Decreased Malondialdehyde Levels Research Articles

Spermine driven water deficit tolerance in early growth phases of sweet corn genotypes under hydroponic cultivation

Sweet corn is highly susceptible to water deprivation, making it crucial to identify effective strategies for enhancing its tolerance to water deficit conditions. This study investigates the novel application of Spermine as a bio-stimulant to improve sweet corn (Zea mays L. var. saccharata) resilience under hydroponic water deficit conditions. Four genotypes (Dessert, Messenger, Tyson, and Royalty) were treated with Spermine (0.2 mM foliar application), polyethylene glycol 6000 (8% and 12%), and their combinations. The impacts on growth parameters, photosynthetic performance, and oxidative stress markers were evaluated. Spermine significantly enhanced biomass parameters, counteracting the severe reductions caused by PEG-induced water deprivation. In the Dessert and Tyson genotypes, total biomass increased by 145%, while it increased by 118% in Messenger and 110% in Royalty when treated with Spermine under severe water deprivation. However, Spermine treatment application did not recorded higher differences compared to control under non water deficit conditions. In the Dessert genotype, root length increased by 36.6% under combined treatment compared to 12% PEG alone. Spermine also mitigated reductions in shoot length, improved by 90.6% and specific leaf area, with a notable 272.6% increase in Tyson under severe water deficit. Photosynthetic performance, including chlorophyll and carotenoid levels, was enhanced, with a 103.1% increase in relative chlorophyll content in Dessert under severe water deprivation. Spermine also reduced oxidative damage, as indicated by a 48.7% decrease in malondialdehyde levels in Tyson, and increased peroxidase activity, enhancing antioxidant defense in Messenger under severe water deprivation. The quantum efficiency of Photosystem II, which was significantly reduced by water deficit, showed substantial improvement with Spermine treatment, with increases of 107.2% in Tyson and 99.4% in Royalty under moderate water deprivation. These results highlight the potential of Spermine as an effective strategy to improve sweet corn resilience under water-limited conditions, offering a novel approach for sustainable crop management.

Molecular mechanisms and enhanced functions of Hibiscus sabdariffa L—nanoliposomes as an emerging therapeutic strategy in UV and galactosamine skin aging-induced model

BackgroundSkin aging is a multifactorial disorder that occurs due to extrinsic and intrinsic factors, where a decrease in natural antioxidant defenses and an imbalance between molecular biomarkers occur. The current study aims to develop nanoliposomes for the dermal delivery of Hs and to investigate their effects on skin biomarkers and skin aging.MethodsChemical profiling performed via high-performance liquid chromatography (HPLC)/ESI‒PDA‒MS revealed enrichment in phenolic metabolite contents. Hs-nanolopeosomes were characterized for their mean size, encapsulation efficiency of Hs and ability to penetrate the skin via confocal microscopy. An aged rat model generated via UV and galactosamine injection was evaluated for reduced glutathione (GSH) and malondialdehyde (MDA) levels, in addition to the levels of collagenase and elastase enzymes in the different study groups, which included a healthy control group, an aged group, a prophylactic group, an aged group treated with Hs-nanoliposomes, and a green tea extract-treated group (positive control). Moreover, the Bcl-2/Bax proteins were determined via ELISA, and MMP-1, MMP-2, MMP-9, and TIMP-1 expression was determined via RT‒qPCR in the study groups.ResultsHs-nanoliposomes (~ 400 nm) proved deep skin localization in confocal images. Compared with the aged group and the green tea extract-treated group, the Hs-liposome-treated group presented elevated reduced glutathione and decreased malondialdehyde levels and inhibited collagenase and elastase enzymes. This treatment also decreased the Bcl-2/Bax ratio and downregulated the expression of MMP-1, MMP-2, and MMP-9. However, upregulation of TIMP-1 expression was detected. The outcomes were confirmed by histopathological assays, which revealed reduced saging and collagen damage in the Hs-nanolipid-treated group.ConclusionThe present study proposed a potential antiaging nanobased formulation that can deliver Hs extract deep in the dermis layer to prevent the oxidative stress that leads to aging.

