Oxidative Stress Index Research Articles

Comparative study of the photosynthetic efficiency and leaf structure of four Cotoneaster species

Plants belonging to the genus Cotoneaster can be valuable sources of phytochemicals with potential therapeutic properties. The natural habitats of most of these species are situated in Asia, Africa and southern Europe. Introducing them into other climatic conditions could expose them to abiotic and biotic stresses, affecting their bioactive properties. The aim of this study was to assess and compare the performance of four non-native Cotoneaster species (C. roseus, C. hissaricus, C. hsingshangensis, C. nebrodensis) grown in eastern Poland in terms of leaf morphology, anatomy, and efficiency of the photosynthetic apparatus in relation to lipid peroxidation level, being an indicator of oxidative stress. Photosynthetic pigments concentration and chlorophyll a fluorescence parameters were used to evaluate the photosynthetic capacity. The morphological and anatomical analysis of leaves did not show any anomalies or stress symptoms. Cotoneaster roseus was characterized by the highest chlorophyll concentration, viability index (Rfd) and a moderate lipid peroxidation level. On the other hand, the lowest values of photochemical quenching (qP), maximum fluorescence (Fm), Rfd, and quantum yield of the photosystem II (QY) observed for C. nebrodensis might indicate an inferior efficiency of the photosynthetic apparatus in this species; however, it demonstrated the lowest lipid peroxidation level. Nevertheless, the content and proportion of the photosynthetic pigments as well as overall chlorophyll a fluorescence parameters and lipid peroxidation levels indicate a good physiological condition of all examined plants. The observed differences between the species may be rather species specific and genetically established and not indicate their sensitivity to non-native growth conditions. This is the first report about the physiological parameters of the four Cotoneaster species, proving they are well adapted to growth in the climatic conditions of central Europe providing thus a raw material with potential for pharmaceutical applications.

Transplantation of human umbilical cord-derived mesenchymal stem cells improves age-related ovarian functional decline via regulating the local renin–angiotensin system on inflammation and oxidative stress

BackgroundAge-related reproductive aging is a natural and irreversible physiological process, and delaying childbearing is increasingly common all over the world. Transplantation of mesenchymal stem cells (MSCs) is considered a new and effective therapy to restore ovarian function, but the relevant mechanisms remain unclear. Recently, it has been found that there is a local Renin–angiotensin system (RAS) in human ovary and it plays a key role.MethodsAfter collecting follicular fluid from women who received oocyte retrieval for pure male factor infertility, the level of RAS components in it were detected, and the correlation analysis by linear regression. Then, the in vivo experiments on female C57BL/6 mice were designed to measure ovarian function, and the transcription and translation levels of RAS pathway were detected by molecular biology methods. Moreover, the role of RAS in regulating inflammation and oxidative stress in the co-culture system were explored in in vitro experiments on KGN cells.ResultsFirst, a total of 139 samples of analyzable follicular fluid were obtained. The local RAS of ovary, which is independent of systemic RAS (P > 0.05), is affected by age (Pearson r < 0, P < 0.05) and related to ovarian function, inflammation, oxidative stress indexes and assisted reproduction laboratory outcomes (P < 0.05). Next, the ovary/body weight of aging mice decreased significantly and serum sex hormones levels changed significantly (P < 0.01). The number of functional follicles decreased, while the atresia follicles increased (P < 0.05). After MSCs transplantation, all the above measures have been partially recovered (P < 0.05). Although several RAS components in aging ovary changed, MSCs only improved the expression level of AT1R (P < 0.05). Furthermore, the secretion ability and mitochondrial membrane potential of aging KGN cells decreased, while the intracellular ROS level and the aging cells ratio increased (P < 0.01). All the above measures have been partially recovered when co-cultured with MSCs (P < 0.05). After Ang(1–7) were added into the co-culture system, the above have been more significantly restored compared with Ang II (P < 0.05). Nevertheless, there was no statistical difference in estradiol level no matter which one was added (P > 0.05).ConclusionsTogether, our findings indicate that a novel possible mechanism to explain how stem cells restore age-related ovarian functional decline.

