Effect of GSH and niacin combination on protein oxidation, ER stress, glycation and aggregation in HLE cells under high glucose condition

2021 ◽  
Vol 2 (1) ◽  
pp. 1-5
Author(s):  
Nina Handayani ◽  
◽  
Hidayat Sujuti ◽  
Achmad Rudijanto ◽  
◽  
...  
Keyword(s):  
Er Stress ◽  
High Glucose ◽  
Active Role ◽  
Protein Carbonyl ◽  
Human Lens ◽  
Control Group ◽  
High Dose ◽  
Protein Carbonyl Content ◽  
Glucose Levels ◽  
High Glucose Condition

AIM: To evaluate the effects of reduced glutathione (GSH) and niacin combination on protein oxidative stress, endoplasmic reticulum (ER) stress, glycation, and aggregation of the αβ crystalline in human lens epithelial (HLE) cells treated with high glucose levels. METHODS: HLE cells were cultured and exposed to 25 mmol/L glucose to promote high glucose conditions. Groups of cells were co-treated with three different combinations of dosages: 10 μmol/L GSH+25 μmol/L niacin (P1), 30 μmol/L GSH+25 μmol/L niacin (P2), and 100 μmol/L GSH+25 μmol/L niacin (P3). After 72h incubation, protein carbonyl content (PCC) and glucose reactive protein (GRP78) content were assessed using ELISA examinations. After two-week incubation, advanced glycation end products (AGEs) were also assessed and the expression of αβ crystalline was measured using Western blot examination. RESULTS: PCC and GRP78 levels in the co-treated groups were not significantly reduced compared to control (P>0.05). In contrast, there was a significant decrease of the AGEs levels in all groups co-treated with GSH and niacin when compared with the control group (P<0.05). In addition, the αβ crystalline expression increased after high dose glucose administration, but decreased in all groups co-treated with GSH and combinations of GSH and niacin. CONCLUSION: Combinations of GSH and niacin inhibit the aggregation of proteins and prevent glycation in hyperglycemic HLE cells. This study shows that this combination may play an active role in preventing diabetic cataract mainly from the AGEs pathway.

Alteration in the oxidative status of Drosophila melanogaster Meigen (Diptera: Drosophilidae) fed with a diet containing Centaurea depressa M. Bieb. (Asteraceae)

2020 ◽  
Vol 70 (2) ◽  
pp. 227-237
Author(s):  
Eda Güneş
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Antioxidant Enzymes ◽  
Total Protein ◽  
Protein Carbonyl ◽  
Control Group ◽  
Carbonyl Content ◽  
Protein Carbonyl Content ◽  
Freeze Dried ◽  
Dried Extract

Abstract The aim of the this study was to evaluate the effects of fresh, dried and freeze-dried Centaurea depressa M. Bieb. (Asteraceae) on the oxidant and antioxidant status of the model organism D. melanogaster Meigen (Diptera: Drosophilidae) experimentally. The study was carried out from 2016 to 2019, and plant leaf extracts (0-50 mg/l) were added to insect standard artificial diets. The total protein, protein carbonyl content and glutathione-S-transferase, superoxide dismutase and catalase activities were quantified at the insect’s third larval stage. Our data showed that protein carbonyl content varied from 2.70 nmol/mg protein in the control group to 59.11 nmol/mg protein in the group fed with fresh leaf extract signifying induction of oxidative stress. All extracts increased the levels of all antioxidant enzymes and decreased the amounts of total protein. Meanwhile, the group fed with the freeze-dried extract showed no significant difference in the levels of total protein and protein carbonyl content except at the 50 mg/l concentration of the extract. Moreover, this group had superoxide dismutase and catalase activities 4 to 5 times higher than in the control group. In conclusion, induction of oxidative stress indicates that the fresh form of C. depressa leaves may have potential as a natural pesticide, whereas induction of endogenous antioxidant enzymes by the freeze-dried extract suggest its potential as an antioxidant.

scholarly journals Iron overload is related to elevated blood glucose levels in obese children and aggravates high glucose-induced endothelial cell dysfunction in vitro

