scholarly journals POSSIBLE PREVENTION OF REACTIVE OXYGEN SPECIES INDUCED HUMAN TRABECULAR MESHWORK CELL DAMAGE BY RESVERATROL AND ASCORBIC ACID.

2019 ◽  
Vol 26 (07) ◽  
pp. 1036-1041
Author(s):  
Muhammad Yaqoob Shahani ◽  
Umbreen Bano ◽  
Shazia Begum Shahani ◽  
Pashmina Shaikh ◽  
Sameena Gul Memon ◽  
...  

Objectives: To analyze the antioxidant activity of Resveratrol and Ascorbic Acid against hydrogen peroxide (an oxidant) mediated cell injury of human trabecular meshwork cells. Study Design: Experimental study. Setting: Molecular Biology Laboratory at Medical Research Centre, Liaquat University of Medical & Health Sciences, Jamshoro. Period: Six months. Materials and Methods: Human Trabecular Meshwork cells were purchased from ScienCell Research Laboratories, USA. TM cell metabolism, TM cell viability and Reactive oxygen species were detected by standard methods in co- and pre- treated TM cells. Results: A significant reduction in TM cell metabolism was observed approximating 61% at 1.0 mM H2O2 compared to Ascorbate – 99% and Resveratrol 99% (p=0.0001). Resveratrol was more effective than Ascorbate even at 4.0 mM H2O2, the TM cell activity was noted 76%. Compared to H2O2- treated TM cells, resveratrol improved mitochondrial function upto 4.0 mM H2O2 (76%). Compared to co-treatment, the pretreatment shows similar results except at 4.0 mM H2O2. At 4.0 mM H2O2 the pre-treat TM cell metabolic activity was found as 11%, 31% and 47% compared to co-treat as 9%, 31% and 76% in controls, ascorbate and resveratrol groups respectively (p<0.05). Resveratrol shows significant decrease in viability was seen in controls compared to Ascorbate and Resveratrol groups. Cell viability showed statistically significant differences at 2.0 and 4.0 mM H2O2 compared to controls (P=0.0001). For reactive oxygen species (ROS), cells were incubated and with Ascorbate and Resveratrol for 24 hours and TM cells were treated with 0.0mM, 0.5 mM, 1.0 mM, 2.0mM and 4.0mM H2O2. Significant decrease in ROS was noted by Resveratrol compared to Ascorbate. Conclusions: Resveratrol and Ascorbate may prove useful in preventing and delaying the glaucoma, and timely institution of these anti – oxidants may help maintain trabecular meshwork functions and prevent visual loss.

Antioxidants ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 107
Author(s):  
Hsin-Yi Chen ◽  
Hsiu-Chuan Chou ◽  
Yi-Jung Ho ◽  
Shing-Jyh Chang ◽  
En-Chi Liao ◽  
...  

Oxidative stress generated by reactive oxygen species (ROS) plays a critical role in the pathomechanism of glaucoma, which is a multifactorial blinding disease that may cause irreversible damage within human trabecular meshwork cells (HTMCs). It is known that the transforming growth factor-β (TGF-β) signaling pathway is an important component of oxidative stress-induced damage related to extracellular matrix (ECM) fibrosis and activates cell antioxidative mechanisms. To elucidate the dual potential roles and regulatory mechanisms of TGF-β in effects on HTMCs, we established an in vitro oxidative model using hydrogen peroxide (H2O2) and further focused on TGF-β-related oxidative stress pathways and the related signal transduction. Via a series of cell functional qualitative analyses to detect related protein level alterations and cell fibrosis status, we illustrated the role of TGF-β1 and TGF-β2 in oxidative stress-induced injury by shTGF-β1 and shTGF-β2 knockdown or added recombinant human TGF-β1 protein (rhTGF-β1). The results of protein level showed that p38 MAPK, TGF-β, and its related SMAD family were activated after H2O2 stimulation. Cell functional assays showed that HTMCs with H2O2 exposure duration had a more irregular actin architecture compared to normal TM cells. Data with rhTGF-β1 (1 ng/mL) pretreatment reduced the cell apoptosis rate and amount of reactive oxygen species (ROS), while it also enhanced survival. Furthermore, TGF-β1 and TGF-β2 in terms of antioxidant signaling were related to the activation of collagen I and laminin, which are fibrosis-response proteins. Succinctly, our study demonstrated that low concentrations of TGF-β1 (1 ng/mL) preserves HTMCs from free radical-mediated injury by p-p38 MAPK level and p-AKT signaling balance, presenting a signaling transduction mechanism of TGF-β1 in HTMC oxidative stress-related therapies.


2020 ◽  
Vol 22 (Supplement_2) ◽  
pp. ii17-ii17
Author(s):  
Shashank Hambarde ◽  
Martyn Sharpe ◽  
David Baskin ◽  
Santosh Helekar

Abstract Noninvasive cancer therapy with minimal side effects would be ideal for improving patient outcome in the clinic. We have developed a novel therapy using strong rotating magnets mounted on a helmet. They generate oscillating magnetic fields (OMF) that penetrate through the skull and cover the entire brain. We have demonstrated that OMF can effectively kill patient derived glioblastoma (GBM) cells in cell culture without having cytotoxic effects on cortical neurons and normal human astrocytes (NHA). Exposure of GBM cells to OMF reduced the cell viability by 33% in comparison to sham-treated cells (p&lt; 0.001), while not affecting NHA cell viability. Time lapse video-microscopy for 16 h after OMF exposure showed a marked elevation of mitochondrial reactive oxygen species (ROS), and rapid apoptosis of GBM cells due to activation of caspase 3. Addition of a potent antioxidant vitamin E analog Trolox effectively blocked OMF-induced GBM cell death. Furthermore, OMF significantly potentiated the cytotoxic effect of the pro-oxidant Benzylamine. The results of our studies demonstrate that OMF-induced cell death is mediated by ROS generation. These results demonstrate a potent oncolytic effect on GBM cells that is novel and unrelated to any previously described therapy, including a very different mechanism of action and different technology compared to Optune therapy. The effect is very powerful, and unlike Optune, can be seen within hours after initiation of treatment. We believe that this technology holds great promise for new, effective and nontoxic treatment of glioblastoma.