Dietary Restriction of Advanced Glycation End-Products (AGEs) in Patients with Diabetes: A Systematic Review of Randomized Controlled Trials

Advanced Glycation End Products (AGEs) are formed through non-enzymatic reactions between reducing sugars and proteins, nucleic acids or lipids (for example through hyperoxidation). In diabetes, elevated glucose levels provide more substrate for AGEs formation. AGEs can also be ingested through the diet from foods cooked at high temperatures, or containing much sugar. The present work aimed to review all published randomized controlled trials (RCT) on low-dietary AGE (L-dAGEs) interventions in patients with diabetes. Pubmed, Scopus and Cochrane databases were searched (until 29 February 2024) with appropriate keywords (inclusion criteria: RCT, patients with diabetes, age &gt; 18 years, outcomes related to inflammation, glucose, and lipids; exclusion criteria: non-RCTs, case-series, case reports and Letter to the Editor, or animal studies). The present review was registered to the Open Science Framework (OSF). From 7091 studies, seven were ultimately included. Bias was assessed with the updated Cochrane Risk of Bias tool. A reduction in circulating AGEs was documented in 3/3 studies. No particular differences were documented in glycemic parameters after a L-dAGEs diet. Reductions in glucose levels were observed in one out of six studies (1/6), while HbA1c and HOMA did not change in any study (0/6 and 0/3, correspondingly). Lipid profile also changed in one out of four studies (1/4). More consistent results were observed for oxidative stress (beneficial effects in 3/3 studies) and inflammatory markers (beneficial effects in 4/4 studies). Other athero-protective effects, such as adiponectin increases, were reported. Limitations included the small sample size and the fact that dietary and physical activity habits were not considered in most studies. In conclusion, a L-dAGEs pattern may minimize AGEs accumulation and have beneficial effects on oxidative stress and inflammation indices, while its effects on glycemic and lipemic parameters are inconsistent and modest in patients with diabetes.

Effects of smoking on local and systemic oxidative stress markers in individuals with periodontitis

Aim: This study aimed to assess the effects of smoking on systemic and local oxidative stress markers in patients with periodontitis. Methods: A total of 72 patients with periodontitis [38 smokers (S +P+), 34 non-smokers (S-P+)] and 54 periodontally healthy individuals [28 smokers (S+P-), 26 non-smokers (S-P-, control)] were included. After clinical measurements and samplings, the cotinine level, total antioxidant capacity (TAOC), total oxidative status (TOS), and malondialdehyde (MDA) level in the serum and saliva were determined, and the oxidative stress index (OSI) was calculated. Kruskal-Wallis and Mann-Whitney U tests were used for multiple and pairwise comparisons. Correlations were analyzed using Pearson correlation coefficient. P&lt;0.05 was considered statistically significant. Results: Smoking and periodontitis decreased the serum and salivary TAOCs and increased the TOS, MDA level, and OSI. The smokers with periodontitis had the lowest TAOC and the highest TOS, MDA level, and OSI, while the controls had the highest TAOC and the lowest TOS, MDA level, and OSI. The systemic and local effects of smoking seemed more pronounced than those of periodontitis in the oxidative stress study, but no significant difference was identified between the smoking (S+P-) and periodontitis (S-P+) groups. The clinical parameters and oxidative stress markers showed both substantial positive and negative relationships in all groups (p&lt;0.01). Conclusions: It can be concluded that smoking and periodontitis (S+P+) are associated with a decrease in serum and salivary TAOCs and an increase in TOS, MDA levels, and OSI. Smoking has a similar effect as periodontitis on local and systemic oxidative stress, and oxidative stress caused by smoking may be a significant factor in the pathophysiology of periodontitis.

Statistical analysis of predictors of effectiveness of complex physiotherapeutic treatment in patients with involutional skin changes

