syedzayyan/paper_mill_benchmark huggingface dataset:
Asymmetric Dimethylarginine Protects Neurons from Oxygen Glucose Deprivation Insult by Modulating Connexin-36 Expression

Asymmetric dimethylarginine (adma) is a nonselective nitric oxide synthase inhibitor.Adma is thought to inhibit the production of nitric oxide (no) by neurons after oxygen-glucose deprivation (ogd).The gap junction protein connexin-36 (cx-36) is involved in the pathophysiology of stroke.We investigated whether adma could protect neurons from ogd insults by regulating the expression of cx-36.Methods.Cultured rat cortical neuronal cells were used.Neurons were treated with ogd with or without adma pretreatment.The lactate dehydrogenase (ldh) release rate was used to assess neuronal injury.Intracellular no levels were determined using 4-amino-5-methylamino-2 ′ ,7 ′ -difluorofluorescein diacetate.Western blotting was performed to detect cx-36 expression.Results.The ldh release rate increased in the supernatant of neurons after the ogd insult, whereas adma treatment reduced the ldh release rate.Intracellular no levels increased following ogd treatment, and this increase was not inhibited by adma treatment.Expression of cx-36 was upregulated in neurons under ogd conditions, and treatment with adma downregulated the expression of cx-36.Conclusions.Adma protects neurons from ogd insult, and cx-36 downregulation may be a possible pathway involved in adma-mediated neuronal protection.

Journal: Oxidative Medicine and Cellular Longevity (2022)
Publication types: Research Article;
Association between Oxidative Burden and Restenosis: A Case-Control Study

In-stent restenosis (isr) is an important clinical complication that occurs following stent implantation.The application of drug-eluting stents (des) and even consumption of drugs such as antiplatelet agents and statins are not completely effective in reducing isr risk.Since the number of these patients continues to rise, it is pivotal to detect patients who are at a higher risk of isr.In addition, identification of biochemical markers of isr could give the right perspective on choosing the proper strategy to treat these patients.Several pathophysiological pathways including oxidative stress (os) are implicated in the progression of isr.Hence, this study aimed to evaluate the association between oxidative/anti-oxidative markers and isr.Methods.This was a case-control study which comprised 21 isr, 26 nisr (non-isr), and 20 healthy subjects.The serum levels of os markers including malondialdehyde (mda), thiol groups (gsh), total antioxidant capacity (tac), and the activity of serum antioxidant enzymes such as glutathione peroxidase (gpx) and superoxide dismutase (sod) were assessed by colorimetric methods.The overall oxidative burden was assessed using a pro-oxidant-antioxidant balance (pab) assay.Results.Mda levels were considerably higher in the isr group when compared to healthy subjects ( p = 0.004 ).Pab also indicated significantly higher values in both isr ( p &lt; 0.001 ) and nisr ( p &lt; 0.001 ) groups related to healthy subjects.No significant differences were observed between the studied groups regarding thiol levels, antioxidant enzyme activities, and tac.Multinomial logistic regression analysis showed that elevated serum levels of mda (or: 1.028, 95% ci: 1.008-1.048; p = 0.006 ) and pab (or: 1.076, 95% ci: 1.017-1.139; p = 0.011 ) were significantly associated with higher isr risk; however, increased values of tac (or: 0.990, 95% ci: 0.982-0.999; p = 0.030 ) were significantly associated with decreased isr risk, while after adjustment for confounders, only sod activity (or: 0.0, 95% ci: 0.0-0.0; p &lt; 0.001 ) and pab value (or: 1.866, 95% ci: 1.856-1.900; p &lt; 0.001 ) showed association with isr risk.Conclusion.According to the present findings, some oxidative and antioxidative markers like pab and sod activity showed the potential in the prediction of isr risk.

