Generation Of Oxidative Stress Research Articles

Effect of isotretinoin (Netlook) on the testis of adult male albino rats and the role of omega 3 supplementation: Ahistological and biochemical study.

Isotretinoin is an oral retinoid which used across the world in the treatment of patients especially adolescents complaining of acne. In spite of the prevalent clinical use of isotretinoin, the generation of oxidative stress with the affection of several organs leads to the limitation and restriction of its use. Omega‐3 (N‐3) is an essential polyunsaturated fatty acid (PUFAs) with powerful antioxidant properties. The aim of this study was to investigate the histological and biochemical changes occurring in the rat testis following isotretinoin intake and to evaluate the role of omega 3 supplementation in ameliorating testicular damage. Thirty adult male albino rats were divided equally into three groups. Group I is the control group, group II received isotretinoin (1.0 mg/kg/day) dissolved in distilled water and group III received isotretinoin (1.0 mg/kg/day) and omega 3 (400 mg/kg/day). Testis samples were collected and processed for light and electron microscopic examination. The blood samples were collected for biochemical assessments. Results indicated that isotretinoin caused histological changes in all stages of spermatogenesis and alterations of the hormonal assay. These changes in the rat testis which were corrected by omega 3 use.

Misuse of Cardiac Lipid upon Exposure to Toxic Trace Elements-A Focused Review.

Heavy metals and metalloids like cadmium, arsenic, mercury, and lead are frequently found in the soil, water, food, and atmosphere; trace amounts can cause serious health issues to the human organism. These toxic trace elements (TTE) affect almost all the organs, mainly the heart, kidney, liver, lungs, and the nervous system, through increased free radical formation, DNA damage, lipid peroxidation, and protein sulfhydryl depletion. This work aims to advance our understanding of the mechanisms behind lipid accumulation via increased free fatty acid levels in circulation due to TTEs. The increased lipid level in the myocardium worsens the heart function. This dysregulation of the lipid metabolism leads to damage in the structure of the myocardium, inclusive fibrosis in cardiac tissue, myocyte apoptosis, and decreased contractility due to mitochondrial dysfunction. Additionally, it is discussed herein how exposure to cadmium decreases the heart rate, contractile tension, the conductivity of the atrioventricular node, and coronary flow rate. Arsenic may induce atherosclerosis by increasing platelet aggregation and reducing fibrinolysis, as exposure interferes with apolipoprotein (Apo) levels, resulting in the rise of the Apo-B/Apo-A1 ratio and an elevated risk of acute cardiovascular events. Concerning mercury and lead, these toxicants can cause hypertension, myocardial infarction, and carotid atherosclerosis, in association with the generation of free radicals and oxidative stress. This review offers a complete overview of the critical factors and biomarkers of lipid and TTE-induced cardiotoxicity useful for developing future protective interventions.

Lutein attenuated methylglyoxal-induced oxidative damage and apoptosis in PC12 cells via the PI3K/Akt signaling pathway.

Methylglyoxal (MGO), a cytotoxic byproduct of glycolysis, causes neuro oxidative damage and apoptosis, and plays key roles in diabetic encephalopathy (DE). The goal of this research was to evaluate the roles of lutein attenuated MGO-induced damage in PC12 cells as well as the underlying mechanisms. The findings of this study showed that lutein has a significant impact on reducing the generation of reactive oxygen species (ROS) and oxidative stress in MGO-induced PC12 cells, which may be attributed to the increased antioxidant enzymes activity and the decreased MDA levels. Moreover, treatment with lutein also alleviated cell apoptosis and mitochondrial damage. Real-time PCR and western blot analysis showed that lutein enhanced the Bcl-2:Bax ratio, inhibited the expression of caspase-3 and caspase-9, and increased the protein level of phosphorylated Akt. The network pharmacology and molecular docking prediction results suggested that the phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) signaling pathway was a potential mechanism of lutein in DE treatment. Furthermore, LY294002, a specific PI3K inhibitor, partially abolished the protective effect of lutein. These results presented that lutein attenuated oxidative damage and apoptosis triggered by MGO in PC12 cells via the PI3K/Akt signaling pathway. PRACTICAL APPLICATIONS: Lutein is a common carotenoid dispersed in fruits and vegetables. This article confirmed a protective effect of lutein on oxidative damage and apoptosis in PC12 cells after MGO damage. These results indicated that lutein could potentially be developed as a nutraceutical or functional food in the prevention of diabetic-related neurodegenerative diseases.