BACKGROUND: Analysis of predictors of the effectiveness of various treatment regimens for diseases, as well as the correction of involutionary processes in the human body, is increasingly becoming a standard in scientific medical research. The technology for identifying them traditionally includes the use of correlation and regression analysis, as well as the principles of correlation adaptometry, which makes it possible to approach the solution of this problem from the position of system analysis. AIM: Analysis of predictors of the effectiveness of correction of involutive skin changes in middle-aged and older women with metabolic syndrome using various therapeutic regimens, including hyaluronic acid laser phoresis and the use of transcranial magnetic therapy in combination with oxygen barotherapy. MATERIALS AND METHODS: The study was carried out with the participation of 60 patients from middle and older age with involutional changes in the skin against the background of metabolic syndrome. All patients were divided into 2 groups using simple fixed randomization. The first group (comparison, 30 patients) received laser phoresis of hyaluronic acid in the form of a 1.5% sodium hyaluronate gel using a laser and laser-vacuum therapy device LAZMIK. Patients of the second group (main group, 30 patients) were prescribed combined physiotherapy. For transcranial magnetic therapy, the Amo-Atos device with the Headband attachment was used, and oxygen barotherapy was carried out in single pressure chambers of the Oka-MT or Irtysh-Shch1 type under a pressure of 2 atm for 1 hour. RESULTS: It was found that in the initial state, the quality of life of patients with involutional changes in the skin against the background of metabolic skin syndrome was largely determined by the presence of pathological correlation galaxies that integrate changes in the condition of the skin, metabolic disorders, indicators of oxidative stress and microhemodynamics, and the activity of proinflammatory cytokines. At the same time, the leading role in the deterioration of the quality of life belonged to the age of the patients, the insulin resistance index, transepidermal water loss and microcirculation indicator. However, predictors of effectiveness varied across different treatment regimens. With laser phoresis of hyaluronic acid, its effectiveness increases in younger women with minimal involutional manifestations of skin aging, tested for the condition of the skin, while combined physiotherapy is also most effective in women with a low average age limit, with minimal manifestations of metabolic syndrome and inflammatory processes, as well as against the background of high activity values of one of the enzymes of antioxidant protection ― superoxide dismutase. CONCLUSION: The results obtained convincingly prove the effectiveness of combination therapy in correcting involutive skin changes in middle-aged and older women due to metabolic syndrome, which is comparable in a number of parameters to the effectiveness of hyaluronic acid laser phoresis. At the same time, predictors of effectiveness depend on the characteristics of the mechanisms of therapeutic action of the treatment regimens used, which allows for a more correct approach to the choice of personalized treatment methods.

Ameliorating arsenic and PVC microplastic stress in barley (Hordeum vulgare L.) using copper oxide nanoparticles: an environmental bioremediation approach

The present study investigates the impact of varying concentrations of PVC microplastics (PVC–MPs) – specifically 0 (no PVC–MPs), 2, and 4 mg L− 1 –alongside different arsenic (As) levels of 0 (no As), 150, and 300 mg kg− 1 in the soil, with the concurrent application of copper oxide–nanoparticles (CuO–NPs) at 0 (no CuO –NPs), 25 and 50 µg mL− 1 to barley (Hordeum vulgare L.) plants. This research primarily aims to assess plant growth and biomass, photosynthetic pigments and gas exchange characteristics, oxidative stress indicators, as well as the response of various antioxidants (both enzymatic and non-enzymatic) and their relevant genes expression, proline metabolism, the AsA–GSH cycle, and cellular fractionation within the plants. The findings showed that increased levels of PVC–MPs and As stress in the soil significantly reduced plant growth and biomass, photosynthetic pigments, and gas exchange characteristics. Additionally, PVC–MPs and As stress increased oxidative stress in the roots and shoots, as evidenced by elevated levels of malondialdehyde (MDA), hydrogen peroxide (H2O2), and electrolyte leakage (EL), which in turn stimulated the production of various enzymatic and non-enzymatic antioxidants, gene expression, and sugar content. Furthermore, a notable increase in proline metabolism, the AsA–GSH cycle, and cellular pigmentation was observed. Conversely, the application of CuO–NPs resulted in a substantial improvement in plant growth and biomass, gas exchange characteristics, and the activity of enzymatic and non-enzymatic antioxidants, along with a reduction in oxidative stress. Additionally, CuO–NPs enhanced cellular fractionation while decreasing proline metabolism and the AsA-GSH cycle in H. vulgare plants. These outcomes provide new insights into sustainable agricultural practices and offer significant potential in addressing the critical challenges of heavy metal contamination in agricultural soils.

Association between systemic zinc and oxidative stress levels and periodontal inflamed surface area.

Zinc is a structural component of some enzymes. The aim of this study was to evaluate the potential associations between serum zinc and oxidative stress levels and periodontal inflamed surface area (PISA). This study included 90 patients divided into three groups: a periodontitis group (P; n = 30), a gingivitis group (G; n = 30), and a periodontal health group (PH; n = 30). Periodontal parameters were recorded and PISA values were calculated. Serum total antioxidant status (TAS), total oxidant status (TOS), and zinc levels were examined biochemically. Oxidative stress index (OSI) levels were calculated. All clinical periodontal parameters, periodontal epithelium surface area, and PISA values were lower in the PH group than the P and G groups (p < 0.05). Serum zinc and TAS values were higher in the PH group than the P and G groups (p < 0.05). Serum TOS and OSI values were lower in the PH group than the G and P groups (p < 0.05). Serum OSI levels were lower in the G group than the P group (p < 0.05). PISA was associated with serum zinc (β = -28.96, 95% CI = (-38.95, -18.98), p < 0.001) and OSI (β = 89.84, 95% CI = (20.63, 159.05), p = 0.011) levels in the multivariate generalized linear model. PISA values were associated with decreasing serum zinc and TAS and increased TOS and OSI levels. Zinc deficiency can be associated with the severity of periodontal disease and higher oxidative stress levels.