Journal: Oxidative Medicine and Cellular Longevity (2022)
Publication types: Clinical Study;
Assessing the Role of Nrf2/GPX4-Mediated Oxidative Stress in Arsenic-Induced Liver Damage and the Potential Application Value of Rosa roxburghii Tratt [Rosaceae]

Arsenic poisoning is a geochemical disease that seriously endangers human health.The liver is one of the important target organs for arsenic poisoning, several studies have shown that oxidative stress plays an important role in arsenic-induced liver damage.However, the specific mechanism of arsenic-induced oxidative stress has not yet been fully elucidated, and currently, there are no effective intervention measures for the prevention and treatment of arsenic-induced liver damage.In this study, the effect of the nrf2/gpx4 signaling pathway and oxidative stress in the arsenic-induced liver damage was first evaluated.The results show that arsenic can activate the nrf2/gpx4 signaling pathway and increase the oxidative stress, which in turn promotes arsenic-induced liver damage in miha cells.Moreover, when we applied the nrf2 inhibitor, the promoting effect of arsenic on liver damage was alleviated by inhibiting the activation of the nrf2/gpx4 signaling pathway.Subsequently, the rosa roxburghii tratt [rosaceae] (rrt) intervention experiments in cells and arsenic poisoning population were designed.The results revealed that rrt can inhibit nrf2/gpx4 signaling pathway to reduce oxidative stress, thereby alleviates arsenic-induced liver damage.This study provides some limited evidence that arsenite can activate nrf2/gpx4 signaling pathway to induce oxidative stress, which in turn promotes arsenic-induced liver damage in miha cells.The second major finding was that kaji-ichigoside f1 may be a potential bioactive compound of rrt, which can inhibit nrf2/gpx4 signaling pathway to reduce oxidative stress, thereby alleviates arsenic-induced liver damage.Our study will contribute to a deeper understanding of the mechanisms in arsenic-induced liver damage, these findings will identify a possible natural medicinal food dual-purpose fruit, rrt, as a more effective prevention and control strategies for arsenic poisoning.

Journal: Oxidative Medicine and Cellular Longevity (2022)
Publication types: Research Article;
Aquaporin 4 Depolarization-Enhanced Transferrin Infiltration Leads to Neuronal Ferroptosis after Subarachnoid Hemorrhage in Mice

The infiltration of blood components into the brain parenchyma through the lymphoid system is an important cause of subarachnoid hemorrhage injury.Aqp4, a water channel protein located at the astrocyte foot, has been reported to regulate blood–brain barrier integrity, and its polarization is disrupted after sah.Neuronal ferroptosis is involved in subarachnoid hemorrhage- (sah-) induced brain injury, but the inducing factors are not completely clear.Transferrin is one of the inducing factors of ferroptosis.This study is aimed at researching the role and mechanism of aqp4 in brain injury after subarachnoid hemorrhage in mice.An experimental mouse sah model was established by endovascular perforation.An aav vector encoding aqp4 with a gfap-specific promoter was administered to mice to achieve specific overexpression of aqp4 in astrocytes.Pi staining, fer-1 intervention, and transmission electron microscopy were used to detect neuronal ferroptosis, and dextran (40 k d) leakage was used to detect bbb integrity.Western blot analysis of perfused brain tissue protein samples was used to detect transferrin infiltration.First, neuronal ferroptosis 24 h after sah was observed by pi staining and fer-1 intervention.Second, a significant increase in transferrin infiltration was found in the brain parenchyma 24 h after sah modeling, while transferrin content was positively correlated with neuronal ferroptosis.Then, we observed that aqp4 overexpression effectively improved aqp depolarization and bbb injury induced by sah and significantly reduced transferrin infiltration and neuronal ferroptosis after sah.Finally, we found that aqp4 overexpression could effectively improve the neurobehavioral ability of sah mice, and the neurobehavioral ability was negatively correlated with transferrin brain content.Taken together, these data indicate that overexpression of aqp4 in the mouse brain can effectively improve post-sah neuronal ferroptosis and brain injury, at least partly by inhibiting transferrin infiltration into the brain parenchyma in the glymphatic system.

Journal: Oxidative Medicine and Cellular Longevity (2022)
Publication types: Research Article;
Applications of Neural Network-Based Plan-Cancer Method for Primary Diagnosis of Mesothelioma Cancer

“malignant mesothelioma (mm)” is an uncommon although fatal form of cancer.The proper mm diagnosis is crucial for efficient therapy and has significant medicolegal implications.Asbestos is a carcinogenic material that poses a health risk to humans.One of the most severe types of cancer induced by asbestos is “malignant mesothelioma.” prolonged shortness of breath and continuous pain are the most typical symptoms of the condition.The importance of early treatment and diagnosis cannot be overstated.The combination “epithelial/mesenchymal appearance of mm,” however, makes a definite diagnosis difficult.This study is aimed at developing a deep learning system for medical diagnosis mm automatically.Otherwise, the sickness might cause patients to succumb to death in a short amount of time.Various forms of artificial intelligence algorithms for successful “malignant mesothelioma illness” identification are explored in this research.In relation to the concept of traditional machine learning, the techniques support “vector machine, neural network, and decision tree” are chosen.Spss has been used to analyze the result regarding the applications of neural network helps to diagnose mm.