2020 ◽  
Vol 8 (1) ◽  
pp. e001426
Author(s):  
Wei Wu ◽  
Jinna Yuan ◽  
Yu Shen ◽  
Yunxian Yu ◽  
Xuefeng Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Iron Overload ◽  
High Glucose ◽  
Metabolic Disorders ◽  
Control Group ◽  
Endothelial Cell Dysfunction ◽  
Obese Children ◽  
Glucose Levels ◽  
Cell Dysfunction ◽  
Blood Glucose Levels

IntroductionThis study was performed to investigate the role of iron overload in the early stage of hyperglycemia-induced vascular functional impairment.Research design and methodsA total of 196 obese children were enrolled, and data regarding ferritin levels, blood glucose levels, intima-media thickness of carotid arteries, liver function and fibrosis index, hemoglobin, blood pressure, blood lipids, and inflammation indicators were collected. Ferritin levels were compared with a control group, which consisted of 148 healthy non-obese children who were age-matched and gender-matched. Endothelial cells were cultured in high glucose medium and supplemented with ferric citrate with or without iron remover (deferoxamine), a reducing agent (N-acetyl-cysteine), or a nuclear factor-κB (NF-κB) inhibitor (BAY 11-7082). Apoptosis, oxidative stress, nitric oxide levels, and endothelin content were evaluated. DNA microarray analysis was performed to analyze the expression of genes in the NF-κB signaling pathway.ResultsObese children have significantly higher ferritin levels compared with the control group. Ferritin level was positively correlated with hemoglobin and was related to metabolic disorders, including impaired glucose tolerance, higher blood pressure, dyslipidemia, and impaired hepatic function. Endothelial cells treated with ferric citrate showed a significantly higher rate of apoptosis, higher levels of oxidative stress, and impaired vasomotor function under high glucose conditions. The above effects were rescued by treatment with an iron remover, reducing agent, or NF-κB inhibitor. Further, detection of phosphorylated-p65 distribution in cells confirmed activation of the NF-κB pathway. DNA microarrays and subsequent gene oncology enrichment analyses revealed the main processes activated in cells.ConclusionIncreased ferritin levels are related to impaired glucose tolerance and other metabolic disorders in obese children. At the cellular level, iron overload aggravated the endothelial cell dysfunction caused by high glucose.

scholarly journals High Glucose Induces Autophagy through PPARγ-Dependent Pathway in Human Nucleus Pulposus Cells

PPAR Research ◽  
2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Chang Jiang ◽  
Shuhao Liu ◽  
Yuanwu Cao ◽  
Hongping Shan
Keyword(s):  
Nucleus Pulposus ◽  
High Glucose ◽  
Beclin 1 ◽  
Control Group ◽  
Peroxisome Proliferator ◽  
Nucleus Pulposus Cells ◽  
Connective Tissues ◽  
Peroxisome Proliferator Activated Receptor ◽  
High Glucose Condition ◽  
Dependent Pathway

Diabetes mellitus is a multiorgan disorder affecting many types of connective tissues, including bone and cartilage. High glucose could accelerate the autophagy in nucleus pulposus (NP) cells. In our present study, we investigated whether peroxisome proliferator-activated receptor γ (PPAR-γ) pathway is involved into autophagy regulation in NP cells under high glucose condition. After NP cells were treated with different high glucose concentrations for 72 hours, the rate of autophagy increased. Moreover, the levels of PPARγ, Beclin-1, and LC3II were significantly increased and p62 was significantly decreased compared to control group. Then, NP cells were treated with high glucose plus PPARγ agonist or PPARγ antagonist, respectively. The rate of autophagy and the levels of Beclin-1 and LC3II increased, but p62 decreased when PPARγ agonist was used. On the contrary, the rate of autophagy and the levels of Beclin-1 and LC3II decreased, while p62 increased when PPARγ antagonist was added. These results suggested that autophagy induced by high glucose in NP cells was through PPARγ-dependent pathway.

scholarly journals Oxycodone Enhances the Effects of Metformin Therapy in Mices With Painful Diabetic Neuropathy Induced by Alloxan

2021 ◽  
Author(s):  
Zahra Askari ◽  
Seyed Javad Boskabadi ◽  
Amirhossein Mahdizade ◽  
Ramin Ataee
Keyword(s):  
Diabetic Neuropathy ◽  
Opioid Receptor ◽  
Diabetic Group ◽  
Control Group ◽  
Diabetic Patients ◽  
High Dose ◽  
Painful Diabetic Neuropathy ◽  
Opioid Agonist ◽  
Protein Carbonyl Content ◽  
Metformin Therapy

