Increased Superoxide Dismutase Activity Research Articles

Protective effects of fermented Rosa roxburghii Tratt juice against ethanol‑induced hepatocyte injury by regulating the NRF2‑AMPK signaling pathway in AML‑12 cells.

Alcohol‑related liver disease (ALD) is a major health concern worldwide. In recent years, there has been growing interest in natural products and functional foods for preventing and treating ALD due to their potential antioxidant and hepatoprotective properties. Rosa roxburghii Tratt, known for its rich content of bioactive compounds, has demonstrated promising health benefits, including anti‑inflammatory and antioxidant effects. Fermentation has been utilized as a strategy to enhance the bioavailability and efficacy of natural products. In the present study, using a mixture of Rosa roxburghii Tratt juice, lotus leaf extract and grape seed proanthocyanidins fermented by Lactobacillus plantarum HH‑LP56, a novel fermented Rosa roxburghii Tratt (FRRT) juice was discovered that can prevent and regulate ethanol‑induced liver cell damage. Following fermentation, the pH was significantly decreased, and the content of VC and superoxide dismutase (SOD) were significantly increased, along with a noticeable enhancement in hydroxyl and 2,2‑diphenyl‑1‑picrylhydrazyl free radical scavenging abilities. Alpha Mouse liver 12 cells were exposed to ethanol for 24 h to establish an in vitro liver cell injury model. The present study evaluated the effects of FRRT on cell damage, lipid accumulation and oxidative stress markers. The results revealed that FRRT pretreatment (cells were pre‑treated with 2.5 and 5 mg/ml FRRT for 2 h) significantly reduced lipid accumulation and oxidative stress in liver cells. Mechanistically, FRRT regulated lipid metabolism by influencing key genes and proteins, such as AMP‑activated protein kinase, sterol regulatory element binding transcription factor 1 and Stearyl‑CoA desaturase‑1. Furthermore, FRRT enhanced antioxidant activity by increasing SOD activity, glutathione and catalase levels, while reducing reactive oxygen species and malondialdehyde levels. It also reversed the expression changes of ethanol‑induced oxidative stress‑related genes and proteins. In conclusion, a novel functional food ingredient may have been discovered with extensive potential applications. These findings indicated that FRRT has antioxidant properties and potential therapeutic benefits in addressing ethanol‑induced liver cell damage through its effects on liver lipid metabolism and oxidative stress.

Metabolic effects of physical exercise on zebrafish (Danio rerio) fed a high-fat diet.

The present study aimed to establish zebrafish as an experimental model for investigations into obesity and physical exercise, as well as to assess the effects of these factors on metabolism. The experiment spanned twelve weeks, comprising a feeding trial during which the last four weeks incorporated a physical exercise protocol. This protocol involved placing fifteen animals in a five-liter aquarium, where they were subjected to swimming at an approximate speed of 0.08m/s for 30min daily. Throughout the experiment, histological analyses of visceral, subcutaneous, and hepatic adipose tissues were conducted, along with biochemical analyses of total cholesterol and its fractions, triglycerides, glucose, lactate, and alanine aminotransferase (ALT) levels. Additionally, oxidative stress markers, such as reactive oxygen species (ROS) levels, superoxide dismutase (SOD) activity, and catalase activity and the formation of thiobarbituric acid-reactive substances, were investigated. The results revealed that the group fed a high-fat diet exhibited an increase in ROS production and SOD activity. In contrast, the group administered the high-fat diet and subjected to physical exercise demonstrated a notable reduction in visceral adipocyte area, hepatic steatosis levels, ALT levels, and SOD activity. These findings indicate that physical exercise has a positive effect on obesity and oxidative stress in zebrafish, providing promising evidence for future investigations in this field.

