scholarly journals Carnosol promotes endothelial differentiation under H2O2-induced oxidative stress

2017 ◽  
Vol 69 (2) ◽  
pp. 299-304
Author(s):  
Shulin Ou ◽  
Jianfeng Lv ◽  
Liming Peng ◽  
Jin Zhao ◽  
Luxiang Chi
Keyword(s):  
Oxidative Stress ◽  
Cell Viability ◽  
Antioxidant Defense ◽  
Caspase 3 ◽  
Defense Mechanism ◽  
Stem Cell Marker ◽  
Endothelial Differentiation ◽  
H2o2 Treatment ◽  
Endothelial Cell Differentiation ◽  
Antiinflammatory Compound

Oxidative stress causes deregulation of endothelial cell differentiation. Carnosol is a potent antioxidant and antiinflammatory compound. In the present study, we examined whether the antioxidant effect of carnosol might protect bone marrow stem cells against H2O2-induced oxidative stress and promote endothelial differentiation. We examined cell viability by the MTT assay; oxidative stress and apoptosis were analyzed through changes in ROS levels, apoptotic ratio and caspase-3 activity; changes in protein expression of OCT-4, Flk-1, CD31 and Nrf-2 were assessed by Western blot analysis. H2O2 treatment increased oxidative stress and reduced cell viability, while the stem cell marker OCT-4 and endothelial markers Flk-1, CD31 were significantly downregulated as a result of the treatment with H2O2. Treatment with carnosol improved the antioxidant status, increased OCT-4 expression and promoted endothelial differentiation. This study provides evidence that carnosol could increase the antioxidant defense mechanism and promote endothelial differentiation.

Oxidative Stress and Antioxidant Defense Mechanism in Glomerular Diseases

1997 ◽  
Vol 22 (1-2) ◽  
pp. 161-168 ◽  
Author(s):  
Sándor Túri ◽  
Ilona Németh ◽  
Attila Torkos ◽  
Levente Sághy ◽  
Ilona Varga ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Defense ◽  
Defense Mechanism ◽  
Glomerular Diseases

scholarly journals Effects of enalapril and paricalcitol treatment on diabetic nephropathy and renal expressions of TNF-α, P53, Caspase-3 and Bcl-2 in STZ-induced diabetic rats

2019 ◽  
Author(s):  
Osama M. Ahmed ◽  
Tarek M. Ali ◽  
Mohamed A. Abdel Gaid ◽  
Ahmed A. Elberry
Keyword(s):  
Oxidative Stress ◽  
Wistar Rats ◽  
Antioxidant Defense ◽  
Caspase 3 ◽  
Enzyme Inhibitor ◽  
Elevated Serum ◽  
Antioxidant Defense System ◽  
Diabetic Rats ◽  
Defense System ◽  
Tnf Α

AbstractThis study aimed to assess the renopreventive effect of the angiotensin converting enzyme inhibitor (ACEI), enalapril, and/or vitamin D receptor (VDR) activator, paricalcitol, on streptozotocin (STZ) diabetes-induced nephropathy and to elucidate the mechanisms of action through investigation of the effects on renal oxidative stress, antioxidant defense system and expressions of TNF-α, P53, caspase-3, and Bcl-2. Diabetes mellitus was induced in fasting male Wistar rats by single intraperitoneal injection of STZ (45 mg /kg b.w.) dissolved in citrate buffer pH 4.5. Ten days after STZ injection, the diabetic rats were treated with enalapril (25 mg/l of drinking water) and/or paricalcitol (8 µg/kg b.w.per os) dissolved in 5% DMSO daily for 4 weeks. The obtained data revealed that the treatment of diabetic Wistar rats with enalapril and/or paricalcitol led to a significant decrease in the elevated serum urea, uric acid, creatinine and sodium, potassium levels; thereby reflecting improvement of the impaired kidney function. The deteriorated kidney lipid peroxidation, GSH content and GST and catalase activities in diabetic rats were significantly ameliorated as a result of treatment with enalapril and/or paricalcitol. The elevated fasting and post-prandial serum glucose levels and the lowered serum insulin and C-peptide levels were also improved. Moreover, the treatment of diabetic rats successfully prevented the diabetes-induced histopathological deleterious changes of kidney and islets of Langerhans of pancreas. In association, the immunohistochemically detected pro-inflammatory cytokine TNF-α and apoptotic mediators P53 and caspase-3 were remarkably decreased in kidney of diabetic rats as a result of treatment, while the expression of anti-apoptotic protein Bcl-2 was increased. Based on these findings, it can be concluded that enalapril and paricalcitol can prevent STZ diabetes-induced nephropathy though amelioration of the glycemic state and antioxidant defense system together with the suppression of oxidative stress, inflammation and apoptosis.