Protective effect of epidermal growth factor on cryopreservation of dromedary camel epididymal spermatozoa: Evidence from in vitro and in silico studies

Epidermal growth factor (EGF) plays a crucial role in maintaining male reproductive capacity in mammals, however, its protective effects on cryopreserved dromedary camel epididymal spermatozoa have not been thoroughly investigated. This study aims to investigate the potential protective role of EGF on cryopreserved camel epididymal spermatozoa, supported by evidence from a molecular docking study. We assessed sperm motility, kinematics parameters, oxidative stress, ultrastructural changes, apoptosis, and molecular docking markers in camel epididymal spermatozoa following cryopreservation. Camel epididymal spermatozoa (n=30 pairs of testes) were collected from local slaughterhouses. The epididymal spermatozoa were diluted with a freezing medium (SHOTOR extender) supplemented with different concentrations of EGF; 0 (EGF0), 50 (EGF50), 100 (EGF100), 200 (EGF200), and 400 (EGF400) ng/mL in SHOTOR extender and cryopreserved using a standard protocol. All EGF groups showed significant improvements in sperm progressive motility, viability, and sperm membrane function after equilibration at 5 °C for 24hours. Regarding frozen-thawed samples, sperm progressive motility and some kinematic parameters (DAP, VSL, VCL and AHL) were significantly higher in the EFG400 group compared to the other groups (P < 0.01). A significant increase in the percentage of live/acrosome-intact sperm was observed, accompanied by a significant decrease in malondialdehyde levels in all EGF groups (P < 0.05). Both the EGF200 and EGF400 groups showed significantly higher sperm viability and significantly lower percentages of apoptotic and necrotic sperm compared to the other groups (P < 0.05). EGF supplementation preserved the ultrastructural integrity and cryotolerance of epididymal camel spermatozoa. The docking analysis indicated that EGF exhibited higher binding affinity with apoptosis sperm markers, including caspase-3 and bcl-2-associated X (Bax) proteins, with binding energies of -502.0 and -621.0kcal/mol, respectively. In conclusion, the addition of EGF to SHOTOR extender was found to have beneficial effects on sperm motility, kinematics parameters, sperm viability, acrosome integrity, sperm ultrastructural features, and reduced oxidative stress and apoptosis-like changes in cryopreserved epididymal camel sperm.

Effect of Ethanol Extract and Ethyl Acetate Fraction of Soursop Leaves administration on Malondialdehyde Levels of Alloxan-Induced Rat Endocrine Cells

Soursop leaves (Annona muricata L.) contain many antioxidant compounds such as phenols and flavonoids that play an active role in inhibiting oxidative stress and can inhibit damage and death in cells, tissues, or organs. The objective of this study was to determine the effect of soursop leaf ethanol extract and ethyl acetate fraction effect on malondialdehyde levels and the quantity of pancreatic endocrine cells in male rats (Mus musculus) induced with alloxan. Method, the test animals were divided into seven groups (n=4). The normal control group was only given feed, the negative control group was given CMC-Na solution, the positive control group was given vitamin C dose of 50 mg/kg.BW, treatment group I was given soursop ethanol extract dose of 50 mg/kg.BW, treatment group II was given soursop ethanol extract dose of 100 mg./kg.BW, ethyl acetate fraction treatment group III was given soursop ethyl acetate fraction dose of 25 mg/kg BW, and treatment group IV was given soursop ethyl acetate fraction dose of 50 mg/kg BW. Results showed that the administration of ethyl acetate fraction of soursop leaves at a dose of 25 mg/kg BW showed the most effective potential significantly (p&lt;0.05) in reducing malondialdehyde levels and cell death. In conclusion, administering ethanol extract and ethyl acetate fraction of soursop leaves to rats which experiencing oxidative stress in their pancreas can stimulate and increase regeneration of endocrine cell in all rat groups. This is proven by a decrease of malondialdehyde levels and the number of necrosis cell necrosis. 1

Memantine/Rosuvastatin Therapy Abrogates Cognitive and Hippocampal Injury in an Experimental Model of Alzheimer's Disease in Rats: Role of TGF-β1/Smad Signaling Pathway and Amyloid-β Clearance

Alzheimer’s disease (AD) is a multifactorial neurodegenerative disorder of complex pathogenesis and multiple interacting signaling pathways where amyloidal-β protein (Aβ) clearance plays a crucial role in cognitive decline. Herein, the current study investigated the possible modulatory effects of memantine/ rosuvastatin therapy on TGF-β1/p-Smad/p21 signaling pathway and their correlation to the blood brain barrier transporters involved in Aβ-clearance and microRNAs as a novel molecular mechanism in AD treatment. AD was induced by a single intracerebroventricular streptozotocin injection (ICV-STZ, 3 mg/kg) in rats and drug therapy was continued for 28 days after AD induction. Efficacy was monitored by applying a battery of behavioral assessments, as well as biochemical, histopathological, molecular and gene expression techniques. The upregulated TGF-β1-signaling in the untreated rats was found to be highly correlated to transporters and microRNAs governing Aβ-efflux; ABCA1/miRNA-26 and LRP1/miRNA-205 expressions, rather than RAGE/miRNA-185 controlling Aβ-influx; an effect that was opposed by the tested drugs and was found to be correlated with the abolished TGF-β1-signaling as well. Combined memantine/rosuvastatin therapy ameliorated the STZ evoked decreases in escape latency and number of crossovers in the Morris water maze test, % spontaneous alternation in the Y-maze test, and discrimination and recognition indices in the object recognition test. The evoked behavioral responses were directly related to the β-amyloid accumulation and the alteration in its clearance. Additionally, drug treatment increased brain glutathione and decreased malondialdehyde levels. These findings were histopathologically confirmed by a marked reduction of gliosis and restoration of neuronal integrity in the CA1 region of the hippocampus of the AD rats. These findings implicated that the memantine/rosuvastatin combination could offer a new therapeutic potential for AD management by abrogating the TGF-β1/p-Smad2/p21 pathway and regulating Aβ-clearance.Graphical