Cereblon deficiency ameliorates carbon tetrachloride-induced acute hepatotoxicity in HepG2 cells by suppressing MAPK-mediated apoptosis

The liver is vulnerable to various hepatotoxins, including carbon tetrachloride (CCl4), which induces oxidative stress and apoptosis by producing reactive oxygen species (ROS) and activating the mitogen-activated protein kinase (MAPK) pathway. Cereblon (CRBN), a multifunctional protein implicated in various cellular processes, functions in the pathogenesis of various diseases; however, its function in liver injury remains unknown. We established a CRBN-knockout (KO) HepG2 cell line and examined its effect on CCl4-induced hepatocellular damage. CRBN-KO cells exhibited reduced sensitivity to CCl4-induced cytotoxicity, as evidenced by decreased levels of apoptosis markers, such as cleaved caspase-3, and aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities. CRBN deficiency enhanced antioxidant defense, with increased superoxide dismutase activity and glutathione ratios (GSH/GSSG), as well as reduced pro-inflammatory cytokine expression. Mechanistically, the protective effects of CRBN deficiency appeared to involve the attenuation of the MAPK-mediated pathways, particularly through decreased phosphorylation of JNK and ERK. Overall, these results suggest the crucial role of CRBN in mediating the hepatocellular response to oxidative stress and inflammation triggered by CCl4 exposure, offering potential clinical implications for liver injury in a wide range of liver diseases.

Lovastatin Combination Therapy Increases the Survival and Proliferation of Rat Bone Marrow-Derived Mesenchymal Stem Cells Against the Inflammatory Activity of Lipopolysaccharide.

Oxidative stress hurts the survival of transplanted mesenchymal stem cells (MSCs). Lipopolysaccharide (LPS) preconditioning inhibits apoptotic death in MSCs. Also, Lovastatin's protective effect was reported on MSCs. Here, we investigated the potential of LPS and Lovastatin combination therapy on the survival and proliferation of MSCs. MSCs harvested from adult rats (240-260 g) femur and tibia bone marrow. Third passage MSCs were divided into 6 groups control group, LPS, LPS + Lovastatin (10 and 15 µM), and Lovastatin (10 and 15 µM). Cell survival and proliferation were assessed using an MTT assay 24 h after LPS, Lovastatin, or LPS + Lovastatin treatment. Also, Malondialdehyde (MDA) as a lipid peroxidation marker and antioxidant enzymes such as Glutathione peroxidase (GPX) and Superoxide dismutase (SOD) activity levels evaluated. Finally, the expression level of tumor protein P53 (P53) and octamer-binding transcription factor 4 (OCT4) genes were measured by qRT-PCR test. Lovastatin 10 μM potentiated proliferation and survival of MSCs. It can increase the activity of GPX and SOD. 10 µM Lovastatin could not affect MDA amounts but decreased the expression levels of P53 and Oct4 significantly. Nevertheless, treatment with LPS reduced the survival and proliferation of MSCs, along with a significant reduction in GPX activity. LPS + Lovastatin could increase SOD activity, however, GPX enzyme activity and MSCs proliferation did not change so, and it was not effective. We propose Lovastatin at the dose of 10 µM as a suitable combination agent to increase the survival and proliferation of MSCs in oxidative stress conditions.

Ripe Musa sapientum Peels Exhibit Neuroprotection Against Lead Acetate-Induced Brain Damage in Wistar Rats