Phytotoxicity Stress Induced by Allelochemicals from Foliar Spray of Sida cordifolia Methanol Leaf Extract on Ageratum conyzoides and Oryza sativa

Allelochemicals are key inhibitors that induce chemical stress in plants. Their mechanisms as agents of oxidative stress are not well understood. A field study was conducted to evaluate herbicidal potential of Sida cordifolia methanol leaf extract (SCLE) on Ageratum conyzoides and Oryza sativa (weedy rice). SCLE concentrations of 0, 3, 6 and 9 g L-1 were prepared and sprayed twice at 7 days interval. The results showed that the SCLE significantly (p&lt;0.05) affected growth attributes, chlorophyll pigments, and proline, and catalase, superoxide dismutase and peroxidase enzyme activities in a concentration-dependent pattern. It was found that high concentrations of SCLE induced greater phytotoxicity against A. conyzoides compared to O. sativa. SCLE spraying stimulated production of reactive oxygen species, boosting their ability to cause damage and inhibit growth. The allelochemicals in the extract stimulated an increased in the level of proline, which is an indicator of oxidative stress. Understanding the physiological and biochemical responses to Sida extract can improve our knowledge on allelochemical target sites and help us to explicate the mechanisms of action of such compounds.

Physiology, gene expression, and behavior as potential indicators of oxidative stress in piglets

The goal of the current study was to develop a pig model to investigate oxidative stress with a low negative impact on piglet welfare. Four independent trials (A, B, C, and D) were performed using a single intraperitoneal shot of lipopolysaccharide (LPS) as an immune challenge, aiming to assess the minimal LPS dose for piglets of different age to trigger a measurable acute oxidative stress response in healthy animals. In trial A, piglets received an LPS dose of 25 µg/KgBW at 41 days post-weaning (p.w.). In trial B, piglets received 25 µg/KgBW of LPS at 28 days p.w., in trials C And D, piglets were injected with 50 µg/KgBW of LPS at 21 days p.w., respectively. Piglets were randomly allocated either to the T1) Control group with saline solution (Ctrl), or T2) LPS challenge (LPS). The oxidative stress response was measured through the enzymatic activity of glutathione peroxidase (GPx), glutathione-S-transferase (GST), superoxide dismutase (SOD), and catalase (CAT), in both plasma and intestinal tissues. Intestinal gene expression of oxidative stress and inflammatory markers was assessed. Discomfort behaviors (panting, prostration, trembling, and vomits) were also recorded. Plasmatic and intestinal oxidative stress response was inconsistent across the four trials even when the dose and pig age were similar, possibly due to individual variability. Relative gene expression differences of anti-inflammatory cytokines (IL10), oxidation precursor (iNOS), and antioxidant markers (GPx4, MnSOD, and CAT) were detected between Ctrl and LPS treatment (P < 0.05) when assessed. Behavioral observations were sensitive to the LPS dose relative to Ctrl (P < 0.05) in all four trials. These results suggest that behavioral observations can be used as a non-invasive methodology to detect the presence of oxidative stress in pigs in challenging conditions. Behavioral observations were more sensitive than other indicators (i.e., biomarkers and gene expression) in the current study. However, a sensitivity scale system needs to be developed to qualify and rank the impact of oxidative stress in pigs.

Sirt1/Nrf2/TNFα; TLR4/Myd88/NF-κB signaling pathways are involved in mediating hepatoprotective effect of bupropion in rat model of myocardial infarction