Biophysical and biochemical study exploring resveratrol protective potential against gamma irradiation effects

BackgroundGamma irradiation causes oxidative stress and disturbs the physiological balance in organisms. Natural antioxidants, like resveratrol (Res), can buffer these effects. The study's goal is to find out whether Res can help reverse changes caused by gamma irradiation in male Wistar rats' total antioxidant capacity (TAC), antioxidant enzyme activity, electrolyte levels, and hemoglobin structure.MethodsTwenty-four rats were divided into four groups: control, Res-treated, irradiated, and Res + irradiated. Blood and tissue samples were collected on the day 16th of the experiment. The levels of antioxidants, catalase (CAT) activity, glutathione (GSH), and glutathione peroxidase (GPx) were estimated along with electrolyte level measurements. UV–FTIR and dielectric spectroscopy were used to assess conformational changes in hemoglobin.ResultsGamma irradiation decreased antioxidant levels and increased markers of oxidative stress. Resveratrol treatment increased the antioxidant capacity and levels of nitric oxide and decreased malondialdehyde levels. Further, Res protected the structure of hemoglobin and decreased the radiation-induced damage.ConclusionResveratrol shows potential as a protective agent against gamma irradiation-induced oxidative stress by enhancing antioxidant defenses and restoring hemoglobin structure.

Ameliorating Effect of Fermented Perilla frutescens on Sleep Deprivation-Induced Cognitive Impairment Through Antioxidant and BDNF Signaling in Mice.

Background: Adequate sleep is essential for maintaining cognitive function, as evidenced by literature. Perilla frutescens var. acuta Kudo (PF) is a traditional medicinal herb reported to improve vascular cognitive impairment and induce sedation. However, the effects of PF on cognitive impairment caused by sleep deprivation (SD) have not yet been evaluated. This study aims to evaluate the effects of fermented PF (FPF) and its underlying mechanisms in a model of SD-induced cognitive impairment. Methods: Mice were subjected to SD to establish cognitive impairment, and FPF was administered once daily for 3 days. Cognitive performance was assessed using Y-maze and passive avoidance tests, followed by molecular mechanisms analyses. Results: FPF treatment improved SD-induced cognitive impairment, as evidenced by increased spontaneous alternation and extended latency time. Histological analysis revealed that SD impaired the hippocampus, and this impairment was alleviated by FPF treatment. FPF demonstrated antioxidant activity by increasing glutathione levels and decreasing malondialdehyde levels. Furthermore, the decreased levels of brain-derived neurotrophic factor (BDNF) observed in sleep-deprived mice were restored with FPF treatment. FPF also enhanced the phosphorylation of tropomyosin receptor kinase B, extracellular signal-regulated kinase, and cAMP response element-binding protein. Conclusions: These results indicate that FPF may have beneficial effects on SD-induced cognitive impairment by protecting against oxidative stress and increasing BDNF expression.

Pueraria lobata extract ameliorates D-GalN/LPS-induced liver injury through targeting TLR4/NF-κB signalling pathway and regulating gut microbiota

AbstractKudzu root (Pueraria lobata), known for its dual role as a medicinal herb and food ingredient, has proven anti-inflammatory and antioxidant properties. This study explored the effects of P. lobata extract (PLE) on D-galactose/lipopolysaccharide (D-GalN/LPS)-induced liver inflammation and oxidative stress in mice, along with its impact on gut microbiota. The in vivo studies indicated that PLE significantly reduced hepatic levels of pro-inflammatory cytokines (tumour necrosis factor-α, interleukin-1β, and interleukin-6) and increased the anti-inflammatory cytokine interleukin-10. It also lowered serum aspartate aminotransferase and alanine aminotransferase activities, indicating reduced liver damage, and mitigated oxidative stress by decreasing malondialdehyde levels while restoring superoxide dismutase activity. Western blot analysis revealed that PLE inhibited the phosphorylation of NF-κB pathway proteins (p65 and IκB) and suppressed TLR4 expression, highlighting its role in this inflammatory pathway. Additionally, PLE ameliorated D-GalN/LPS-induced gut microbiota dysbiosis, reducing Proteobacteria abundance and promoting beneficial genera such as Lactobacillus, Bifidobacterium, and Akkermansia. These findings suggest that PLE protects against liver inflammation and oxidative stress, while improving gut microbiota composition, offering potential therapeutic strategies for liver-related diseases.