Objective: Human health has continued to be at risk from lead exposure. This study explored the antioxidative potential of ethanol extract of ripe Musa sapientum peels to protect against lead acetate-induced neuronal insult in female wistar rats. Methods: Thirty adult female rats (120-160 g) were randomly divided into six groups (n = 5): Group 1 (control group) received 10 mL/kg of distilled water; Group 2 received 100 mg/kg lead acetate. Group 3 received 2.5 mg/kg of donepezil. Groups 4 to 6 received 100, 200, and 400 mg/kg ethanol extract of ripe M sapientum, respectively, via oral gavage. Groups 2 to 5 were co-treated with 100 mg/kg lead acetate for 21 days. Neurobehavioral parameter, biochemical and histological analyses of the hippocampus were determined. Recognition memory was evaluated using Novel Object Recognition Test. Results: There was a significant ( p < 0.05) increase in total exploration, discrimination index, and percentage alternation in the ethanol extract M sapientum-treated groups compared with the lead acetate-induced group. M sapientum ethanol extract and dopamine significantly ( p < 0.05) reduced acetylcholinesterase enzyme (AChE) and malondialdehyde (MDA) activities in a dose-dependent manner and significantly ( p < 0.05) increased superoxide dismutase activity (SOD) dose dependently, respectively. In the histopathological analysis of the hippocampal area, there were mild vacuolation (V), mild degeneration as well as mild granular cell atrophy in the treated groups, suggesting that M sapientum may have neuroprotective properties. Conclusion: Ethanol extract of ripe M sapientum peels enhanced cognitive functions and may be beneficial in preventing neurodegenerative disorders via antioxidant mechanism.

Impact of ocean acidification on microzooplankton grazing dynamics

This study examines the potential impacts of projected atmospheric carbon dioxide (pCO2) levels reaching 800 ppm by the end of the century, focusing on ocean acidification effects on marine ecosystems in the coastal areas of Bohai. We investigated how acidification affects the grazing patterns of microzooplankton using dilution techniques and ecophysiological methods. Our findings indicate that acidic conditions shift the phytoplankton community structure, changing dominant species. Elevated CO2 concentrations reduced grazing pressure on phytoplankton, with less steep declines in growth rates at 800 ppm CO2 (spring: 2.43 d−1 vs. 2.16 d−1, summer: −0.46 d−1 vs. −0.73 d−1, autumn: −0.45 d−1 vs. −0.90 d−1) and significant decreases in grazing pressure percentages (%Pp from 0.84 to 0.58 and %Pi from 0.64 to 0.46). Short-term acid exposure significantly increased superoxide dismutase activity in both microplankton (from 0.03 to 0.08 U mg−1, p<0.01) and nanoplankton (from 0.05 to 0.09 U mg−1, p<0.001), indicating an adaptive response to oxidative stress. These results highlight that elevated CO2 levels primarily boost phytoplankton growth by reducing microzooplankton grazing pressure, resulting in higher growth rates and a shift towards smaller-sized phytoplankton, reflecting complex short-term ecological responses to acidification. Further research is needed to understand the long-term effects of ocean acidification on microzooplankton and their role in marine secondary productivity.

Dapagliflozin dampens liver fibrosis induced by common bile duct ligation in rats associated with the augmentation of the hepatic Sirt1/AMPK/PGC1α/FoxO1 axis

Liver fibrosis is considered an epidemic health problem due to different insults that lead to death. Dapagliflozin (DAPA), a sodium-glucose cotransporter-2 (SGLT2) inhibitor, is one of the newer anti-diabetic drugs used to manage type 2 diabetes mellitus (T2DM). DAPA exerted beneficial effects in many human and rat models due to its antioxidant, anti-inflammatory and antifibrotic activities. AimDue to previously reported capabilities related to DAPA, we designed this study to clarify the beneficial role of DAPA in liver fibrosis triggered by common bile duct ligation (CBL) in male rats. MethodsFor 14 or 28 days after CBL procedures, DAPA was administered to the rats orally at a dose of 10 mg/kg once daily. The effects of DAPA were evaluated by assaying liver enzymes, hepatic oxidant/antioxidant parameters, serum levels of tumor necrotic factor alpha (TNF-α), and AMP-activated protein kinase (AMPK). In addition, we measured the hepatic expression of fibrosis regulator-related genes along with evaluating liver histological changes. Key findingsDAPA successfully decreased hepatic enzymes and malondialdehyde levels, increased superoxide dismutase activity, elevated catalase levels, decreased serum levels of TNF-α, elevated serum levels of AMPK, decreased liver hydroxyproline content, upregulated Sirt1/PGC1α/FoxO1 liver gene expressions, down-regulated fibronectin-1 (Fn-1), collagen-1 genes in liver tissues, and improved the damaged liver tissues. Deteriorated biochemical parameters and histological liver insults associated with CBL were more pronounced after 28 days, but DAPA administration for 14 and 28 days showed significant improvement in most parameters and reflected positively in the histological structures of the liver. SignificanceThe significance of this study lies in the observation that DAPA mitigated CBL-induced liver fibrosis in rats, most likely due to its antioxidant, anti-inflammatory, and antifibrotic effects. These results suggest that DAPA's beneficial impact on liver fibrosis might be attributed to its interaction with the Sirt1/AMPK/PGC1α/FoxO1 pathway, indicating a potential mechanistic action for future exploration.