Role of NLRP3 Inflammasome and Its Inhibitors as Emerging Therapeutic Drug Candidate for Alzheimer's Disease: a Review of Mechanism of Activation, Regulation, and Inhibition.

Alzheimer’s disease (AD) is one of the most prevalent neurodegenerative disorders. The etiology and pathology of AD are complicated, variable, and yet to be completely discovered. However, the involvement of inflammasomes, particularly the NLRP3 inflammasome, has been emphasized recently. NLRP3 is a critical pattern recognition receptor involved in the expression of immune responses and has been found to play a significant role in the development of various immunological and neurological disorders such as multiple sclerosis, ulcerative colitis, gout, diabetes, and AD. It is a multimeric protein which releases various cytokines and causes caspase-1 activation through the process known as pyroptosis. Increased levels of cytokines (IL-1β and IL-18), caspase-1 activation, and neuropathogenic stimulus lead to the formation of proinflammatory microglial M1. Progressive researches have also shown that besides loss of neurons, the pathophysiology of AD primarily includes amyloid beta (Aβ) accumulation, generation of oxidative stress, and microglial damage leading to activation of NLRP3 inflammasome that eventually leads to neuroinflammation and dementia. It has been suggested in the literature that suppressing the activity of the NLRP3 inflammasome has substantial potential to prevent, manage, and treat Alzheimer’s disease. The present review discusses the functional composition, various models, signaling molecules, pathways, and evidence of NLRP3 activation in AD. The manuscript also discusses the synthetic drugs, their clinical status, and projected natural products as a potential therapeutic approach to manage and treat NLRP3 mediated AD.

Application of nickel chitosan nanoconjugate as an antifungal agent for combating Fusarium rot of wheat

Agro-researchers are endlessly trying to derive a potential biomolecule having antifungal properties in order to replace the application of synthetic fungicides on agricultural fields. Rot disease often caused by Fusarium solani made severe loss of wheat crops every year. Chitosan and its metallic nano-derivatives hold a broad-spectrum antifungal property. Our interdisciplinary study deals with the application of nickel chitosan nanoconjugate (NiCNC) against Fusarium rot of wheat, in comparison with chitosan nanoparticles (CNPs) and commercial fungicide Mancozeb. CNPs and NiCNC were characterized on the basis of UV–Vis spectrophotometry, HR-TEM, FESEM, EDXS and FT-IR. Both CNPs and NiCNC were found effective against the fungal growth, of which NiCNC at 0.04 mg/mL showed complete termination of F. solani grown in suitable medium. Ultrastructural analysis of F. solani conidia treated with NiCNC revealed pronounced damages and disruption of the membrane surface. Fluorescence microscopic study revealed generation of oxidative stress in the fungal system upon NiCNC exposure. Moreover, NiCNC showed reduction in rot disease incidence by 83.33% of wheat seedlings which was further confirmed through the observation of anatomical sections of the stem. NiCNC application helps the seedling to overcome the adverse effect of pathogen, which was evaluated through stress indices attributes.

Grandiflorenic acid from Wedelia trilobata plant induces apoptosis and autophagy cell death in breast adenocarcinoma (MCF7), lung carcinoma (A549), and hepatocellular carcinoma (HuH7.5) cells lines