Gastrodin ameliorates diabetic nephropathy by activating the AMPK/Nrf2 pathway.

Diabetic nephropathy (DN) is a leading cause of end-stage kidney failure, contributing to elevated morbidity and mortality rates in individuals with diabetes. Despite its potential renoprotective effects, the molecular mechanism by which gastrodin (GSTD) impacts DN remains unclear. To investigate this, mice were initially induced with DN via intraperitoneal streptozotocin (STZ) injection (50mg/kg) and subsequently treated with varying doses of GSTD (5, 10, 20mg/kg). Furthermore, the potential molecular mechanism of GSTD in mitigating DN was explored in vivo in conjunction with compound C, an inhibitor of 5'-AMP-activated protein kinase (AMPK). Subsequently, the blood weight, fasting blood glucose levels, and renal injury markers of DN-afflicted mice were assessed. Additionally, renal tissues were subjected to quantitative reverse-transcriptase-polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA) to evaluate inflammatory factor levels, colorimetric assays to measure renal malondialdehyde (MDA) levels, and immunoblotting analysis to examine AMPK/nuclear factor erythroid 2-related factor 2 (Nrf2) pathway. The results demonstrated that a 6-week GSTD regimen effectively improved metabolic manifestations associated with DN, including reductions in fasting blood glucose levels, 24-hour urine output, renal indices, amelioration of glomerular histopathological abnormalities, diminished glycogen accumulation, and fibrosis. Furthermore, DN-afflicted renal tissues exhibited decreased MDA levels and elevated expression of AMPK/Nrf2 pathway-associated proteins. The beneficial effects of GSTD on DN and its protein modulation were reversed upon co-intervention with compound C. Together, our findings imply that GSTD improves DN by activating the AMPK/Nrf2 pathway, thereby mitigating STZ-induced renal damage, inflammatory responses, and oxidative stress.

Abstract 029: Malondialdehyde as a Clinical Indicator for Oxidative Stress and Functional Outcomes in Acute Ischemic Stroke

Introduction Acute Ischemic stroke (AIS) is a leading cause of death and disability worldwide, with Social Isolation (SI) being a contributing factor to worse functional outcomes. The molecular and metabolic changes that occur after AIS are not fully understood. One mechanism known to trigger systemic inflammatory responses and neuronal death characteristic of stroke is the rapid increase in Reactive Oxygen Species (ROS), leading to oxidative stress (OS). New data reports that SI has been shown to increase OS in mouse models. One emerging biomarker able to reliably measure OS is Malondialdehyde (MDA), a reactive carbonyl compound originating from polyunsaturated fatty acid oxidation and lipid peroxidation. Due to its composition, MDA readily reacts with lipid membranes, making it a sensitive OS biomarker. This study assessed MDA levels in the plasma of AIS patients to evaluate its ability to predict long‐term functional outcomes and complications arising from SI. Hypothesis We hypothesized that OS levels correlate with long‐term functional outcomes in AIS patients and varies based on non‐modifiable risk factors such as sex and race. Methods In this study, we used peripheral blood plasma from healthy volunteers (HV, N=24), and from AIS patients (N=27) at 3d and 7d post‐stroke to capture the temporal profile of MDA after injury. Social Isolation was measured utilizing ULCA Loneliness scale and Lubben Social Network Scale collected during patients’ hospitalization. Results AIS patients had an increase in MDA levels compared to the control group, as seen in prior literature. We found a significant positive correlation with age of AIS patients and higher levels of MDA (p&lt;0.05). There was a positive trend with BMI and levels of MDA. As expected, non‐lonely AIS patients had increased levels of MDA when compared to non‐lonely HV (p&lt;0.05). Interestingly, lonely AIS patients had a decrease in MDA when compared to their lonely HV counterparts (p&lt;0.001). Stroke patients with larger social networks had decreased MDA levels. There was no relationship between levels of MDA during hospitalization and functional outcome at 3 months post discharge. Conclusion MDA appears to be a promising biomarker for oxidative stress in AIS patients, with notable associations with age, BMI, and social network and isolation. These findings underscore the complex relationship between OS, social factors, and stroke outcomes. Further research is needed to understand the impact of OS and its correlation with SI so that new treatment plans can be developed for stroke survivors.