Hederagenin reduces Aβ-induced oxidative damage, decreases Aβ deposition and promotes cell survival by the P13 K/Akt signaling pathway.

Alzheimer's disease (AD) is a neurodegenerative disease characterized by memory loss and cognitive impairment. β-amyloid (Aβ) is one of the typical pathological features of AD, and its accumulation leads to neuronal death from oxidative stress. Here, we found that hederagenin (HG), a natural product, exhibits anti-tumor, anti-inflammatory, anti-depressant, anti-neurodegenerative biological activities. However, whether HG has anti-Aβ activity remains unclear. Based on the characteristics of HG, it is hypothesized that HG has biological activity against Aβ injury. Therefore, Aβ-injured SH-SY5Y cells were constructed, and the protective effect of HG against Aβ injury was further evaluated using C. elegans. The results showed that HG increased superoxide dismutase activity, effectively reduced Aβ-induced oxidative damage, and reduced apoptosis via the PI3 K/Akt signaling pathway. HG inhibited Aβ deposition and delayed senescence and paralysis in the C. elegans strain, CL4176. HG showed inhibitory effects on Aβ; therefore, more natural active products are expected to be applied in AD therapy.

Salvianolic acid A alleviates H2O2-induced endothelial oxidative injury via miR-204-5p

Oxidative stress induced endothelial dysfunction plays a particularly important role in promoting the development of cardiovascular diseases (CVDs). Salvianolic acid A (SalA) is a water-soluble component of traditional Chinese medicine Salvia miltiorrhiza Bunge with anti-oxidant potency. This study aims to explore the regulatory effect of SalA on oxidative injury using an in vitro model of H2O2-induced injury in human umbilical vein endothelial cells (HUVECs). In the study, we determined cell viability, the activities of Lactate dehydrogenase (LDH) and Superoxide dismutase (SOD), cell proliferation rate and intracellular reactive oxygen species (ROS). Flow cytometry was used to detect cell apoptosis. Western-blotting was used to evaluate the expression of cell senescence, apoptosis, autophagy and pyroptosis protein factors. The expression level of miRNA was determined by qRT-PCR. Compared with H2O2-induced HUVECs, SalA promoted cell viability and cell proliferation rate; decreased LDH and ROS levels; and increased SOD activity. SalA also significantly attenuated endothelial senescence, inhibited cell apoptosis, reversed the increase of LC3 II/I ratio and NLRP3 accumulation. Furthermore, miR-204-5p was regulated by SalA. Importantly, miR-204-5p inhibitor had similar effect to that of SalA on H2O2-induced HUVECs. Our results indicated that SalA could alleviate H2O2-induced oxidative injury by downregulating miR-204-5p in HUVECs.

Anti-Vasculogenic, Antioxidant, and Anti-Inflammatory Activities of Sulfated Polysaccharide Derived from Codium tomentosum: Pharmacokinetic Assay.