Journal: BioMed Research International (2023)
Publication types: Research Article;
Apoptotic and Antioxidant Activity of Gold Nanoparticles Synthesized Using Marine Brown Seaweed: An In Vitro Study

A major paradigm shift in the field of nanobiotechnology is the invention of an eco‐friendly, economical, and green approach for synthesis of metal nanoparticles.In the present study, we have synthesized gold nanoparticles (au nps) using aqueous extracts of marine brown seaweed sargassum longifolium.The synthesized nanoparticle was subjected to characterization using different techniques such as uv‐vis spectroscopy, fourier transform infrared spectroscopy, atomic force microscope, scanning electron microscope, transmission electron microscope, and elemental dispersive x‐ray diffraction.Further, the seaweed extract and the synthesized au nps were evaluated for its anticancer effect using mg‐63 human osteosarcoma cells besides in vitro antioxidant effect.The formation of s.Longifolium‐mediated synthesis of gold nanoparticles was demonstrated by uv‐vis spectroscopy.Presence of elemental gold was confirmed by edx analysis.Tem analysis demonstrated spherical morphology of the synthesized au nps and sem analysis revealed the particle size to be in the range of 10‐60 nm.The ftir showed the presence of hydroxyl functional groups.The toxicity of s.Longifolium extract and the synthesized au nps was tested using brine shrimp lethality assay at different concentrations with results showing both seaweed extract and au nps to be nontoxic.Both s.Longifolium and au nps exhibited significant antioxidant activity by scavenging dpph free radicals and h 2 o 2 radicals.Significant antiproliferative effect was observed against mg‐63 osteosarcoma cells.It was also shown that the seaweed extract and the au nps induced cytotoxicity in cell lines by mechanism of apoptosis.In conclusion, this study provided insight on au nps synthesized from s.Longifolium as a potent antioxidant and anticancer agent.

Journal: BioMed Research International (2022)
Publication types: Research Article;
Apatinib Promotes Apoptosis of Pancreatic Cancer Cells through Downregulation of Hypoxia-Inducible Factor-1 α and Increased Levels of Reactive Oxygen Species

At present, apatinib is considered a new generation agent for the treatment of patients with gastric cancer.However, the effects of apatinib on pancreatic cancer have not been clarified.This study investigated the impact of apatinib on the biological function of pancreatic cancer cells and the potential mechanism involved in this process.Using the cell counting kit-8 method, we confirmed that apatinib treatment inhibited cell proliferation in vitro .Moreover, the migration rate of pancreatic cells was inhibited.The effects of apatinib on apoptosis and cell cycle distribution of pancreatic carcinoma cells were detected by flow cytometry.The number of apoptotic cells was significantly increased, and the cell cycle was altered.Furthermore, we demonstrated that apatinib inhibited the expression of hypoxia-inducible factor-1 α (hif-1 α ), vascular endothelial growth factor, and markers of the phosphoinositide 3-kinase (pi3k)/akt/m tor signaling pathway, which increased the levels of reactive oxygen species in vitro.Apatinib significantly inhibited the biological function of pancreatic cancer cells.It promoted apoptosis, downregulated the expression of hif-1 α , and increased the levels of reactive oxygen species.

Journal: Oxidative Medicine and Cellular Longevity (2019)
Publication types: Research Article;
Antiviral Activity of Plantago asiatica Polysaccharide against Pseudorabies Virus In Vitro

Pseudorabies (pr) is an acute infectious disease of various domestic animals and wild animals caused by pseudorabies virus (prv).It is mainly characterized by fever, itching, encephalomyelitis, and respiratory and neurological disorders.Plantago asiatica polysaccharide (plp), extracted from the whole plant of plantago asiatica l., showed immunomodulatory and antioxidation effects, but the antiviral activity had not been reported.In this study, the inhibitory effect of plp on prv infection was studied.Our study first revealed that plp could inhibit prv infection in a dose-dependent manner.By adding plp at different stages of the virus’s life cycle, we revealed that plp could reduce the attachment and penetration of prv into pk15 cells.The inhibition of prv attachment was better than inhibition of prv penetration.However, plp did not affect prv replication and inactivation.In addition, plp decreased the intracellular ros levels in infected cells significantly, and ros scavenger nac decreased prv infection.Therefore, our study provided preliminary data of anti-prv activity of plp, which was established to be a novel anti-prv infection agent.