2016 ◽  
Vol 52 (27) ◽  
pp. 4888-4890 ◽  
Author(s):  
V. N. Carroll ◽  
C. Truillet ◽  
B. Shen ◽  
R. R. Flavell ◽  
X. Shao ◽  
...  

We report the radiosynthesis of an endogenous redox pair, [11C]ascorbic acid and [11C]dehydroascorbic acid and their application to ROS sensing.


2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Mingyan Hu ◽  
Ping Ye ◽  
Hua Liao ◽  
Manhua Chen ◽  
Feiyan Yang

Metformin is a first-line drug for the management of type 2 diabetes. Recent studies suggested cardioprotective effects of metformin against ischemia/reperfusion injury. However, it remains elusive whether metformin provides direct protection against hypoxia/reoxygenation (H/R) injury in cardiomyocytes under normal or hyperglycemic conditions. This study in H9C2 rat cardiomyoblasts was designed to determine cell viability under H/R and high-glucose (HG, 33 mM) conditions and the effects of cotreatment with various concentrations of metformin (0, 1, 5, and 10 mM). We further elucidated molecular mechanisms underlying metformin-induced cytoprotection, especially the possible involvement of AMP-activated protein kinase (AMPK) and Jun NH(2)-terminal kinase (JNK). Results indicated that 5 mM metformin improved cell viability, mitochondrial integrity, and respiratory chain activity under HG and/or H/R (P<0.05). The beneficial effects were associated with reduced levels of reactive oxygen species generation and proinflammatory cytokines (TNF-α, IL-1α, and IL-6) (P<0.05). Metformin enhanced phosphorylation level of AMPK and suppressed HG + H/R induced JNK activation. Inhibitor of AMPK (compound C) or activator of JNK (anisomycin) abolished the cytoprotective effects of metformin. In conclusion, our study demonstrated for the first time that metformin possessed direct cytoprotective effects against HG and H/R injury in cardiac cells via signaling mechanisms involving activation of AMPK and concomitant inhibition of JNK.


Author(s):  
Young Sook Kim ◽  
Heung Joo Yuk ◽  
Dong-Seon Kim

Oxidative stress is a major contributor to muscle aging and loss of muscle tissue. Jakyakgamcho-tang has been used in traditional Eastern medicine to treat muscle pain. Here, we compared various solvent-based Jakyakgamcho-tang extracts in terms of their effects against hydrogen peroxide-induced oxidative stress in murine C2C12 skeletal muscle cells. Total phenolic content and total flavonoid content in 30% ethanol extracts of Jakyakgamcho-tang were higher than those of water extracts of Jakyakgamcho-tang. Ethanol extracts of Jakyakgamcho-tang had stronger antioxidant and 2,2-azino-bis-3-ethylbenzothiazoline-6-sulfonic acid and 2,2&acute;-diphenyl-1-picrylhydrazyl-scavenging activity than water extracts of Jakyakgamcho-tang. The ethanol extract of Jakyakgamcho-tang inhibited peroxide-induced cell viability and intracellular reactive oxygen species generation more effectively than the water extract of Jakyakgamcho-tang in a dose-dependent manner. These results suggest that the ethanol extract of Jakyakgamcho-tang is relatively more efficacious at protecting against oxidative stress-induced muscle cell death because it prevents reactive oxygen species generation in C2C12 cells. Moreover, the current study indicated that the effective dose of the ethanol extract of Jakyakgamcho-tang required to alleviate muscle pain might be lower than that required for Jakyakgamcho-tang.


Nutrients ◽  
2020 ◽  
Vol 12 (1) ◽  
pp. 159
Author(s):  
Sonali Nashine ◽  
Anthony B. Nesburn ◽  
Baruch D. Kuppermann ◽  
Maria Cristina Kenney

Resveratrol is a phytoalexin, stilbenoid compound with antioxidant properties attributable to its bioactive trans-resveratrol content. This study characterized the effects of over-the-counter (OTC) resveratrol nutritional supplements and a HPLC-purified resveratrol formulation, in human transmitochondrial age-related macular degeneration (AMD) retinal pigment epithelial (RPE) patient cell lines. These cell lines, which were created by fusing blood platelets obtained from dry and wet AMD patients with mitochondria-deficient (Rho0) ARPE-19 cells, had identical nuclei (derived from ARPE-19 cells) but different mitochondria that were derived from AMD patients. After resveratrol treatment, the levels of cell viability and reactive oxygen species production were measured. Results demonstrated that treatment with different resveratrol formulations improved cell viability and decreased reactive oxygen species generation in each AMD patient cell line. Although further studies are required to establish the cytoprotective potential of resveratrol under different physiological conditions, this novel study established the positive effects of OTC resveratrol supplements in macular degeneration patient cybrid cell lines in vitro.


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