The purpose of this paper was to investigate the anti-inflammatory and anti-angiogenic activities of sulfated polysaccharide from C. tomentosum (PCT) using carrageenan (CARR)-induced paw edema in a rat model and anti-vasculogenic activity on a chorioallantoic membrane assay (CAM) model. Based on in vitro tests of anti-radical, total antioxidant, and reducing power activities, PCT presents a real interest via its antioxidant activity and ability to scavenge radical species. The in vivo pharmacological tests suggest that PCT possesses anti-inflammatory action by reducing paw edema and leukocyte migration, maintaining the redox equilibrium, and stabilizing the cellular level of several pro-/antioxidant system markers. It could significantly decrease the malondialdehyde levels and increase superoxide dismutase, glutathione peroxidase, and glutathione activities in local paw edema and erythrocytes during the acute inflammatory reaction of CARR. PCT pretreatment was effective against DNA alterations in the blood lymphocytes of inflamed rats and reduced the hematological alteration by restoring blood parameters to normal levels. The anti-angiogenic activity results revealed that CAM neovascularization, defined as the formation of new vessel numbers and branching patterns, was decreased by PCT in a dose-dependent manner, which supported the in silico bioavailability and pharmacokinetic findings. These results indicated the therapeutic effects of polysaccharides from C. tomentosum and their possible use as anti-proliferative molecules based on their antioxidant, anti-inflammatory, and anti-angiogenic activities.

Effect of cadmium and polystyrene nanoplastics on the growth, antioxidant content, ionome, and metabolism of dandelion seedlings

Cadmium is the most prevalent heavy metal pollutant in the environment and can be readily combined with micro/nanoplastics (M/NPs) to change their bioavailability. In the present study, we comprehensively investigated the effect of polystyrene (PS) NPs on dandelion plants grown under Cd stress. Cd exposure significantly inhibited the growth of dandelion seedlings, resulting in a decrease in seedling elongation from 26.47% to 28.83%, a reduction in biomass from 29.76% to 54.14%, and an exacerbation of lipid peroxidation and oxidative stress. The interaction between PS NPs and Cd resulted in the formation of larger aggregates, with the Cd bioavailability reduced by 12.56%. PS NPs affect ion absorption by regulating reactive oxygen production and increasing superoxide dismutase activity, thereby mitigating the adverse effects of Cd. PSCd aggregates induced significant changes in the metabolic profiles of dandelions, affecting various carbohydrates related to alcohols, organic acids, sugar metabolism, and bioactive components related to flavonoids and phenolic acids. Furthermore, based on a structural equation model, exposure to PSCd activated oxidative stress and nutrient absorption, thereby affecting plant growth and Cd accumulation. Overall, our study provides valuable insights into the effects of PS NPs on Cd bioavailability, accumulation, and plant growth, which are crucial for understanding the food safety of medicinal plants in a coexistence environment.

The Effects of Antioxidants and Hyperbaric Oxygenation at Severe Thermal Injury: a Prospective Study

INTRODUCTION. Severe thermal injury (STI) characterized, among others, by hypoxia and oxidative stress (OS). The possibility of maintaining the antioxidant system through the antioxidants usage is proposed, but their effectiveness and duration are debatable issues. On the other hand, correction of OS at STI is theoretically possible by hyperbaric oxygenation (HBO) sessions, but there is a need to assess the benefit-risk ratio. AIM. Investigate the effect of antioxidants and hyperbaric oxygenation sessions on the course of oxidative stress at severe thermal injury. MATERIALS AND METHODS. This study involved conditionally healthy individuals (n = 25), and patients with STI (n = 31), randomized into 3 groups: standard methods (n = 11), supplemented with antioxidants (daily injecting of 250 g vitamin C, 1.494 g “Cernevit” and 10 ml “Addamel N” during 14 days, n = 11) or HBO sessions (50–60 minutes in pressure chambers BLKS-30, BLKS-307/1 in the “low dose” at 1.3 Ata, n = 9). Plasma and erythrocytes were evaluated for free radical oxidation (FPO) and total antioxidant activity, malonic dialdehyde (MDA) concentration, activity of superoxide dismutase (SOD), catalase, and glutathione reductase. RESULTS AND DISCUSSION. At the antioxidant usage was found SOD activity increase by 11 % (p 0.01) on the second day, a decrease in FROer by 13 % (p = 0.012) on the 9th day, and MDAer by 13 % (p = 0.036) on the 6th day. In the HBO group, there was 9 % increase in SOD activity (p = 0.038) after the first session, an increase in glutathione reductase activity by 15 % (p = 0.028) by the 9th day. Thus, it is possible to pre-limit the period of potentially favorable use of antioxidants and HBO, which contributes to the maximum therapeutic effect. The negative consequences caused by the use of antioxidants or HBO have not been identified in this work. CONCLUSION. The antioxidant usage at STI contributes to the growth of the antioxidant protection of erythrocytes. The HBO usage leads to an improvement in cellular respiration and antioxidant enzymes activity and does not cause a deepening of OS. The optimal duration of prescribing antioxidants is the first 6–8 days, HBO — 9–11 days from the beginning of therapy.