Introduction: Wedelia trilobata (Sphagneticola trilobata) is a plant used in this popular medicine for treating infectious, sores and swellings in some rural communities, and their extract has antioxidant, anti-inflammatory, antitumor and hepatoprotective effect. Cancer is a molecularly heterogeneous disease caused by environmental and, genetic factors, among others. Since the complexity of the disease leads to low response rates to the different treatments used, it is necessary to find alternative drugs aimed at its control. The objective of our study was to assess whether grandiflorenic acid (GFA) has antitumor activity on breast (MCF7), liver (HuH7.5), and lung (A549) tumor cell lines. Methods: We used cell integrity assessment methods to assess whether (GFA) would be cytotoxic for tumor cell lines at doses ranging from and the pattern of death involved in this effect. Results: Treatment using GFA significantly inhibited cell proliferation in the three studied cells, followed by a decrease in cell size. The assessment of the death mechanisms showed the treatments increased the production of reactive oxygen species, caused exposure of phosphatidylserine, depolarization of the mitochondrial membrane, and, decrease plasma membrane integrity, indicating mechanisms related to apoptosis. Besides, we found the formation of autophagy vacuoles in our tests. Conclusion: Finally, our study found the effect of GFA on breast (MCF7), lung (A549), and liver (HuH7.5) tumor cell lines induce cytotoxicity and patterns of death associated with apoptosis and autophagy, and oxidative stress generation plays a role in these two pathways of cell death. Thus, this study revealed GFA exhibits anti-cancer activity in vitro and could help future studies to improve strategies for cancer treatment with involving natural compounds.

Naringenin ameliorates myocardial injury in STZ-induced diabetic mice by reducing oxidative stress, inflammation and apoptosis via regulating the Nrf2 and NF-κB signaling pathways

Diabetes-induced myocardial damage leads to diabetic cardiomyopathy and is closely associated with the generation of oxidative stress and inflammation. Naringenin (NG) exhibits antioxidant and anti-inflammatory effects. However, whether NG has cardioprotective effects against diabetic cardiomyopathy by regulating oxidative stress and inflammation remains unknown. This study investigated the effect of NG on diabetic cardiomyopathy based on an analysis of streptozotocin (STZ)-induced type 1 diabetic mice. The results indicated that NG reduced cardiac fibrosis and cardiomyocyte apoptosis in this diabetic model, accompanied by reduced blood glucose. NG inhibited pro-inflammatory cytokines, the level of reactive oxygen species and the expression of nuclear factor kappa-B (NF-κB), whereas the expression of antioxidant enzymes and nuclear factor erythroid 2-related factor 2 (Nrf2) were greatly enhanced by NG. Furthermore, in high glucose-treated H9C2 myocardial cells, NG effectively reduced cell apoptosis by inhibiting the formation of reactive oxygen species and pro-inflammatory cytokines. NG's antioxidant and anti-inflammatory activities were mechanistically associated with NF-κB inhibition and Nrf2 activation in animal and cell experiments. Data analysis showed that NG could regulate Nrf2 and NF-κB pathways to protect against diabetes-induced myocardial damage by reducing oxidative stress and inhibiting inflammation.

Oxidative stress-mediated memory impairment during aging and its therapeutic intervention by natural bioactive compounds.

Aging and associated neurodegenerative diseases are accompanied by the decline of several brain functions including cognitive abilities. Progressive deleterious changes at biochemical and physiological levels lead to the generation of oxidative stress, accumulation of protein aggregates, mitochondrial dysfunctions, loss of synaptic connections, and ultimately neurodegeneration and cognitive decline during aging. Oxidative stress that arises due to an imbalance between the rates of production and elimination of free radicles is the key factor for age-associated neurodegeneration and cognitive decline. Due to high energy demand, the brain is more susceptible to free radicals-mediated damages as they oxidize lipids, proteins, and nucleic acids, thereby causing an imbalance in the homeostasis of the aging brain. Animal, as well as human subject studies, showed that with almost no or few side effects, dietary interventions and plant-derived bioactive compounds could be beneficial to recovering the memory or delaying the onset of memory impairment. As the plant-derived bioactive compounds have antioxidative properties, several of them were used to recover the oxidative stress-mediated changes in the aging brain. In the present article, we review different aspects of oxidative stress-mediated cognitive change during aging and its therapeutic intervention by natural bioactive compounds.