Journal: Oxidative Medicine and Cellular Longevity (2022)
Publication types: Research Article;
Antioxidative Capacity of Liver- and Adipose-Derived Mesenchymal Stem Cell-Conditioned Media and Their Applicability in Treatment of Type 2 Diabetic Rats

Type 2 diabetes mellitus (t2dm) is mainly characterized by insulin resistance and impaired insulin secretion, which cannot be reversed with existing therapeutic strategies.Using mesenchymal stem cells (mscs), cell‐based therapy has been demonstrated in displaying therapeutic effects in t2dm for their self‐renewable, differentiation potential, and immunosuppressive properties and higher levels of angiogenic factors.Stem cell therapies are complicated and have a serious adverse effect including tumor formation and immunogenicity, while using mesenchymal stem cell‐conditioned media (msc‐cm) significantly reduces stem cell risk, maintaining efficacy and showing significantly higher levels of growth factors, cytokines, and angiogenic factors that stimulate angiogenesis and promote fracture healing in diabetes.In the present study, we investigated the therapeutic potential of the liver and adipose msc‐cm in diabetic endothelial dysfunction compared with standard insulin therapy.Fifty adult male sprague dawley rats were divided equally into 5 groups as follows: control, diabetic, diabetic+insulin, diabetic+liver msc‐cm, and diabetic+adipose msc‐cm; all treatments continued for 4 weeks.Finally, we observed that liver msc‐cm therapy had the most apparent improvement in levels of blood glucose; hb a1c; ages; lipid panel (cholesterol, tg, ldl, hdl, and total lipids); renal function (urea, uric acid, creatinine, and total protein); liver function (ast, alt, alp, bilirubin, and albumin); cpk; c‐peptide; ho‐1; inflammatory markers including il‐6, tnf‐ α , and crp; growth factors (liver and serum igf‐1); amylase; histopathological changes; pancreatic cell oxidative stress; and antioxidant markers (mda, gsh, ros, cat, sod, ho‐1, and xo) toward the normal levels compared with insulin and adipose mscs‐cm.Moreover, both the liver and adipose msc‐cm relieved the hyperglycemic status by improving pancreatic islet β cell regeneration, promoting the conversion of alpha cells to beta cells, reducing insulin resistance, and protecting pancreatic tissues against oxidative stress‐induced injury as well as possessing the ability to modulate immunity and angiogenesis.These results indicated that msc‐cm infusion has therapeutic effects in t2dm rats and may be a promising novel therapeutic target.

Journal: Oxidative Medicine and Cellular Longevity (2021)
Publication types: Research Article;
Antioxidant, Anticancer, and PXR-Dependent CYP3A4 Attributes of Schweinfurthia papilionacea (Burm.f.) Boiss., Tricholepis glaberrima DC. and Viola stocksii Boiss

Present study established the biological potential of schweinfurthia papilionacea, tricholepis glaberrima and viola stocksii extracts for their potential applications in drug formulations.Initially, ftir was performed to ascertain functional groups and then plant extracts were prepared using five solvents depending on the polarity.Total phenolic contents were observed in the range of 36.36 ± 1.08 mg gae/g to 95.55 ± 2.46 mg gae/g while flavonoid contents were found in the range of 10.51 ± 0.25 mg qe/g to 22.17 ± 1.79 mg qe/g.Antioxidant activity was determined using trp, cuprac, tac and dpph assays and was recorded highest in s.Papilionacea followed by t.Glaberrima extracts.Tpc and tfc were found to be strongly correlated with trp (r &gt; 0.50), cuprac (r &gt; 0.53) and dpph (r = 0.31 and 0.72) assay while weakly correlated with tac (r = 0.08 and 0.03) as determined by pearson correlation analysis.Anticancer activity showed that s.Papilionacea chloroform extracts possess highest cell viability (85.04 ± 4.24%) against hep g2 cell lines while t.Glaberrima chloroform extracts exhibited highest activity (82.80 ± 2.68%) against ht144 cell lines.Afterwards, highest pxr activation was observed in t.Glaberrima (3.49 ± 0.34 μg/m l fold) at 60 μg/m l and was correlated with increase in cyp3a4 activity (15.0 ± 3.00 μg/m l ic50 value).Furthermore, antimalarial activity revealed &gt;47600 ic50 value against p.Falciparum d6 and p.Falciparum w2 and antimicrobial assay indicated highest activity (32 ± 2.80 mm) in s.Papilionacea against c.Neoformans.At the end, gc-ms analysis of n-hexane plant extracts showed 99.104% of total identified compounds in t.Glaberrima and 94.31% in v.Stocksii.In conclusion, present study provides insight about the different biological potentials of s.Papilionacea and t.Glaberrima extracts that rationalize the applications of these extracts in functional foods and herbal drugs for the management of oxidative-stress related diseases, antimicrobial infections and liver and skin cancer.