scholarly journals The Long Non-Coding RNA SNHG1 Attenuates Cell Apoptosis by Regulating miR-195 and BCL2-Like Protein 2 in Human Cardiomyocytes

2018 ◽  
Vol 50 (3) ◽  
pp. 1029-1040 ◽  
Author(s):  
Ning Zhang ◽  
Xin Meng ◽  
Lijun Mei ◽  
Jian Hu ◽  
Chedong Zhao ◽  
...  
Keyword(s):  
Cell Viability ◽  
Cell Apoptosis ◽  
Molecular Mechanisms ◽  
Caspase 3 ◽  
Heart Diseases ◽  
Cardiomyocyte Apoptosis ◽  
Luciferase Reporter ◽  
H2o2 Treatment ◽  
Human Cardiomyocytes

Background/Aims: Long non-coding RNAs (lncRNAs) are theorized to play key roles in the development of heart diseases. However, the role of lncRNAs in cardiomyocyte apoptosis is largely unknown. The present study examined the role of lncRNA SNHG1 in the human cardiomyocytes (HCMs) apoptosis and explored the underlying molecular mechanisms. Methods: SNHG1, miR-195 and mRNA expression was detected by qRT-PCR; protein level was determined by western blot; cell viability was detected by MTT assay; cell apoptosis was evaluated by flow cytometry and caspase-3 activity assay; the interaction between SNHG1 and miR195 was examined by using luciferase reporter assay. Results: Hydrogen peroxide (H2O2) treatment significantly suppressed cell viability and increased cell apoptotic rate and caspase-3 activity in HCMs. Overexpression of SNHG1 attenuated the effects of H2O2 on HCMs viability and apoptosis; while SNHG1 exerted the opposite effects. SNHG1 was found to sponge miR-195 and suppress the expression of miR-195 in HCMs. Overexpression of miR-195 suppressed cell viability and induced apoptosis in HCMs, and miR-195 was found to negatively regulate the expression of BCL-2 like protein 2 (BCL2L2) via targeting its 3’ untranslated region. Overexpression of BCL2L2 partially reversed the effects of miR-195 overexpression on cell viability and cell apoptosis of HCMs. MiR-195 overexpression or BCL2L2 knockdown attenuated the effects of SNHG1 overexpression on cell viability, cell apoptosis and protein levels of cleaved caspase-3, cleaved caspase-9 and Bax in H2O2-treated HCMs. Conclusion: Our results suggest a novel SNHG1/miR-195/BCL2L2 axis in the regulation of cardiomyocyte apoptosis. Modulation of SNHG1 may represent a novel strategy to treat cardiomyocyte apoptosis-related heart diseases.

scholarly journals The Relevance of Oxidative Stress Status in One Week and One Month Alcohol Abstinent Patients

2014 ◽  
Vol 33 (3) ◽  
pp. 284-290 ◽  
Author(s):  
Ovidiu Alexinschi ◽  
Roxana Chirita ◽  
Alin Ciobica ◽  
Padurariu Manuela ◽  
Romeo Dobrin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alcohol Withdrawal ◽  
Antioxidant Defense ◽  
Defense Mechanism ◽  
Specific Activity ◽  
Oxidative Stress Marker ◽  
Control Group ◽  
Stress Markers ◽  
Oxidative Stress Status ◽  
Markers Of Oxidative Stress

Abstract Background: Although it is generally accepted that there is an increased oxidative stress status in alcoholics, the separate relevance of oxidative stress following alcohol withdrawal is still not understood to this date. There are reports stating that the increased oxidative stress status in alcoholics may persist independently of the constant presence of alcohol intake, while on the other side, it was demonstrated that the antioxidant defense mechanism could significantly increase after alcohol withdrawal. Methods: In the present work, we were interested in studying the relevance of oxidative stress status in the alcohol withdrawal processes, by determining some oxidative stress markers (two antioxidant enzymes: superoxide dismutase - SOD and glutathione peroxidase - GPX and a lipid peroxidation maker - MDA) after one week and one month of abstinence, as compared to the baseline and a control group of subjects. Results: Our data confirmed the increased oxidative stress status in alcoholic patients and, more importantly, we de m - onstrated here a significant decrease of the oxidative stress status one week and one month following the withdrawal, as showed by a significant increase in the specific activity of SOD (p<0.003), as well as by a decrease in MDA levels (p<0.019). Still, in the case of all three markers of oxidative stress status which we determined, the levels after one week or one month of abstinence were significantly altered when compared to controls. Conclusions: This suggests that severe and prolonged deficiency in the oxidative stress marker levels needs longer than one month of abstinence to normalize.