Protective effects of coenzyme Q10 nanoparticles on hepatotoxicity induced by monocrotophos in rats

The present study was executed to evaluate the efficacy of coenzyme Q10 nanoparticles (CoQ10 NPs) against monocrotophos (MCP) exposure-induced hepatotoxicity in rats. Albino Wistar rats were divided into 1) Control, 2) CoQ10 NPs treated, 3) MCPexposed and 4) CoQ10 NPs + MCP cotreated groups. Exposure to MCP elevated oxidative stress markers and significantly depleted antioxidant status. Besides the oxidative injuries, histological alterations in liver tissue were also observed in liver tissues of MCPexposed rats. CoQ10 NPs treatment significantly prevented oxidative stress generation and replenished antioxidant status. Treatment of CoQ10 NPs also prevented histological alterations in MCP-exposed rats. In conclusion, the results suggest that CoQ10 NPs have therapeutic potential against MCP-induced toxicity.

Anti-Aging Effects of R-Phycocyanin from Porphyra haitanensis on HUVEC Cells and Drosophila melanogaster.

Aging has become a global public health challenge. Many studies have revealed that the excessive generation of ROS and oxidative stress could be the major causative factors contributing to aging. In this study, R-phycocyanin (R-PC) was isolated from Porphyra haitanensis, and its anti-aging ability was explored by natural aging Drosophila melanogaster and H2O2-induced HUVEC cells as the aging model. Results showed that R-PC α and β subunits expressed have antioxidant activity and can inhibit the generation of radicals, exhibiting a protective effect against H2O2-induced apoptotic HUVEC cells death. R-PC prevented the H2O2-induced HUVEC cell cycle phase arrest by regulating cell cycle-related protein. Furthermore, R-PC prevented the H2O2-induced HUVEC cell cycle phase arrest by regulating cell-cycle-related protein expression. In vivo study also indicated that R-PC significantly increased the survival time and alleviated the oxidative stress of Drosophila melanogaster. Moreover, R-PC notably decreased levels of ROS in natural aging flies and inhibited lipid peroxidation by enhancing the expressions of the endogenous stress marker genes (SOD1, SOD2, CAT of Drosophila melanogaster). Taken together, a study on the antioxidation extract from Porphyra haitanensis, such as R-PC, may open a new window for the prevention of anti-aging.

Proanthocyanidins alleviate pentylenetetrazole-induced epileptic seizures in mice via the antioxidant activity.

The role of oxidative stress in the initiation and progress of epilepsy is well established. Proanthocyanidins (PACs), a naturally occurring polyphenolic compound, have been reported to possess a broad spectrum of pharmacological and therapeutic properties against oxidative stress. However, the protective effects of proanthocyanidins against epilepsy have not been clarified. In the present study, we used the pentylenetetrazole (PTZ)-induced epilepsy mouse model to explore whether proanthocyanidins could help to reduce oxidative stress and protect against epilepsy. Mice were allocated into four groups (n = 14 per each group): control, PTZ (60mg/kg, intraperitoneally), PACs + PTZ (200mg/kg, p.o.) and sodium valproate (VPA) + PTZ (200mg/kg, p.o.). PTZ injection caused oxidative stress in the hippocampal tissue as represented by the elevated lipid peroxidation and NO synthesis and increased expression of iNOS. Furthermore, depleted levels of anti-oxidants, GSH, GR, GPx, SOD, and CAT also indicate that oxidative stress was induced in mice exposed to PTZ. Additionally, a state of neuroinflammation was recorded following the developed seizures. Moreover, neuronal apoptosis was recorded following the development of epileptic convulsions as confirmed by the elevated Bax and caspase-3 and the decreased Bcl2 protein. Moreover, AChE activity, DA, NE, 5-HT, brain-derived neurotrophic factor levels, and gene expression of Nrf2 have decreased in the hippocampal tissue of PTZ exposed mice. However, pre-treatment of mice with PACs protected against the generation of oxidative stress, apoptosis, and neuroinflammation in the PTZ exposed mice brain as the biomarkers for all these conditions was bought to control levels. In addition, the gene expression of Nrf2 was significantly upregulated following PACs treatment. These results suggest that PACs can ameliorate oxidative stress, neuroinflammation, and neuronal apoptosis by activating the Nrf2 signaling pathway in PTZ induced seizures in mice.