Background The aim of the current study is to identify the possible protective effect of bupropion (BUP) on liver injury in rat model of myocardial infarction (MI). BUP was administered in the presence and absence of MI. Materials and methods Thirty-two Wistar adult male rats were randomly arranged into four groups: control, BUP (30 mg/kg/day, intraperitoneal) for 28 days, isoproterenol (ISO) was injected subcutaneous (85 mg/kg) in the 26th and 27th days and BUP/ISO groups. Cardiac and hepatic enzymes were measured, also Hepatic oxidative stress indicators, as well as inflammatory and apoptotic biomarkers, were evaluated. Cardiac and hepatic histopathological examination and hepatic nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) immunohistochemical study were also detected. Results ISO significantly increased cardiac and hepatic enzymes, hepatic oxidative stress, inflammatory, apoptotic, with a histopathological picture of cardiac and hepatic damage and high hepatic NF-κB immunoexpression were detected. BUP significantly normalized the upraised oxidative, inflammatory, and apoptotic parameters, with an impressive improvement in the histopathological picture and a reduction in hepatic NF-κB immunoexpression. Conclusion BUP protects against liver injury on top of MI in rat model via modulation of Sirtuin type 1 (Sirt1)/Nuclear factor (erythroid-derived 2)-like 2 (Nrf2)/tumor necrosis factor α (TNFα); Toll-like receptor 4 (TLR4)/Hepatic myeloid differentiation primary response 88(Myd88)/NF-κB signaling pathways.

The Apoptotic, Cytotoxic, and Anti-migration Effects of Sodium Deoxycholate in a Breast Cancer Cell Line and its Modulation on PON1 as a Predictive Risk Marker.

Breast cancer is the most prevalent cancer among women and is usually treated with antineoplastic drugs. The present study examines the influence of sodium deoxycholate on the molecular pathways underlying apoptosis, cytotoxicity, and the modulation of PON1 in the MCF-7 breast cancer cell line. Various doses were administered to test the hypothesis that it could potentially affect cancer cells. The study examined the cytotoxic effect of sodium deoxycholate on MCF-7 cells and human mammary epithelial cells (CRL-4010) using the MTT method to detect its anticancer properties. Subsequently, the efficacy of the active dose on DNA fragmentation and apoptosis was examined using the apoptotic DNA ladder and Western blot methods. Additionally, oxidative stress index and cell migration tests were conducted. Notably, sodium deoxycholate did not cause DNA damage despite demonstrating cytotoxic effects on cells. The study found that sodium deoxycholate increased the levels of several pro-apoptotic proteins, leading to apoptosis. Moreover, it markedly diminishes the activity of paraoxonase and arylesterase of PON1, which are predictive risk markers for cancer. Furthermore, it was found to delay cell migration in a time-dependent manner. These findings suggest that sodium deoxycholate exhibits an antimetastatic effect in breast cancer cells, could be a valuable subject for further cancer research.

Gastrointestinal toxicity following sub-acute exposure of erythrosine in rats: biochemical, oxidative stress, DNA damage and histopathological studies.

Erythrosine, a synthetic food dye, has been controversial due to its potential health risks. This study examines the effect of erythrosine on activity of antioxidative enzymes, oxidative stress indices, DNA damage through comet assay, and histopathological changes on stomach, intestine, and colon over a period of 28 days in rats. Twenty-four rats were randomly divided into four groups (n = 6). The first is the control group and then one each for three doses of erythrosine based on acceptable daily intake (¼ ADI, ½ ADI, and ADI, 0.1 mg/kg body weight). The results revealed that with increasing dosages the activity of catalase decreased in stomach and intestine but in colon, the catalase activity increased. Superoxide dismutase and glutathione-S-transferase activity decreased in dose-dependent manner in all three tissues. While, in stomach and intestine, the acetylcholinesterase activity showed increment in ¼ ADI dose group and then declined in ½ ADI and ADI dose-administered rats. The oxidative stress indicators showed elevated levels of lipid peroxidation, hydrogen peroxide concentration, and lactate dehydrogenase activity suggesting heightened free radical activity and potential oxidative damage. The comet test was used to evaluate DNA damage, revealing substantial damage in the erythrosine administered groups. Histopathological examination showed inflammatory infiltration and other degenerative changes in gastrointestinal tract, highlighting the dye's adverse effects. The research underscores the need for a comprehensive reevaluation of the safety and toxicity of food dyes like erythrosine, especially considering the inconsistencies in existing studies regarding the dye's safety.

Ginsenoside Re Regulates Oxidative Stress through the PI3K/Akt/Nrf2 Signaling Pathway in Mice with Scopolamine-Induced Memory Impairments.

While Ginsenoside Re has been shown to protect the central nervous system, reports of its effects on memory in the model of scopolamine-induced memory impairment are rare. The aim of this study was to investigate the effects of Ginsenoside Re on scopolamine (SCOP)-induced memory damage and the mechanism of action. Male ICR mice were treated with SCOP (3 mg/kg) for 7 days and with or without Ginsenoside Re for 14 days. As evidenced by behavioral studies (escape latency and cross platform position), brain tissue morphology, and oxidative stress indicators after Ginsenoside Re treatment, the memory damage caused by SCOP was significantly ameliorated. Further mechanism research indicated that Ginsenoside Re inhibited cell apoptosis by regulating the PI3K/Akt/Nrf2 pathway, thereby exerting a cognitive impairment improvement effect. This research suggests that Ginsenoside Re could protect against SCOP-induced memory defects possibly through inhibiting oxidative stress and cell apoptosis.