Inhibiting Ferroptosis Prevents the Progression of Steatotic Liver Disease in Obese Mice.

Ferroptosis, a form of regulated cell death characterized by lipid peroxidation and iron accumulation, has been implicated in the progression of metabolic-dysfunction-associated steatohepatitis (MASH) in obesity. This study investigated the role of ferroptosis in the development of hepatic steatosis and MASH in obese mice and assessed the therapeutic potential of ferrostatin-1, a ferroptosis inhibitor. C57BL/6J wild-type (n = 8) and ob/ob mice (n = 16) were maintained on a standard chow diet. Mice were divided into three groups that included C57BL/6 (n = 8), ob/ob (n = 8), and ob/ob + ferrostatin-1 (FER) (n = 8), with the latter group receiving an intraperitoneal injection of 5 μM/kg ferrostatin three times per week for eight weeks. Following treatment, serum and tissue samples were collected for analysis. Significant hepatic steatosis and increased lipogenesis markers were observed in ob/ob mice, which were restored to baseline levels in the ob/ob + FER group treated with ferrostatin-1. Elevated oxidative stress was indicated by increased reactive oxygen species (ROS) and malondialdehyde (MDA) levels in the ob/ob group, while glutathione peroxidase 4 (GPX4) activity was significantly reduced. Ferrostatin-1 treatment decreases MDA levels and restores GPX4 activity. Additionally, ferrostatin mitigates iron overload and promotes macrophage polarization from M1 to M2, thereby reducing liver inflammation and fibrosis. Ferrostatin treatment reversed mitochondrial dysfunction in ob/ob mice. Our findings revealed that ferroptosis plays a significant role in the progression of obesity to hepatic steatosis and MASH. Inhibiting ferroptosis using ferrostatin-1 effectively improves liver histology, reduces oxidative stress, normalizes lipogenesis, and modulates macrophage polarization. This study highlights the potential of targeting ferroptosis as a therapeutic strategy for obesity-related liver diseases, warranting further investigation in clinical settings.

Green synthesis of silver nanoparticles containing Cichorium intybus to treat the sepsis-induced DNA damage in the liver of Wistar albino rats

Abstract Sepsis is a severe reaction of the body to an infection, presenting a critical medical crisis. It represents an imbalance between the body’s anti- and pro-inflammatory reactions. The occurrence of sepsis, which leads to multiple-organ failure and increased mortality, is marked by dysfunction in the lungs, heart, kidneys, and liver. The involvement of reactive oxygen species is believed to contribute to the progression of sepsis. Data suggest potential advantages of phenolic compounds derived from plants in combating sepsis. Plant polyphenols can be antioxidants by scavenging free radicals, chelating metals, and binding to proteins. In this research, silver nanoparticles (AgNPs) were produced by the aqueous extract of Cichorium intybus leaf for the purpose of treating sepsis-induced DNA harm. The recent study focused on the biological aspect including the cytotoxicity properties on normal (HUVEC) cell line. The AgNPs were analyzed by transmission electron microscopy (TEM), scanning electron microscopy (SEM), fourier-transform infrared spectroscopy, X-ray powder diffraction, and UV-Vis. The TEM and SEM images of AgNPs exhibited the average size of 35.29 nm with spherical morphology. In the in vivo study, the animals were categorized into four groups: sepsis-induced, sham, AgNPs-20, and AgNPs-100. AgNPs treatment resulted in a significant decrease in tissues damage (p &lt; 0.01). The sepsis-induced group showed a significantly elevated malondialdehyde (MDA) level in comparison to the sham group (p &lt; 0.01). Nevertheless, the groups that received AgNPs experienced a decrease in MDA levels and an increase in glutathione and superoxide dismutases levels (p &lt; 0.01). Additionally, the rats treated with AgNPs exhibited a reduction in the IL-1β mRNA expression levels (p &lt; 0.01).

Mitigating effects of agmatine on myocardial infarction in rats subjected to isoproterenol.

