Alzheimers disease. Zinc induces tau hyperphosphorylation via mTOR/P70S6K activation in vitro. However, the involvement of mTOR/P70S6K pathway in zinc-induced oxidative stress, tau degeneration, synaptic and cognitive impairment, has not been fully elucidated in vivo. Here we assessed in the effect of pathological concentration of zinc in SH-SY5Y cells by using biochemical assays and immunofluorescence staining. Rats (n = 18, male) were lateral ventricularly-injected with zinc and treated with rapamycin (intraperitoneal injection) for one week and assessed using Morris water maze. Evaluation of the oxidative stress, tau phorsphylation and synaptic impairment were performed using the hippocampus tissue of the rats by biochemical assays and immunofluorescence staining. Results from Morris water maze showed that the capacity of spatial memory is impaired in zinc-treated rats. Zinc sulfate significantly increased the levels of P-mTOR Ser2448, P-p70S6K Thr389, and P-tau Ser356, and decreased levels of Nrf2 and HO-1 in SH-SY5Y cells and in zinc-treated rats compared with control groups. Increased expressions of reactive oxygen species were observed in zinc sulfate-induced SH-SY5Y cells as well as in the hippocampus of zinc-injected rats. Rapamycin, an inhibitor of mTOR, rescued the zinc-induced increases in mTOR/p70S6K activations, tau phosphorylation and oxidative stress, as well as Nrf2/HO-1 inactivation, cognitive impairment and synaptic impairment reduced the expression of synapse-related proteins in zinc-injected rats. In conclusion, our findings imply that rapamycin prevents zinc-induced cognitive impairment and protects neurons from tau pathology, oxidative stress and synaptic impairment, by decreasing mTOR/p70S6K hyperactivity and increasing Nrf2/HO-1 activity.

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Vitamin C supplementation improves blood pressure and oxidative stress after acute exercise in patients with poorly controlled type 2 diabetes mellitus: A randomized, placebo-controlled, cross-over study

The Chinese Journal of Physiology ◽

10.4103/cjp.cjp_95_20 ◽

2021 ◽

Vol 64 (1) ◽

pp. 16

Author(s):

Naruemon Leelayuwat ◽

Chongchira Boonthongkaew ◽

Terdthai Tong-Un ◽

Yupaporn Kanpetta ◽

Nisa Chaungchot ◽

...

Keyword(s):

Oxidative Stress ◽

Diabetes Mellitus ◽

Blood Pressure ◽

Type 2 Diabetes ◽

Type 2 Diabetes Mellitus ◽

Vitamin C ◽

Acute Exercise ◽

Vitamin C Supplementation ◽

And Oxidative Stress

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Paracetamol-induced changes of haematobiochemical and oxidative stress parameters in rat blood: Protective role of vitamin C and β-glucan

Kragujevac Journal of Science ◽

10.5937/kgjsci1638135m ◽

2016 ◽

pp. 135-146 ◽

Cited By ~ 2

Author(s):

Milos Matic ◽

Marija Milosevic ◽

Milica Paunovic ◽

Branka Ognjanovic ◽

Andras Stajn ◽

...

Keyword(s):

Oxidative Stress ◽

Vitamin C ◽

Protective Role ◽

Rat Blood ◽

Oxidative Stress Parameters ◽

Induced Changes ◽

And Oxidative Stress ◽

Stress Parameters

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Evaluation of the effect of vitamin C on caspase 9 and oxidative stress in rheumatoid arthritis patients

African Journal of Biochemistry Research ◽

10.5897/ajbr2018.0992 ◽

2018 ◽

Vol 12 (10) ◽

pp. 94-101

Author(s):

M. Elshamy Amira ◽

K. Gaafar Nagah ◽

E. ElAshwah Nadia ◽

A. Wagih Ayman ◽

A. Shahba Abeer

Keyword(s):

Rheumatoid Arthritis ◽

Oxidative Stress ◽

Vitamin C ◽

Caspase 9 ◽

And Oxidative Stress

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Patients Undergoing Myeloablative Chemotherapy and Hematopoietic Stem Cell Transplantation Exhibit Depleted Vitamin C Status in Association with Febrile Neutropenia

Nutrients ◽

10.3390/nu12061879 ◽

2020 ◽

Vol 12 (6) ◽

pp. 1879 ◽

Cited By ~ 1

Author(s):

Anitra C. Carr ◽

Emma Spencer ◽

Andrew Das ◽

Natalie Meijer ◽

Carolyn Lauren ◽

...

Keyword(s):

Oxidative Stress ◽

Febrile Neutropenia ◽

Vitamin C ◽

Thiobarbituric Acid ◽

Thiobarbituric Acid Reactive Substances ◽

C Reactive Protein ◽

Hematopoietic Stem ◽

Reactive Protein ◽

Myeloablative Chemotherapy ◽

And Oxidative Stress

Patients undergoing myeloablative chemotherapy and hematopoietic stem cell transplantation (HSCT) experience profound neutropenia and vulnerability to infection. Previous research has indicated that patients with infections have depleted vitamin C status. In this study, we recruited 38 patients with hematopoietic cancer who were undergoing conditioning chemotherapy and HSCT. Blood samples were collected prior to transplantation, at one week, two weeks and four weeks following transplantation. Vitamin C status and biomarkers of inflammation (C-reactive protein) and oxidative stress (protein carbonyls and thiobarbituric acid reactive substances) were assessed in association with febrile neutropenia. The vitamin C status of the study participants decreased from 44 ± 7 µmol/L to 29 ± 5 µmol/L by week one (p = 0.001) and 19 ± 6 µmol/L by week two (p < 0.001), by which time all of the participants had undergone a febrile episode. By week four, vitamin C status had increased to 37 ± 10 µmol/L (p = 0.1). Pre-transplantation, the cohort comprised 19% with hypovitaminosis C (i.e., <23 µmol/L) and 8% with deficiency (i.e., <11 µmol/L). At week one, those with hypovitaminosis C had increased to 38%, and at week two, 72% had hypovitaminosis C, and 34% had outright deficiency. C-reactive protein concentrations increased from 3.5 ± 1.8 mg/L to 20 ± 11 mg/L at week one (p = 0.002), and 119 ± 25 mg/L at week two (p < 0.001), corresponding to the development of febrile neutropenia in the patients. By week four, these values had dropped to 17 ± 8 mg/L (p < 0.001). There was a significant inverse correlation between C-reactive protein concentrations and vitamin C status (r = −0.424, p < 0.001). Lipid oxidation (thiobarbituric acid reactive substances (TBARS)) increased significantly from 2.0 ± 0.3 µmol/L at baseline to 3.3 ± 0.6 µmol/L by week one (p < 0.001), and remained elevated at week two (p = 0.003), returning to baseline concentrations by week four (p = 0.3). Overall, the lowest mean vitamin C values (recorded at week two) corresponded with the highest mean C-reactive protein values and lowest mean neutrophil counts. Thus, depleted vitamin C status in the HSCT patients coincides with febrile neutropenia and elevated inflammation and oxidative stress.

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