Effects of Lactone- and Ketone-Brassinosteroids of the 28-Homobrassinolide Series on Barley Plants under Water Deficit.

The aim of this work was to study the ability of 28-homobrassinolide (HBL) and 28-homocastasterone (HCS) to increase the resistance of barley (Hordeum vulgare L.) plants to drought and to alter their endogenous brassinosteroid status. Germinated barley seeds were treated with 0.1 nM HBL or HCS solutions for two hours. A water deficit was created by stopping the watering of 7-day-old plants for the next two weeks. Plants responded to drought through growth inhibition, impaired water status, increased lipid peroxidation, differential effects on antioxidant enzymes, intense proline accumulation, altered expression of genes involved in metabolism, and decreased endogenous contents of hormones (28-homobrassinolide, B-ketones, and B-lactones). Pretreatment of plants with HBL reduced the inhibitory effect of drought on fresh and dry biomass accumulation and relative water content, whereas HCS partially reversed the negative effect of drought on fresh biomass accumulation, reduced the intensity of lipid peroxidation, and increased the osmotic potential. Compared with drought stress alone, pretreatment of plants with HCS or HBL followed by drought increased superoxide dismutase activity sevenfold or threefold and catalase activity (by 36%). The short-term action of HBL and HCS in subsequent drought conditions partially restored the endogenous B-ketone and B-lactone contents. Thus, the steroidal phytohormones HBL and HCS increased barley plant resistance to subsequent drought, showing some specificity of action.

Rosmarinic acid ameliorated oxidative stress, neuronal injuries, and mitochondrial dysfunctions mediated by polyglutamine and ɑ-synuclein in Caenorhabditis elegans models.

Numerous natural antioxidants have been developed into agents for neurodegenerative diseases (NDs) treatment. Rosmarinic acid (RA), an excellent antioxidant, exhibits neuroprotective activity, but its anti-NDs efficacy remains puzzling. Here, Caenorhabditis elegans models were employed to systematically reveal RA-mediated mechanisms in delaying NDs from diverse facets, including oxidative stress, the homeostasis of neural and protein, and mitochondrial disorders. Firstly, RA significantly inhibited reactive oxygen species accumulation, reduced peroxide malonaldehyde production, and strengthened the antioxidant defense system via increasing superoxide dismutase activity. Besides, RA reduced neuronal loss and ameliorated polyglutamine and ɑ-synuclein-mediated dyskinesia in NDs models. Further, in combination with the data and molecular docking results, RA may bind specifically to Huntington protein and ɑ-synuclein to prevent toxic protein aggregation and thus enhance proteostasis. Finally, RA ameliorated mitochondrial dysfunction including increasing adenosine triphosphate and mitochondrial membrane potential levels and rescuing mitochondrial membrane proteins' expressions and mitochondrial structural abnormalities via regulating mitochondrial dynamics genes and improving the mitochondrial kinetic homeostasis. Thus, this study systematically revealed the RA-mediated neuroprotective mechanism and promoted RA as a promising nutritional intervention strategy to prevent NDs.