Isoproterenol (ISO) usage is limited by its potential for cardiotoxicity. We sought to investigate the potential of agmatine in mitigating ISO-induced cardiotoxicity. Agmatine (100mg/kg/day) was intraperitoneally administered to Wistar rats for 7days in the presence or absence of cardiotoxicity induced by subcutaneous injection of ISO (85mg/kg) on the sixth and seventh days. ECG parameters, lactate dehydrogenase (LDH), malondialdehyde (MDA), and creatinine phosphokinase (CPK) were investigated. Changes in cardiac tissue were also investigated using H&E staining. The heart weight/body weight ratio increased in ISO-treated rats. In the agmatine + ISO group, the increased heart rate observed in ISO-treated rats was reversed (317.2 ± 10.5 vs 452.2 ± 10.61, P < 0.001). Agmatine ameliorated the change in PR, RR, and ST intervals and the QRS complex, which was reduced by ISO. Treatment with saline, ISO, and agmatine had no significant effect on papillary muscle stimulation (P > 0.05). The administration of agmatine to ISO-receiving group could mitigate several parameters when compared to ISO-receiving group including increasing papillary muscle contraction (0.83 vs 0.71 N/M2 respectively, P < 0.01), decreasing LDH levels (660ng/ml vs 1080ng/ml, respectively, P < 0.05), decreasing CPK levels (377 U/l vs 642 U/l, respectively, P < 0.05) and decreasing MDA levels (20.32µM/l vs 46.83µM/l, P < 0.001). Coadministration of agmatine and ISO is capable of ameliorating ISO cardiotoxicity by antioxidant effects and controlling the hemostasis of calcium in myocytes.

Potential protection of resveratrol-tempeh against nephrotoxic and hepatotoxic histological damage in mice induced by aluminum

Aluminum is a widely distributed metal that, while generally safe at low levels, can become toxic when accumulated in the body. Its exposure is daily through various sources, including food, water, and medications. High levels of aluminum have been shown to adversely affect the kidneys and liver, leading to significant organ damage. Resveratrol-tempeh is a safe protective agent against organ damage caused by aluminum. Here, we investigated the impact of resveratrol on liver and kidney toxicity and Al-induced levels of catalase and malondialdehyde. The mice group was the control group, Al-group, Al+REST5-group, and Al+REST10-group. Aluminum and resveratrol were administered intraperitoneally to mice for four weeks, but resveratrol was administered one hour after exposure to aluminum. Mice were killed by cervical dislocation; the liver and kidney were isolated for slide, and the level of an antioxidant enzyme of catalase and oxidant of malondialdehyde was measured. The results showed that administration of aluminum at a dose of 200 mg/kg body weight caused glomerular shrinkage and proximal tubule degeneration in the kidneys. In addition, it also caused liver tissue damage, with hepatocytes undergoing degeneration, sinusoids dilating, and decreased body weight in the mice. Administration of resveratrol-tempeh tended to decrease malondialdehyde levels and increase catalase activity, although the changes were not significant. It seems that resveratrol-tempeh can repair liver and kidney damage and restore them to normal conditions. Conclusion: Aluminum at 200 mg/kg is toxic to mice. Resveratrol-tempeh can be considered a potential candidate to protect kidney and liver damage caused by aluminum chloride toxicity.

Application of Fluorescent Composite Materials as a Sustained Release System in Treatment of Polycystic Ovary Syndrome.

Polycystic ovary syndrome (PCOS) is a multifactorial disease characterized by oxidative stress and follicular dysfunction, leading to menstrual irregularities, hyperandrogenism, and infertility. Traditional drug delivery methods often result in drug loss and side effects on normal tissues. To address these issues, we synthesized two novel Co(II)-containing coordination polymers (CPs), {[Co(L)(H2O)2]·2H2O}n (1) and {[Co(L)(H2O)2]·1.5H2O}n (2), through the reaction of the T-shaped ligand (4 - 3'-pyridyl-,6 - 4'-carboxylphenyl)picolinic acid (H2L) with Co(NO3)2·6H2O via a solvothermal process. Fluorescence spectroscopy revealed that the fluorescence emission of the CPs originates from the ligand, indicating their potential application as blue fluorescence materials. Subsequently, we encapsulated these CPs with hyaluronic acid (HA) and carboxymethyl chitosan (CMCS) hydrogels to create two types of metal gel particles carrying spironolactone (HA/CMCS-CPs@spironolactone). SEM and TEM analyses showed that the material consists of tightly stacked sheet-like structures with an average size of approximately 100nm. Thermogravimetric analysis (TGA) indicated that the material begins to decompose at around 115°C, demonstrating good thermal stability. We assessed the inhibitory effects of these materials on oxidative stress induced by PCOS. The results showed that both types of spironolactone-loaded metal gel particles significantly reduced malondialdehyde (MDA) levels, particularly the particles constructed with CP2. HA/CMCS-CP1@spironolactone reduced MDA levels by approximately 17% and 46% at low and high concentrations, respectively, while HA/CMCS-CP2@spironolactone decreased MDA levels by about 55% and 39% at high and low concentrations, respectively. Therefore, the novel drug delivery system reported in this study has the potential to become a safe and effective option for the localized treatment of PCOS.