scholarly journals New insight into the effects of lead modulation on antioxidant defense mechanism and trace element concentration in rat bone

2009 ◽  
Vol 2 (1) ◽  
pp. 18-23 ◽  
Author(s):  
Bhardwaj Payal ◽  
Harkiran Kaur ◽  
Durg Rai
Keyword(s):  
Oxidative Stress ◽  
Alkaline Phosphatase ◽  
Antioxidant Defense ◽  
Element Concentration ◽  
Defense Mechanism ◽  
Trace Element Concentration ◽  
Nucleic Acid Content ◽  
Glutathione S Transferase ◽  
Insight Into ◽  
Rat Bone

New insight into the effects of lead modulation on antioxidant defense mechanism and trace element concentration in rat boneRisks of heavy metals-induced severe bone disorders generate interest to their toxicity. The present study was undertaken to monitor the biochemical and antioxidant status of bone of 30 and 80 days old male Wistar rats exposed to 5 week lead treatment. At the end of study, the rats were sacrificed, their long bone i.e. femur were excised, cleaned of soft tissue, minced and homogenized. Nucleic acid content, alkaline phosphatase, lipid peroxidation, catalase, glutathione S-transferase and superoxide dismutase were determined in bone. In both groups of treated animals lead treatment increased the production of malondialdehyde, while reducing activities of catalase, glutathione S-transferase and superoxide dismutase, indicating that it causes oxidative stress. Parallely with these effects lead significantly reduced the nucleic acid content and the activity of alkaline phosphatase, considered as biomarkers of osteoblast's function, conditions and development of bones. Moreover the concentrations of copper, zinc, iron and sodium were reduced in the excised bones. The present study indicates that the lead induced bone toxicity and its deteriorated development is the consequence of a primary oxidative stress. Our results may be helpful in understanding the modulation of biochemical parameters under lead toxicity.

scholarly journals PTEN inhibitor bpV(HOpic) confers protection against ionizing radiation

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ankit Chauhan ◽  
Dhananjay Kumar Sah ◽  
Neeraj Kumari ◽  
Namita Kalra ◽  
Ravi Soni ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Repair ◽  
Ionizing Radiation ◽  
Antioxidant Defense ◽  
Defense Mechanism ◽  
Akt Signaling ◽  
Proliferation Index ◽  
Membrane Phospholipids

AbstractExposure to Ionizing radiation (IR) poses a severe threat to human health. Therefore, there is an urgent need to develop potent and safe radioprotective agents for radio-nuclear emergencies. Phosphatidylinositol-3-kinase (PI3K) mediates its cytoprotective signaling against IR by phosphorylating membrane phospholipids to phosphatidylinositol 3,4,5 triphosphate, PIP3, that serve as a docking site for AKT. Phosphatase and Tensin Homolog on chromosome 10 (PTEN) antagonizes PI3K activity by dephosphorylating PIP3, thus suppressing PI3K/AKT signaling that could prevent IR induced cytotoxicity. The current study was undertaken to investigate the radioprotective potential of PTEN inhibitor (PTENi), bpV(HOpic). The cell cytotoxicity, proliferation index, and clonogenic survival assays were performed for assessing the radioprotective potential of bpV(HOpic). A safe dose of bpV(HOpic) was shown to be radioprotective in three radiosensitive tissue origin cells. Further, bpV(HOpic) significantly reduced the IR-induced apoptosis and associated pro-death signaling. A faster and better DNA repair kinetics was also observed in bpV(HOpic) pretreated cells exposed to IR. Additionally, bpV(HOpic) decreased the IR-induced oxidative stress and significantly enhanced the antioxidant defense mechanism in cells. The radioprotective effect of bpV(HOpic) was found to be AKT dependant and primarily regulated by the enhanced glycolysis and associated signaling. Furthermore, this in-vitro observation was verified in-vivo, where administration of bpV(HOpic) in C57BL/6 mice resulted in AKT activation and conferred survival advantage against IR-induced mortality. These results imply that bpV(HOpic) ameliorates IR-induced oxidative stress and cell death by inducing AKT signaling mediated antioxidant defense system and DNA repair pathways, thus strengthening its potential to be used as a radiation countermeasure.

scholarly journals A Neuroprotective Bovine Colostrum Attenuates Apoptosis in Dexamethasone-Treated MC3T3-E1 Osteoblastic Cells