Antitumoral potential of Chartergellus-CP1 peptide from Chartergellus communis wasp venom in two different breast cancer cell lines (HR+ and triple-negative)

Breast cancer represents the most incident cancer in women. Surgery, chemotherapy, radiation therapy, and hormone therapy remain the main treatment for this type of cancer. However, increasing resistance to anti-cancer drugs through poor response for some types of breast cancer to treatments highlights the need to develop new therapeutic agents to fight the disease. In this study, we evaluated the anti-tumor potential of the Chartergellus-CP1 peptide isolated from the wasp venom of Chartergellus communis in human breast cancer cell lines MCF-7 (HR+) and MDA-MB-231 (triple-negative). Cells viability, morphology, cell cycle dynamics, reactive oxygen species (ROS) production, and apoptosis were assessed for both cell lines after exposure to Chartergellus-CP1 during 24 and 48 h. The results showed that Chartergellus-CP1 led to a significant increase of cells in the S phase in addition to a high generation of ROS (being more evident in the MCF-7 cell line) associated with apoptotic cell death. This work demonstrates, for the first time, the cytotoxic effects of Chatergellus-CP1 on human breast cancer cell lines including cell cycle profile, oxidative stress generation, and cell death mechanisms.

A REVIEW ON GREEN-SYNTHESIS OF CERIUM OXIDE NANOPARTICLES: FOCUS ON CENTRAL NERVOUS SYSTEM DISORDERS

Green Synthesized Cerium oxide nanoparticles (CeO2NPs) have sparked a lot of interest in numerous disciplines of science and Technology during the past decade. A wide range of biological resources has been employed in synthesizing CeO2NPs, including plants, microorganisms, and other biological products. Biosynthesis procedures, current knowledge, and prospects in the synthesis of Green synthesis of CeO2NPs are also discussed. Neurodegenerative diseases, such as aging, trauma, Alzheimer's and Parkinson's, and other neurological problems, are linked to higher oxidative stress and superoxide radicals generation. Cerium oxide nanoparticles' antioxidant properties suggest that they may be useful in the treatment of CNS diseases. The biological antioxidant benefits of cerium oxide nanoparticles on extending cell and organism lifespan, preventing a free radical attack, and preventing trauma-induced neurological damage are discussed in this section. CeO2NPs, an aspect of nanotechnology, would emerge as a novel drug delivery carrier through therapeutic strategies. In several diseases oxidative stress and inflammation. CeO2NPs exhibited a remarkable ability to switch between+3 and+4 oxidation states making this an efficient therapeutic option and an effective drug delivery agent. Further Reactive oxygen and nitrogen species. The overall goal of this study is to provide reasonable insight into CeO2NPs as new therapeutic agents and to solve the challenges, of safely and effectively employing these CeO2NPs for efficient management of Central Nervous System diseases.

Exploring Nrf2 as a therapeutic target in testicular dysfunction.

Testicular dysfunction, a major contributory factor to infertility, has received a lot of attention over the recent years. Several studies have linked abnormal sperm function and morphology with an enhanced generation of reactive oxygen species (ROS) and oxidative stress. The nuclear factor erythroid-derived 2 (Nrf2) is a transcriptional response to cellular stresses (intrinsic or extrinsic) that regulates the oxidative status, mitochondrial dysfunction, inflammation, and proteostasis. In this review, the therapeutic role of Nrf2 was explored. To do so, scientific data were retrieved from databases such as Elsevier, Wiley, Web of Science, Springer, PubMed, Taylor and Francis, and Google Scholar using search terms such as "Nrf2" and "testis," "sperm," "testicular function," and "testosterone." It has been noted that Nrf2 influences the physiology and pathology of testicular dysfunction, especially in the spermatogenic process, by regulating cellular resistance to oxidative stress, inflammation, and environmental toxicants. However, numerous compounds serve as activators and inhibitors of testicular Nrf2. Nrf2 activators might play a therapeutic role in the prevention and treatment of testicular dysfunction, while molecules that inhibit Nrf2 might induce dysfunction in testis components. Nrf2 activators protect cells against oxidative damage and activate Nrf2/KEAP1 signaling which promotes its movement to the nucleus, and increased Nrf2 function and expression, along with their downstream antioxidant gene. Nrf2 inhibitors facilitate oxidative stress via interfering with the Nrf2 signal pathway. The Nrf2 activation could serve as a promising therapeutic target for testicular dysfunction. This review explored the effect of Nrf2 on testicular function while highlighting potential activators and inhibitors of Nrf2.