Unraveling Mitochondrial Reactive Oxygen Species Involvement in Psoriasis: The Promise of Antioxidant Therapies.

Psoriasis is a chronic inflammatory skin disorder characterized by immune dysregulation and aberrant keratinocyte proliferation. Despite tremendous advances in understanding its etiology, effective therapies that target its fundamental mechanisms remain necessary. Recent research highlights the role of reactive oxygen species dysregulation and mitochondrial dysfunction in psoriasis pathogenesis. Mitochondrial reactive oxygen species mediate cellular signaling pathways involved in psoriasis, such as proliferation, apoptosis, and inflammation, leading to oxidative stress, exacerbating inflammation and tissue damage if dysregulated. This review explores oxidative stress biomarkers and parameters in psoriasis, including myeloperoxidase, paraoxonase, sirtuins, superoxide dismutase, catalase, malondialdehyde, oxidative stress index, total oxidant status, and total antioxidant status. These markers provide insights into disease mechanisms and potential diagnostic and therapeutic targets. Modulating mitochondrial reactive oxygen species levels and enhancing antioxidant defenses can alleviate inflammation and oxidative damage, improving patient outcomes. Natural antioxidants like quercetin, curcumin, gingerol, resveratrol, and other antioxidants show promise as complementary treatments targeting oxidative stress and mitochondrial dysfunction. This review aims to guide the development of personalized therapeutic methods and diagnostic techniques, emphasizing the importance of comprehensive clinical studies to validate the efficacy and safety of these interventions, paving the way for more effective and holistic psoriasis care.

Rhoifolin Attenuates Concanavalin A-Induced Autoimmune Hepatitis in Mice via JAKs/STATs Mediated Immune and Apoptotic Processes.

Rhoifolin (ROF) exhibits a diverse range of biological activities, encompassing anticancer, hepatoprotective, antidiabetic, antirheumatic, and antiviral properties. However, the specific protective effects and possible mechanisms of the compound against T-cell-mediated autoimmune hepatitis have not been previously elucidated. In the present study, adult male mice were administered Con A (20 mg/kg, intravenously) for 8 h. In the treated groups, mice were pretreated with ROF daily (20 mg/kg and 40 mg/kg, orally) for 7 days before Con A intoxication. The results showed that ROF significantly decreased serum biochemical indices (ALT, AST, ALP, and LDH) and regulated related oxidative stress indicators (MDA, SOD, and GSH), reduced hepatic necrosis areas and immune cells infiltration, inhibited the release of various inflammatory factors (TNF-α, IFN-γ, IL-2, and IL-17), and improved hepatic tissue apoptosis, thereby alleviating hepatic damage induced by Con A. Additionally, we have also confirmed that ROF efficiently inhibited Th1/Th17 cells polarization via modulation of the JAK2/JAK3/STAT1/STAT3 signaling pathways both in vivo and in vitro. Moreover, the molecular mechanism examination also demonstrated that ROF regulated apoptotic cascade signaling through IL-6/JAK2/STAT1/STAT3 controlling BNIP3 activity in primary hepatocytes. These effects were in good agreement with the bioinformatics analysis of ROF treatment for AIH. In conclusion, our findings provide new insights into the potential use of ROF for AIH therapy, which may result from the specific regulation of the T cell subtype polarization and the apoptosis of liver cells via modulation of the JAKs/STATs signaling pathways.

Anti-oxidant, anti-apoptotic and anti-inflammatory effects of geraniin in spinal cord injury in rat: role of COX-2.