Anti irradiation nanoparticles shelter immune organ from radio-damage via preventing the IKK/IκB/NF-κB activation

BackgroundNormal tissue and immune organ protection are critical parts of the tumor radiation therapy process. Radiation-induced immune organ damage (RIOD) causes several side reactions by increasing oxidative stress and inflammatory responses, resulting in unsatisfactory curability in tumor radiation therapy. The aim of this study was to develop a novel and efficient anti irradiation nanoparticle and explore its mechanism of protecting splenic tissue from radiation in mice.MethodsNanoparticles of triphenylphosphine cation NIT radicals (NPs-TPP-NIT) were prepared and used to protect the spleens of mice irradiated with X-rays. Splenic tissue histopathology and hematological parameters were investigated to evaluate the protective effect of NPs-TPP-NIT against X-ray radiation. Proteomics was used to identify differentially expressed proteins related to inflammatory factor regulation. In addition, in vitro and in vivo experiments were performed to assess the impact of NPs-TPP-NIT on radiation therapy.ResultsNPs-TPP-NIT increased superoxide dismutase, catalase, and glutathione peroxidase activity and decreased malondialdehyde levels and reactive oxygen species generation in the spleens of mice after exposure to 6.0 Gy X-ray radiation. Moreover, NPs-TPP-NIT inhibited cell apoptosis, blocked the activation of cleaved cysteine aspartic acid–specific protease/proteinase, upregulated the expression of Bcl-2, and downregulated that of Bax. We confirmed that NPs-TPP-NIT prevented the IKK/IκB/NF-κB activation induced by ionizing radiation, thereby alleviating radiation-induced splenic inflammatory damage. In addition, when used during radiotherapy for tumors in mice, NPs-TPP-NIT exhibited no significant toxicity and conferred no significant tumor protective effects.ConclusionsNPs-TPP-NIT prevented activation of IKK/IκB/NF-κB signaling, reduced secretion of pro-inflammatory factors, and promoted production of anti-inflammatory factors in the spleen, which exhibited radiation-induced damage repair capability without diminishing the therapeutic effect of radiation therapy. It suggests that NPs-TPP-NIT serve as a potential radioprotective drug to shelter immune organs from radiation-induced damage.

Extraction, Characterization, and Antioxidant Activity of Eucommia ulmoides Polysaccharides.

Herein, the ultrasound-assisted extraction conditions affecting the yield of EUPS (Eucommia ulmoides polysaccharide) were analyzed using a Box-Behnken response surface design. The alleviation effect of EUPS on diquat-induced oxidative stress in mice was also studied. A maximum EUPS yield of 2.60% was obtained under the following optimized conditions: an extraction temperature of 63 °C, extraction time of 1 h, and ratio of liquid to raw materials of 22:1. EUPS exhibited strong 1,1-diphenyl-2-picryl-hydrazyl (DPPH) radical-scavenging ability (87.05%), 2'-Azinobis-(3-ethylbenzthiazoline-6-sulphonate) (ABTS) radical-scavenging ability (101.17%), and hydroxyl radical-scavenging ability (62.92%). The administration of EUPS increased the activities of superoxide dismutase, catalase, and glutathione peroxidase and decreased malondialdehyde levels in the livers of mice exposed to diquat. EUPS may inhibit the downregulation of NAD(P)H:quinoneoxidoreductase 1 and heme oxygenase 1 mRNA expression in the livers of diquat-administered mice through the Nrf2-Keap1 signaling pathway. Moreover, the abundance of Firmicutes and Ligilactobacillus was enhanced, whereas that of Helicobacter decreased in the gut of the remaining groups of mice compared with that of the diquat-treated mice. Therefore, EUPS exhibited an antioxidant effect and improved oxidative stress and intestinal flora abundance in mice.

Comparison of Dietary Supplementation with Krill Oil, Fish Oil, and Astaxanthin on an Experimental Ethanol-Induced Gastric Ulcer Model: A Biochemical and Histological Study

Background/Objectives: Despite advances in ulcer treatment research, the search for new, safe, and effective strategies for preventing and treating ulcer diseases persists. Methods: In this study, the protective effects of dietary supplementation with krill oil (KO), fish oil (FO), and astaxanthin (ASX) on an ethanol-induced gastric ulcer model were compared during biochemical and histological observations. Sprague–Dawley (n = 64) rats randomly divided into four groups—normal control (vehicle), KO, FO, and ASX groups—received the supplements via the orogastric route at a rate of 2.5% (v/w) of their daily feed consumption for 4 weeks. Then, ulcer induction was performed with ethanol. Results: The ulcer group showed increased levels of malondialdehyde (MDA), chemiluminescence (CL), and myeloperoxidase (MPO) activity and decreased levels of glutathione in the gastric tissues. While KO, FO, and ASX supplementation decreased chemiluminescence levels in the ulcer group, only ASX supplementation decreased MDA levels and MPO activity. Conclusions: In conclusion, supplementation with KO or FO has a similar protective effect against ethanol-induced ulcer damage, as it inhibits ROS formation and reduces lipid peroxidation. However, ASX supplementation has a higher protective effect than KO or FO supplementations against experimental ethanol-induced gastric lesions in rats, as it inhibits ROS formation and reduces neutrophil infiltration and lipid peroxidation.