Abstract Background DN (diabetic neuropathy) is a common disorder and two thirds of diabetic patients have clinical or subclinical neuropathy. Pain in DN can be spontaneous or stimulus induced and aggravate in nights. µ-opioid receptor make weak-reply to an antinociceptive effect of opioid agonist but κ-opioid receptors create antinociceptive response appropriately. Methods Diabetic animals were treated intraperitoneally for 3weeks in 9 groups including different doses of oxycodone and codeine with constant dose of metformin (200mg/kg). The normal saline group was considered as a negative control group and diabetic group as positive control. After 3 weeks Hot plate and tail flic test were done and fasting blood glucose was measured. After that Animals were sacrificed and oxidative stress biomarkers including lipid peroxidation, protein carbonyl content, and glutathione content were measured in brain and liver isolated mitochondria. Conclusion In this study finding demonstrated that Oxycodone (high dose 8mg/kg) with effect on both µ-opioid receptor and κ-opioid receptor significantly enhances the effects of metformin therapy in mices with painful diabetic neuropathy. In addition, opioid drugs induced stress oxidative and MDA formation in brain and liver.As well as, in diabetic mices, glucose level in all drug groups significantly decreased in compared to positive diabetic group.

scholarly journals UJI EFEKTIVITAS ANTIDIABETES KOMBINASI EKSTRAK DAUN MENIRAN (Phyllanthus niruri L.) Dan KELOPAK BUNGA ROSELLA (Hibiscus sabdariffa L.) PADA TIKUS JANTAN PUTIH

2019 ◽  
Vol 2 (1) ◽  
pp. 24-28
Author(s):  
Herviani Sari ◽  
Vera Estefania Kaban ◽  
Friska Raulina Situmorang ◽  
Firdaus Fahdi
Keyword(s):  
Blood Glucose ◽  
Leaf Extract ◽  
Negative Control Group ◽  
Positive Control ◽  
Negative Control ◽  
Control Group ◽  
High Dose ◽  
Glucose Levels ◽  
White Rats ◽  
Blood Glucose Levels

Purpose: To determine the effect of decreasing blood glucose levels in white rats using a combination of meniran and rosella compared to glibenclamide. Method: This research was carried out experimentally. Simplicia of meniran leaves and rosella macerated using 80% ethanol. The research used 21 rats that were induced by alloxan and divided into 7 groups and all compared using glibenclamide.Group 1 (negative control) CMC Na 1%, group 2 (positive control) glibenclamide dose 0.45 mg/kgMB, group 3 single roselle extract dose 130 mg/kgMB, group 4 single meniran leaf extract dose 200 mg/kgMB, group 5 combination of meniran leaf extract dose of 100 mg/kgMB and rosella extract dose of 65 mg/kgMB, group 6 combination of meniran leaf extract dose of 200 mg/kgMB and rosella extract dose of 130 mg/kgMB, and group 7 meniran leaf extract combination dose 400 mg/kgMB and rosella extract dose 195 mg/kgMB. Result: The results showed that rats had hyperglycemia after being induced by alloxan.Data were analyzed using one way ANOVA method followed by LSD and tukeys' B post hoct test. Having a difference in the decrease in blood glucose levels between the positive control group and the five doses of meniran extract and rosella gave a significant effect compared to the negative control group did not have a significant effect in reducing blood glucose levels. Conclusion: Single meniran extract and high-dose combination extract are more effective than glibenclamide.