CircRNA Samd4 induces cardiac repair after myocardial infarction by blocking mitochondria-derived ROS output

Reactive oxygen species (ROS) derived from oxygen-dependent mitochondrial metabolism are the essential drivers of cardiomyocyte (CM) cell-cycle arrest in adulthood. Mitochondria-localized circular RNAs (circRNAs) play important roles in regulating mitochondria-derived ROS production, but their functions in cardiac regeneration are still unknown. Herein, we investigated the functions and underlying mechanism of mitochondria-localized circSamd4 in cardiac regeneration. We found that circSamd4 was selectively expressed in fetal and neonatal CMs. The transcription factor Nrf2 controlled circSamd4 expression by binding to the promoter of circSamd4 host gene. CircSamd4 overexpression reduced while circSamd4 silenced increased mitochondrial oxidative stress and subsequent oxidative DNA damage. Moreover, circSamd4 overexpression induced CM proliferation and prevented CM apoptosis, which reduced the size of the fibrotic area and improved cardiac function after myocardial infarction (MI). Mechanistically, circSamd4 reduced oxidative stress generation and maintained mitochondrial dynamics by inducing the mitochondrial translocation of the Vcp protein, which downregulated Vdac1 expression and prevented the mitochondrial permeability transition pore (mPTP) from opening. Our findings suggest that circSamd4 is a novel therapeutic target for heart failure after MI.

Pathological Mechanism and Targeted Drugs of COPD.

Chronic obstructive pulmonary disease (COPD) includes chronic bronchitis, emphysema, and small airway obstruction. Incompletely reversible airflow limitation, inflammation, excessive mucus secretion and bronchial mucosal epithelial lesions are the main pathological basis of the disease. The prevalence of COPD is increasingly worldwide, which has caused the burden on individuals and society. This paper summarizes the pathogenesis of COPD and clarifies the effect and mechanism of the latest targeted drugs for COPD. Besides, we focus on NOD-like receptor thermal protein domain associated protein 3 inflammasome (NLRP3 inflammasome). NLRP3 can promote production of interleukin-1β (IL-1β) and interleukin-18 (IL-18). NLRP3 is an important factor in the migratory aggregation of macrophages and neutrophils and the generation of oxidative stress. Inhibition of NLRP3 inflammasome indirectly blocks the inflammatory effects of IL-1β and IL-18, which may be regarded as an ideal target for COPD treatment.

Melatonin Prevents NaAsO2-Induced Developmental Cardiotoxicity in Zebrafish through Regulating Oxidative Stress and Apoptosis.

Melatonin is an indoleamine hormone secreted by the pineal gland. It has antioxidation and anti-apoptosis effects and a clear protective effect against cardiovascular diseases. Our previous studies demonstrated that embryonic exposure to sodium arsenite (NaAsO2) can lead to an abnormal cardiac development. The aim of this study was to determine whether melatonin could protect against NaAsO2-induced generation of reactive oxygen species (ROS), oxidative stress, apoptosis, and abnormal cardiac development in a zebrafish (Danio rerio) model. We found that melatonin decreased NaAsO2-induced zebrafish embryonic heart malformations and abnormal heart rates at a melatonin concentration as low as 10−9 mol/L. The NaAsO2-induced oxidative stress was counteracted by melatonin supplementation. Melatonin blunted the NaAsO2-induced overproduction of ROS, the upregulation of oxidative stress-related genes (sod2, cat, gpx, nrf2, ho-1), and the production of antioxidant enzymes (Total SOD, SOD1, SOD2, CAT). Melatonin attenuated the NaAsO2-induced oxidative damage, DNA damage, and apoptosis, based on malonaldehyde and 8-OHdG levels and apoptosis-related gene expression (caspase-3, bax, bcl-2), respectively. Melatonin also maintained the control levels of heart development-related genes (nkx2.5, sox9b) affected by NaAsO2. In conclusion, melatonin protected against NaAsO2-induced heart malformations by inhibiting the oxidative stress and apoptosis in zebrafish.