Spinal cord injury (SCI) is devastating diseases affecting the degeneration of the spinal column, and vascular problems. However, the currently available therapeutic interventions are insufficient to address the effect of SCI which leads to significant impact on the morbidity and mortality of patients. In the present manuscript, we intend to investigate the pharmacological effect of geraniin on the SCI in Sprague-Dawley (SD) rats. The SCI in rats were induced by the conventional weight-drop method and treated with GER (2.5, 5, and 10 mg/kg). Subsequently, the locomotor activity of rats with SCI was assessed using Basso, Beattie, and Bresnahan (BBB) scores, while oxidative stress indicators and inflammatory variables were analyzed using commercially available kits. Additionally, neuronal death was quantified using TUNEL labeling. The enzymatic activity of caspase 3, 8, and 9 was also assessed. Furthermore, the expression levels of Bcl2, Bax, and COX-2 in rat spinal cords after SCI were analyzed by RT-PCR analysis. Our research indicated that therapy with GER in a manner that depends on the dosage could enhance the functional recovery, as well as reduce the occurrence of apoptosis, mitigate the inflammatory and oxidative response in rats with SCI. Furthermore, it was observed that GER increased the expression of Bcl2 and decreased the expression of Bax and COX-2. The concentration of caspase-3, -8, and -9 was observed to be decreased in SCI rats treated with GER. GER might protect the spinal cord from SCI by reducing apoptosis, oxidative stress, and inflammatory response through the inhibition of COX-2.

A broad appraisal of decompression-induced physiological stress in different simulated dive profiles

Background: The present study was designed to observe if different decompression profiles, calculated as a function of tissue supersaturation during ascent, would result in significantly different outcomes, measured through different physiological stress indicators, even in the absence of symptoms of decompression sickness. Aim: The aim of this study was to evaluate if simulated decompression profiles would affect the immune system, oxidative stress indicators, and heart rate variability. Methods: A total of 23 volunteers participated in two different experimental protocols in a dry hyperbaric chamber. These simulated dives comprised two different compression–decompression arrangements with the same maximum pressure and duration but different decompression profiles. Results: The shallow decompression profile with shorter deeper stops and longer shallow stops presented an increase in the standard deviation of the normal-to-normal R-R interval (a wide indicator of overall variability); the deep decompression profile with longer deeper stops and shorter shallow stops did not exhibit such increase. The shallow decompression profile resulted in an increase in neutrophil count and its microparticles (MPs), but no changes were observed for platelet count and its MPs, as well as for endothelial-derived MPs. In contrast, the deep decompression profile resulted in no changes in neutrophil count and its MPs, but a decrease in platelet count along with an increase in MPs from both platelets and endothelial cells. The observed difference might be related to different levels of decompression-related activation of immune system responses and oxidative processes triggered by different levels of inert gas supersaturation upon surfacing. Conclusion: From previous results and literature data, we present a tentative schematic of how the velocity of ascent would trigger (or not) pro-inflammatory and immune system responses that could ultimately lead to the development of decompression sickness. Relevance for patients: Increasing safety in exposure to hyperbaric environments and subsequent decompression by evaluating individual physiological responses to the process.

Zhachong Shisanwei pill drug-containing serum protects H2O2-Induced PC12 cells injury by suppressing apoptosis, oxidative stress via regulating the MAPK signaling pathway.

Zhachong Shisanwei Pill (ZSP) is a classical Mongolian formula that combines 13 types of Chinese medicinal materials and has been used for treating ischemic stroke (IS) for centuries. However, the underlying molecular mechanisms have yet to be fully elucidated. The aim of this study is to explore potential mechanism of ZSP on nerve cells in cerebral ischemic injury. To simulate the pathological process of oxidative stress following IS, an injury model using PC12 cells was induced with hydrogen peroxide (H2O2). Afterward, PC12 cells were treated with ZSP medicated serum at low, medium, and high doses. Various assays were conducted to assess cell viability and oxidative stress indicators, including lactate dehydrogenase (LDH), malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), reactive oxygen species (ROS), and mitochondrial membrane potential (MMP). Cell apoptosis was evaluated through morphological assessment and flow cytometry. Additionally, the expression levels of apoptosis-related proteins (Bcl-2, Bax, Caspase-9, Caspase-3, PARP) and signaling pathway proteins (JNK, phosphorylated JNK, ERK, phosphorylated ERK, p38, and phosphorylated p38) were measured using automated Western blotting. Our findings indicate that ZSP medicated serum preconditioning improves the condition of PC12 cells injured by H2O2. Specifically, it increased cell survival rates and reduced LDH release. Additionally, ZSP treatment decreased ROS levels and MDA content, while enhancing the activity of SOD and CAT in the injured PC12 cells. ZSP also reversed the depolarization of mitochondrial membrane potential and protected cells from apoptosis by modulating the expression of apoptosis-related proteins, including Bcl-2, Bax, Caspase-9, Caspase-3, and PARP. Furthermore, the overactivation of the MAPK signaling pathway due to H2O2-induced injury was inhibited, as evidenced by the downregulation of phosphorylated JNK, ERK, and p38 levels. Mongolian medicine ZSP demonstrates protective effects against H2O2-induced oxidative stress and apoptosis in PC12 cells. The underlying mechanism may involve the inhibition of the MAPK signaling pathway, enhancement of antioxidant enzyme activity, reduction of intracellular peroxidation levels, and suppression of intrinsic apoptosis pathways.