Effects of high doses of zearalenone on some antioxidant enzymes and locomotion of Tenebrio molitor larvae (Coleoptera: Tenebrionidae).

The mealworm Tenebrio molitor L. (Coleoptera: Tenebrionidae) feeds on wheat bran and is considered both a pest and an edible insect. Its larvae contain proteins and essential amino acids, fats, and minerals, making them suitable for animal and human consumption. Zearalenone (ZEA) is the mycotoxin most commonly associated with Fusarium spp. It is found in cereals and cereal products, so their consumption is a major risk for mycotoxin contamination. One of the most important effects of ZEA is the induction of oxidative stress, which leads to physiological and behavioral changes. This study deals with the effects of high doses of ZEA (10 and 20mg/kg) on survival, molting, growth, weight gain, activity of antioxidant enzymes superoxide dismutase (SOD) and glutathione S-transferase (GST), and locomotion of mealworm larvae. Both doses of ZEA were found to (i) have no effect on survival, (ii) increase molting frequency, SOD, and GST activity, and (iii) decrease body weight and locomotion, with more pronounced changes at 20mg/kg. These results indicated the susceptibility of T. molitor larvae to high doses of ZEA in feed.

Cobalt protoporphyrin modulates antioxidant enzyme activity in the hypothalamus and motor cortex of female rats.

Cobalt protoporphyrin (CoPP) is a synthetic heme analog that has been observed to reduce food intake and promote sustained weight loss. While the precise mechanisms responsible for these effects remain elusive, earlier research has hinted at the potential involvement of nitric oxide synthase in the hypothalamus. This study aimed to delve into CoPP's impact on the activities of crucial antioxidant enzymes: superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione-S-transferase (GST) across seven distinct brain regions (hippocampus, hypothalamus, prefrontal cortex, motor cortex, striatum, midbrain, and cerebellum), as well as in the liver and kidneys. Female Wistar rats weighing 180 to 200 grams received a single subcutaneous dose of 25 μmol/kg CoPP. After six days, brain tissue was extracted to assess the activities of antioxidant enzymes and quantify malondialdehyde levels. Our findings confirm that CoPP administration triggers the characteristic effects of decreased food intake and reduced body weight. Moreover, it led to an increase in SOD activity in the hypothalamus, a pivotal brain region associated with food intake regulation. Notably, CoPP-treated rats exhibited elevated enzymatic activity of catalase, GR, and GST in the motor cortex without concurrent signs of heightened oxidative stress. These results underscore a strong connection between the antioxidant system and food intake regulation. They also emphasize the need for further investigation into the roles of antioxidant enzymes in modulating food intake and the ensuing weight loss, using CoPP as a valuable research tool.

Integrated evaluation of the biological response of the earthworm Eisenia fetida using two glyphosate exposure strategies: soil enriched and soils collected from crops in Southeastern Mexico.

Under laboratory conditions, the toxicological effects of pesticides tend to be less variable and realistic than under field conditions, limiting their usefulness in environmental risk assessment. In the current study, the earthworm Eisenia fetida was selected as a bioindicator for assessing glyphosate toxic effects in two different trials to solve this dilemma. In Trial 1, the worms were exposed for 7 and 14days to concentrations of a commercial glyphosate formulation (1 to 500mg a.i. kg-1) currently used in the field. In Trial 2, the worms were kept in nine soils collected from different plots with crops for 14days of exposure. In both experiments, glutathione S-transferase (GST), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and acetylcholinesterase (AChE) activities and contents of lipid peroxidation (LPO) were evaluated. In T1, the glyphosate formulation produced a 40% inhibition of AChE activity and a significant increase in GST, SOD, CAT, and GPx activities and LPO contents in E. fetida on day 7. In T2, higher concentrations of glyphosate were detected in the soils of soybean, papaya, and corn (0.92, 0.87, and 0.85mgkg-1), which induced a positive correlation between the levels of glyphosate residues with GST, SOD, CAT, GPx, and LPO and a negative correlation with AChE. These findings indicate that crop soils polluted with glyphosate elicited higher oxidative stress than under laboratory conditions, confirmed by IBRv2, PCA, and AHC analyses.