Sufentanil Affects High Glucose-Induced Oxidative Stress in and Apoptosis of Cardiomyocytes by Regulation of miR-142-3p Expression

2021 ◽  
Vol 11 (3) ◽  
pp. 466-470
Author(s):  
Zhiyong Liu ◽  
Cuiqing Ding ◽  
Changqing Yao ◽  
Jinhui Chen
Keyword(s):  
Oxidative Stress ◽  
High Glucose ◽  
Molecular Mechanisms ◽  
Caspase 3 ◽  
Control Group ◽  
High Dose ◽  
Dependent Manner ◽  
Sod Activity ◽  
Apoptosis Rate ◽  
Mda Content

To explore the effects and molecular mechanisms of sufentanil on high glucose-induced oxidative stress in and apoptosis of cardiomyocytes, cardiomyocytes H9c2 cells were classified into groups based on different treatments as high-glucose (HG), HG with low, medium, or high-dose sufentanil, HG with high-dose sufentanil and anti-miR-NC, HG with high-dose sufentanil and anti-miR-142-3p, and control. The cells’ superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were detected using respective kits. The apoptosis rate in each group was detected by flow cytometry. The expressions of cleaved caspase-3 and pro-caspase3 were determined using western blotting. The expression of miR-142-3p in cardiomyocytes was detected using real-time fluorescent quantitative PCR. Compared with the control group, the HG group had decreased SOD activity, pro-caspase-3 expression, and miR-142-3p expression and increased MDA content, apoptosis, and cleaved caspase-3 expression (P < 0.05). Compared with the HG group, the SOD activity and pro-caspase-3 expression increased and the MDA content, apoptosis rate, and cleaved caspase-3 expression decreased in HG cells treated with low, medium, or high-dose sufentanil. The expression of miR-142-3p was increased in a dose-dependent manner (P < 0.05). The interference of miR-142-3p reversed the effect of sufentanil on high glucose-induced oxidative stress in and apoptosis of cardiomyocytes. Sufentanil may inhibit high glucose-induced oxidative stress in and apoptosis of cardiomyocytes by upregulating miR-142-3p expression.

N-acetylcysteine and taurine prevent hyperglycemia-induced insulin resistance in vivo: possible role of oxidative stress

2003 ◽  
Vol 285 (4) ◽  
pp. E744-E753 ◽  
Author(s):  
C. Andrew Haber ◽  
Tony K. T. Lam ◽  
Zhiwen Yu ◽  
Neehar Gupta ◽  
Tracy Goh ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
High Glucose ◽  
Muscle Protein ◽  
Fold Increase ◽  
Protein Carbonyl ◽  
Protein Carbonyl Content ◽  
High Concentrations

Exposure to high concentrations of glucose and insulin results in insulin resistance of metabolic target tissues, a characteristic feature of type 2 diabetes. High glucose has also been associated with oxidative stress, and increased levels of reactive oxygen species have been proposed to cause insulin resistance. To determine whether oxidative stress contributes to insulin resistance induced by hyperglycemia in vivo, nondiabetic rats were infused with glucose for 6 h to maintain a circulating glucose concentration of 15 mM with and without coinfusion of the antioxidant N-acetylcysteine (NAC), followed by a 2-h hyperinsulinemic-euglycemic clamp. High glucose (HG) induced a significant decrease in insulin-stimulated glucose uptake [tracer-determined disappearance rate (Rd), control 41.2 ± 1.7 vs. HG 32.4 ± 1.9 mg · kg–1 · min–1, P < 0.05], which was prevented by NAC (HG + NAC 45.9 ± 3.5 mg · kg–1 · min–1). Similar results were obtained with the antioxidant taurine. Neither NAC nor taurine alone altered Rd. HG caused a significant (5-fold) increase in soleus muscle protein carbonyl content, a marker of oxidative stress that was blocked by NAC, as well as elevated levels of malondialdehyde and 4-hydroxynonenal, markers of lipid peroxidation, which were reduced by taurine. In contrast to findings after long-term hyperglycemia, there was no membrane translocation of novel isoforms of protein kinase C in skeletal muscle after 6 h. These data support the concept that oxidative stress contributes to the pathogenesis of hyperglycemia-induced insulin resistance.