Physicochemical, structural, and biological properties of novel water-soluble polysaccharide derived from the Tunisian Hammada scoparia plant and its application on beef meat preservation

This work aims to characterize a novel water-soluble polysaccharide from Hammada scoparia leaves named PSP. The Infrared (FT-IR) and nuclear magnetic resonance (NMR) spectra confirmed the presence of different polysaccharide functional bands. The High-Performance Liquid Chromatography (HPLC) analysis identified a heteropolysaccharide composed of two monosaccharides. A semi-crystalline structure of PSP was proved using the X-ray diffraction (XRD) and Scanning Electron Microscopy (SEM) analysis. The evaluation of the antioxidant activity revealed an interesting potential to prevent oxidative stress.Additionally, PSP showed interesting functional propreties such as good oil and water retention abilities, higher foaming stability, and higher emulsifying capacity and stability. However, the effect of PSP on the oxidation of lipids in the ground beef meat was established during nine days at 4 °C. Obtained data revealed a significant decrease in malondialdehyde levels, inhibition of metmyoglobin (MetMb) accumulation, and significant inhibition of microbial growth compared with the control sample during storage. Moreover, incorporating PSP in minced meat proved color pH and moisture stability. Overall, the findings in the present study confirmed that PSP could be considered a natural bioactive polymer for food applications.

Evaluation of Antioxidant Effects of Coenzyme Q10 against Hyperglycemia-Mediated Oxidative Stress by Focusing on Nrf2/Keap1/HO-1 Signaling Pathway in the Liver of Diabetic Rats.

Hyperglycemia-induced oxidative stress can damage the liver and lead to diabetes complications. Coenzyme Q10 (CoQ-10) reduces diabetes-related oxidative stress. However, its molecular mechanisms are still unclear. This study aimed to examine CoQ-10's antioxidant capabilities against hyperglycemia-induced oxidative stress in the livers of diabetic rats, specifically targeting the Nrf2/Keap1/ARE signaling pathway. This study was conducted between 2020-2021 at Arak University of Medical Sciences. A total of 30 male adult Wistar rats (8 weeks old) weighing 220-250 g were randomly assigned to five groups (n=6 in each group): control healthy, sesame oil (CoQ-10 solvent), CoQ-10 (10 mg/Kg), diabetic, and diabetic+CoQ-10. Liver oxidative stress indicators, including malondialdehyde, catalase, glutathione peroxidase, and glutathione, were estimated using the spectrophotometry method. Nrf2, Keap1, HO-1, and NQO1 gene expressions were measured using real-time PCR tests in the liver tissue. All treatments were conducted for 6 weeks. Statistical analysis was performed using SPSS software. One-way ANOVA followed by LSD's or Tukey's post hoc tests were used to compare the results of different groups. P<0.05 was considered statistically significant. The findings showed that induction of diabetes significantly increased Keap1 expression (2.1±0.9 folds, P=0.01), and significantly inhibited the mRNA expression of Nrf2 (0.38±0.2 folds, P=0.009), HO-1 (0.27±0.1 folds, P=0.02), and NQO1 (0.26±0.1 folds P=0.01), compared with the healthy group. In the diabetic group, the activity of glutathione peroxidase, catalase enzymes, and glutathione levels was decreased with an increase in malondialdehyde level. CoQ-10 supplementation significantly up-regulated the expressions of Nrf2 (0.85±0.3, P=0.04), HO-1 (0.94±0.2, P=0.04), NQO1 (0.88±0.5, P=0.03) genes, and inhibited Keap1 expression (1.1±0.6, P=0.02). Furthermore, as compared to control diabetic rats, CoQ-10 ameliorated oxidative stress by decreasing malondialdehyde levels and increasing catalase, glutathione peroxidase activities, and glutathione levels in the liver tissues of the treated rats in the treatment group. The findings of this study revealed that CoQ-10 could increase the antioxidant capacity of the liver tissue in diabetic rats by modulating the Nrf2/Keap1/HO-1/NQO1 signaling pathway.