2021 ◽  
Vol 22 (19) ◽  
pp. 10195
Author(s):  
Sagrario Martin-Aragon ◽  
Paloma Bermejo-Bescós ◽  
Juana Benedí ◽  
Carlos Raposo ◽  
Franklim Marques ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Viability ◽  
Caspase 3 ◽  
Neuronal Damage ◽  
Dairy Product ◽  
Preliminary Evidence ◽  
Bovine Colostrum ◽  
Osteoblastic Cells ◽  
Osteoblastic Cell ◽  
Induced Apoptosis

Glucocorticoid-induced osteoporosis (GIO) is one of the most common secondary forms of osteoporosis. GIO is partially due to the apoptosis of osteoblasts and osteocytes. In addition, high doses of dexamethasone (DEX), a synthetic glucocorticoid receptor agonist, induces neurodegeneration by initiating inflammatory processes leading to neural apoptosis. Here, a neuroprotective bovine colostrum against glucocorticoid-induced neuronal damage was investigated for its anti-apoptotic activity in glucocorticoid-treated MC3T3-E1 osteoblastic cells. A model of apoptotic osteoblastic cells was developed by exposing MC3T3-E1 cells to DEX (0–700 μM). Colostrum co-treated with DEX was executed at 0.1–5.0 mg/mL. Cell viability was measured for all treatment schedules. Caspase-3 activation was assessed to determine both osteoblast apoptosis under DEX exposure and its potential prevention by colostrum co-treatment. Glutathione reduced (GSH) was measured to determine whether DEX-mediated oxidative stress-driven apoptosis is alleviated by colostrum co-treatment. Western blot was performed to determine the levels of p-ERK1/2, Bcl-XL, Bax, and Hsp70 proteins upon DEX or DEX plus colostrum exposure. Colostrum prevented the decrease in cell viability and the increase in caspase-3 activation and oxidative stress caused by DEX exposure. Cells, upon colostrum co-treated with DEX, exhibited higher levels of p-ERK1/2 and lower levels of Bcl-XL, Bax, and Hsp70. Our data support the notion that colostrum may be able to reduce DEX-induced apoptosis possibly via the activation of the ERK pathway and modulation of the Hsp70 system. We provided preliminary evidence on how bovine colostrum, as a complex and multi-component dairy product, in addition to its neuroprotective action, may affect osteoblastic cell survival undergoing apoptosis.

scholarly journals Nrf2 Inhibits Periodontal Ligament Stem Cell Apoptosis under Excessive Oxidative Stress

2017 ◽  
Author(s):  
Yanli Liu ◽  
Hongxu Yang ◽  
Yinhua Zhao ◽  
Min Zhang ◽  
Yongjin Chen
Keyword(s):  
Oxidative Stress ◽  
Periodontal Ligament ◽  
Caspase 3 ◽  
Oxidative Enzymes ◽  
Tunel Staining ◽  
Caspase 8 ◽  
Caspase 9 ◽  
Periodontal Ligament Stem Cells ◽  
H2o2 Treatment ◽  
Periodontal Ligament Stem Cell

The present study aimed to analyze novel mechanisms underlying Nrf2-mediated anti-apoptosis in periodontal ligament stem cells (PDLSCs) in the periodontitis oxidative microenvironment. We created an oxidative stress model with H2O2-treated PDLSCs. Herein, we used real-time PCR, western blotting, TUNEL staining, fluorogenic assay and transfer genetics to confirm the degree of oxidative stress and apoptosis as well as the Nrf2 function. Surprisingly, we demonstrated that with up-regulated ROS and MDA levels, the effect of oxidative stress was obvious under H2O2 treatment. Anti-oxidative molecules were changed after the H2O2 exposure, whereby the anti-oxidative signaling of Nrf2 was activated with the increase of its downstream effectors, HO-1, NQO1 and &gamma;-GCS. Additionally, the apoptosis levels gradually increased with oxidative stress and changes in the caspase-9, caspase-3, Bax and c-Fos levels, but not with caspase-8 and down-regulated Bcl-2. The enhanced antioxidant effect could not resist the occurrence of apoptosis. Furthermore, Nrf2 overexpression effectively improved the anti-oxidative levels and increased cell proliferation. At the same time, overexpression effectively restrained TUNEL staining and decreased the molecular levels of caspase-9, caspase-3, et al, but not that of caspase-8. By contrast, silencing the expression Nrf2 levels had the opposite effect. Collectively, Nrf2 alleviates PDLSCs via its effects on anti-oxidative and anti-intrinsic apoptosis by the activation of anti-oxidative enzymes.

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