Relationship among superoxide-related enzyme, PPARs, and endothelium-dependent relaxation in murine aortas previously organ-cultured in high-glucose conditions

2010 ◽  
Vol 88 (7) ◽  
pp. 760-769 ◽  
Author(s):  
Yasuhiro Takenouchi ◽  
Tsuneo Kobayashi ◽  
Kumiko Taguchi ◽  
Takayuki Matsumoto ◽  
Katsuo Kamata
Keyword(s):  
Protein Expression ◽  
High Glucose ◽  
Peroxisome Proliferator ◽  
High Concentration ◽  
Glucose Levels ◽  
High Glucose Condition ◽  
Lower Protein ◽  
Related Enzyme ◽  
Peroxisome Proliferator Activated Receptors ◽  
Endothelium Dependent Relaxation

The aim of the present study was to investigate the relationship among superoxide anion, peroxisome proliferator-activated receptors (PPARs), and endothelium-dependent relaxation in murine aortas organ-cultured in a high-glucose condition. Aortas organ-cultured with a high concentration of glucose (40 mmol/L, 20 h; HG group) exhibited the following characteristics (versus aortas cultured in serum-free medium): (i) significantly weaker relaxation to acetylcholine, but unchanged relaxation to SNP and unchanged contractions to norepinephrine and isotonic K+, (ii) significantly greater superoxide generation (indicated by the amount of nitroblue tetrazolium reduced, (iii) significantly higher protein expression levels of gp91phox, NAD(P)H oxidase subunits, and endothelial NO synthase, (iv) significantly lower protein expression level of Mn-superoxide dismutase (SOD), and (v) markedly greater reduction in the protein expression of PPARγ than in that of PPARα. The HG-induced impairment of endothelium-dependent relaxation was prevented by cotreatment with tempol (a SOD mimetic). These results suggest that in the mouse aorta, exposure to high glucose levels may lead to an excessive generation of superoxide via increased gp91phox and decreased Mn-SOD protein expression and that this may in turn trigger an impairment of endothelium-dependent relaxation. Moreover, such protein changes in gp91phox and Mn-SOD may be secondary to a decreased expression of PPARγ protein.

UJI EFEKTIVITAS ANTIDIABETES KOMBINASI EKSTRAK DAUN MENIRAN (Phyllanthus niruri L.) dan KELOPAK BUNGA ROSELLA (Hibiscus sabdariffa L.) pada TIKUS JANTAN PUTIH SEBAGAI HEWAN PERCOBAAN

2019 ◽  
Vol 2 (1) ◽  
pp. 19-23
Author(s):  
Herviani Sari ◽  
Vera Estefania Kaban ◽  
Friska Raulina Situmorang ◽  
Firdaus Fahdi
Keyword(s):  
Blood Glucose ◽  
Leaf Extract ◽  
Negative Control Group ◽  
Positive Control ◽  
Negative Control ◽  
Control Group ◽  
High Dose ◽  
Glucose Levels ◽  
White Rats ◽  
Blood Glucose Levels

Background : Diabetes mellitus (DM) is a chronic disease caused by the body's inability to produce the hormone insulin or due to ineffective use of insulin production. Diabetes has become a global problem, DM prevalence of 4.6%, estimated in 2000 amounted to 5.6 million. One of the plants that can reduce blood glucose levels is meniran and rosella which are found in Indonesia. Objective : To determine the effect of decreasing blood glucose levels in white rats using a combination of meniran and rosella compared to glibenclamide.Method : This research was carried out experimentally. Simplicia of meniran leaves and rosella macerated using 80% ethanol. The research used 21 rats that were induced by alloxan and divided into 7 groups and all compared using glibenclamide.Group 1 (negative control) CMC Na 1%, group 2 (positive control) glibenclamide dose 0.45 mg / kgBB, group 3 single roselle extract dose 130 mg / kgBB, group 4 single meniran leaf extract dose 200 mg / kgBB, group 5 combination of meniran leaf extract dose of 100 mg / kgBB and rosella extract dose of 65 mg / kgBB, group 6 combination of meniran leaf extract dose of 200 mg / kgBB and rosella extract dose of 130 mg / kgBB, and group 7 meniran leaf extract combination dose 400 mg / kgBB and rosella extract dose 195 mg / kgBB. Result : The results showed that rats had hyperglycemia after being induced by alloxan.Data were analyzed using one way ANOVA method followed by LSD and tukeys' B post hoct test. Having a difference in the decrease in blood glucose levels between the positive control group and the five doses of meniran extract and rosella where p <0.05 gave a significant effect compared to the negative control group p> 0.05 did not have a significant effect in reducing blood glucose levels. Conclusion : Single meniran extract and high-dose combination extract are more effective than glibenclamide.

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