Identification of Active Component of Hachimi-jio-gan Ameliorating Diabetic Nephropathy

Conventional medicine-based Chinese herbal prescriptions, have fascinatedmuch attention due to their extensive and unique diversity of biologicaleffects without toxicity and/or adverse effects. Treatment with Hachimijio-gan (Ba-Wei-Di-Huang-Wan in Chinese) improved the dysregulatedlevels of hyperglycemic condition-related oxidative stress generation,advanced glycation endproduct generation, and renal function parameters.These results indicate that Hachimi-jio-gan is a prospective therapeuticagent against the pathogenesis of diabetic nephropathy. Cornel iridoidglycosides and polyphenol are the active compounds of Corni Fructus, theactive component of Hachimi-jio-gan, against kidney damage caused bydiabetes. Additionally, major components of the Corni Fructus, morronisideand 7-O-Galloyl-D-sedoheptulose (GS) are considered to be importantcontributors to prevent and/or delay the onset of kidney damage caused bydiabetes. Chief of all, GS is expected to be developed as a novel therapeuticdrug for the diabetes-accelerated kidney damage.

Biomarkers of Oxidative Stress Tethered to Cardiovascular Diseases.

Cardiovascular disease (CVD) is a broad term that incorporated a group of conditions that affect the blood vessels and the heart. CVD is a foremost cause of fatalities around the world. Multiple pathophysiological mechanisms are involved in CVD; however, oxidative stress plays a vital role in generating reactive oxygen species (ROS). Oxidative stress occurs when the concentration of oxidants exceeds the potency of antioxidants within the body while producing reactive nitrogen species (RNS). ROS generated by oxidative stress disrupts cell signaling, DNA damage, lipids, and proteins, thereby resulting in inflammation and apoptosis. Mitochondria is the primary source of ROS production within cells. Increased ROS production reduces nitric oxide (NO) bioavailability, which elevates vasoconstriction within the arteries and contributes to the development of hypertension. ROS production has also been linked to the development of atherosclerotic plaque. Antioxidants can decrease oxidative stress in the body; however, various therapeutic drugs have been designed to treat oxidative stress damage due to CVD. The present review provides a detailed narrative of the oxidative stress and ROS generation with a primary focus on the oxidative stress biomarker and its association with CVD. We have also discussed the complex relationship between inflammation and endothelial dysfunction in CVD as well as oxidative stress-induced obesity in CVD. Finally, we discussed the role of antioxidants in reducing oxidative stress in CVD.

Maackiain Prevents Amyloid-Beta-Induced Cellular Injury via Priming PKC-Nrf2 Pathway.

Amyloid-beta (Aβ) peptide induces neurotoxicity through oxidative stress and inflammatory response. Brain deposition of a large amount of amyloid-beta (Aβ), in particular Aβ42, promotes the development of Alzheimer's disease (AD). Maackiain is extracted from traditional Chinese medicine peony root and possesses antioxidative, antiosteoporosis, antitumor, and immunoregulatory effects. Whether Maackiain can reduce neurotoxicity caused by Aβ accumulation remains elusive. Herein, we found that Maackiain downregulated Aβ42-induced cell injury and apoptosis in PC12 cells. Moreover, Maackiain prevented Aβ42 stimulation-induced generation of oxidative stress and reduced Aβ42-caused impairment of mitochondrial membrane potential in PC12 cells. Maackiain increased the superoxide dismutase activity and decreased malondialdehyde content that was induced by Aβ42. Mechanistic studies showed that Maackiain increased intranuclear Nrf2 expression. Consistently, Nrf2 silencing by RNA interference weakened the protective role of Maackiain against Aβ exposure. In addition, calphostin C, a specific antagonist of protein kinase C, attenuated the promoting effects of Maackiain on Nrf2 nuclear translocation. Moreover, calphostin C attenuated the antioxidant and anti-inflammatory capabilities of Maackiain in PC12 cells. Collectively, Maackiain promoted Nrf2 activation through the PKC signaling pathway, thus preventing PC12 cells from Aβ-induced oxidative stress and cell injury, suggesting that Maackiain is a potential drug for AD treatment.