Journal: Oxidative Medicine and Cellular Longevity (2022)
Publication types: Research Article;
Antioxidant and Anti-Inflammatory Activities of Coenzyme-Q10 and Piperine against Cyclophosphamide-Induced Cytotoxicity in HuH-7 Cells

Cyclophosphamide (cp) alkylates dna and rna produce crosslinks that cause gene expression and protein synthesis inhibition to exert its anticancer effect.However, adverse effects of cp have restricted the cp application in cancer treatment.We investigate coenzyme‐q10 (q10) and piperine (p) protective role on cp oxidant and inflammatory effect.Hu h‐7 cells were exposed to varying concentrations and combinations of q10, p, and cp and evaluated intracellular ros generation as well as inflammatory responses upon exposure.Our results showed q10 and/or p suppressed both basal and cp‐induced ros generation without upsetting the balance in activities of sod, catalase, and gsh levels.Analysis of proinflammatory cytokine gene expression showed that cp treatment alone only induced expression of il-6β .However, coexposure of the cells to both q10 and cp caused significant suppression of basal cox-2 and tnf-α gene expression, while coexposure of the cells to cp and p with co‐q10 suppressed basal il-1β gene expression.Q10 also suppressed cp‐induced expression of cox-1 .P and cp suppressed basal expression of il-6β and il-12β , while p and q10 suppressed cp‐induced il1-α gene expression.Taken together, both q10 and p seem to be inhibiting nf κβ pathway to suppress cp‐mediated inflammation.In conclusion, q10 and/or p induced suppression of ros generation mediated by cp and also suppressed cp‐induced inflammation by inhibiting expression of specific inflammatory cytokine.

Journal: BioMed Research International (2022)
Publication types: Research Article;
Antileukemic Effects of Anti-miR-146a, Anti-miR-155, Anti-miR-181a, and Prednisolone on Childhood Acute Lymphoblastic Leukemia

Prednisolone has been used frequently in the treatment of acute lymphoblastic leukemia.However, to overcome the challenges of the treatment, the development of additional therapies is of great importance.Small, non‐protein‐coding rnas, namely, micro rnas (mi rnas), are critical epigenetic regulators with physiological and pathological importance.This study is aimed at determining the effects of mi r‐146a, mi r‐155, and mi r‐181a inhibition with their corresponding anti‐mi rs on both leukemic and healthy cells, individually and with prednisolone.Leukemic (sup‐b15) and healthy b‐lymphocyte (nci‐bl 2171) cell lines were used in this study.A total of 12 experimental groups included individual and combinational silenced all‐associated mi rnas (hsa‐mi r‐155, hsa‐mi r‐146a, and hsa‐mi r‐181a) and their combination with prednisolone.Cytotoxicity, proliferation, cell cycle, and apoptosis analyses were performed by using wst‐1, trypan blue, apc‐brd u, annexin v, and jc‐1 methods in each study group, respectively.To control the effectiveness of anti‐mi r transfection and prednisolone application, mi rna expression analysis was performed from all groups.Anti‐mi r application was effective on the viability, proliferation, cell cycle, and apoptosis of leukemia cells, and this effect was increased with prednisolone administration.In addition, this activity was found to be very low on healthy cells.In conclusion, anti‐mi r applications may have the potential for clinical use of adjuvant to or as an alternative to conventional therapies for childhood acute lymphoblastic leukemia.

Journal: BioMed Research International (2021)
Publication types: Research Article;