Alleviative effect of iron chlorin e6 on isoproturon phytotoxicity to wheat

Abstract Isoproturon phytotoxicity to wheat (Triticum aestivum L.) is a worry for many farmers in chemical control of weeds in wheat fields, especially in subzero weather conditions. Iron chlorin e6 (ICe6), a new plant growth regulator, has been reported to enhance crop stress resistance to alleviate damage caused by stress; however, it is not clear whether ICe6 has an alleviative effect on isoproturon phytotoxicity to wheat. We determined the alleviative effect of ICe6 on isoproturon phytotoxicity to wheat, and 0.018 g ai ha−1 was the optimal dose. Meanwhile, we also studied the photosynthetic pigment content, photosynthetic parameters, oxidative stress indicators, and antioxidant enzyme activity of wheat treated with the three different treatments. We found that the photosynthetic pigment content, antioxidant enzyme activity, and photosynthesis of wheat damaged by isoproturon were significantly lower than those of the control, and the hydrogen peroxide (H2O2) and malondialdehyde (MDA) content increased. These results indicate that isoproturon stress significantly weakened the photosynthetic and antioxidant capacity of wheat. The photosynthetic pigment content, photosynthetic parameters (excluding intercellular CO2 concentration), and antioxidant enzyme activity of isoproturon+ICe6– treated wheat were significantly higher than those of isoproturon-treated wheat. The H2O2 and MDA content was significantly lower than that of isoproturon-treated wheat. These results indicate that ICe6 treatment maintained the photosynthetic pigment content of wheat and relatively improved photosynthetic capacity, allowing photosynthesis to proceed normally. ICe6 treatment also limits the decrease in antioxidant enzyme activity, effectively clearing excess reactive oxygen species and ultimately alleviating membrane lipid peroxidation damage. In summary, ICe6 not only enhances stress resistance and increases yield in crops such as soybean [Glycine max (L.) Merr.] and canola (Brassica napus L.), but also has an alleviating effect on the isoproturon phytotoxicity to wheat, which is manifested by the improvement of photosynthetic and antioxidant abilities, ultimately leading to an increase in wheat shoot height and shoot fresh weight.

6-Shogaol Abrogates Parkinson’s Disease in Rotenone-Induced Rodents: Based on In Silico Study and Inhibiting TNF-α/NF-κB/IL-1β/MAO-B

Background/Objectives: 6-Shogaol is a comparatively innovative anti-Parkinson’s remedy with antioxidant and anti-inflammatory characteristics. This investigation intended to determine the role of 6-shogaol in the Parkinson’s disease (PD) paradigm in rotenone-induced rats. Methods: Thirty male Wistar rats (10–12 weeks old; 180 ± 20 g) were divided into five groups. Animals with rotenone-induced experimental PD were subsequently treated with 6-shogaol-10 at 20 mg/kg for 28 days. After the experimental duration, behavioural investigations were performed, i.e., open field test, forced swim test, rotarod test, and catalepsy test. Biochemical assessments like AChE, GSH, CAT, SOD, MDA, nitrite, ceruloplasmin, proinflammatory markers such as IL-1β, NF-κB, TNF-α, and catecholamines markers (DA, GABA, and MAO-B) were determined. The docking procedure was conducted using the AutoDock Vina docking protocol. Furthermore, histopathology was performed. Results: Rotenone significantly increased the level of MAO-B, oxidative, nitrative, and pro-inflammatory markers. However, there was a decline in ceruloplasmin, dopamine, and endogenous antioxidants. Treatment with 6-shogaol (10 and 20 mg/kg) considerably sustained the elevation of oxidative stress and inflammatory indicators and decreased AChE activity and dopamine levels. In the histology of the brain, 6-shogaol improved the neuronal structure and reduced the degeneration of neurons. Based on the binding energy values, compound 6-shogaol demonstrates a favourable binding affinity to AChE, MAO-B, DA, and GABA with respective binding energies of −8.214, −8.133, −7.396 and −6.189 kcal/mol. Conclusions: In this study, 6-shogaol exhibited neuroprotective properties against PD, which could be employed as a prospective medication for PD.