Comparative analysis of antioxidant enzyme activity and defence responses in root‐knot nematode resistant and susceptible carrot cultivars

AbstractRoot‐knot nematodes (RKNs) are one of the most serious pests of carrot plants. Resistance cultivars are a cost‐effective and ecofriendly management strategy for nematodes. To develop these, it is essential to understand the genetic, molecular and biochemical aspects underpinning RKN infection. Here, Meloidogyne javanica penetration and development, defence reactions and antioxidant enzyme activity were investigated in a resistant carrot cultivar (TN‐99‐129) compared to the susceptible cultivar TN‐99‐62. No significant difference was found in the number of J2s penetrating the roots of both cultivars. At 2 days post‐inoculation (DPI), necrosis symptoms were observed around the head of penetrated nematodes. Cell death also increased in the roots of the nematode‐infected TN‐99‐129 cultivar. Callose deposition happened at 6 DPI, and lignin content increased with delay (21 DPI) in the inoculated resistant cultivar. In addition, the reactive oxygen species metabolism process in resistant and susceptible cultivars was significantly different. In TN‐99‐129, catalase activity inhibition was observed at the early (2 DPI) phases of infection, and increasing superoxide dismutase activity and a relative decrease in catalase activity during nematode development. The activity of guaiacol peroxidase also increased significantly in the resistant cultivar, but no significant difference was observed in the activity of ascorbate peroxidase. This study explains the process of defence reactions in the TN‐99‐129 carrot cultivar during RKN penetration and development. The exhaustive characterization of the defence mechanism of a novel source of resistance to RKN in carrots constitutes a significant step toward their use in crop breeding.

Vincamine alleviates brain injury by attenuating neuroinflammation and oxidative damage in a mouse model of Parkinson's disease through the NF-κB and Nrf2/HO-1 signaling pathways.

Parkinson's disease (PD)is a neurodegenerative disease featured by progressive loss of nigrostriatal dopaminergic neurons, the etiology of which is associated with the existence of neuroinflammatory response and oxidative stress. Vincamine is an indole alkaloid that was reported to exhibit potent anti-inflammatory and antioxidant properties in many central and/or peripheral diseases. Nevertheless, the specific role of vincamine in PD development remains unknown. In our study, dopaminergic neuron loss was determined through immunohistochemistry staining and western blot analysis of tyrosine hydroxylase (TH)expression in the substantia nigra (SN)of PD mice. Reactive oxygen species (ROS)production and malondialdehyde (MDA),superoxide dismutase (SOD),and glutathione (GSH)levels were detected through DHE staining and commercially available kits to assess oxidative stress. Pro-inflammatorycytokine (TNF-α,IL-1β, and IL-6)levels in the SN were measured via RT-qPCRand western blot analysis. Microglial and astrocyte activation was examined through immunofluorescence staining of Iba-1 (microglia marker) and GFAP (astrocyte marker) in the SN. The regulation of vincamine on the NF-κBand Nrf2/HO-1pathway was estimated through western blot analysis. Our results showed that vincamine treatment decreased TNF-α,IL-1β,and IL-6 mRNA and protein levels, reduced GFAP and Iba-1 expression, decreased ROS production and MDA level, and increased SOD activity and GSH level in the SN of PD mice. Mechanically, vincamine repressed the phosphorylation levels of p65, IKKβ, and IκBα but enhanced the protein levels of Nrf2 and HO-1 in PD mice. Collectively, vincamine plays a neuroprotective role in PD mouse models by alleviating neuroinflammation and oxidative damage via suppressing the NF-κBpathway and activating the Nrf2/HO-1pathway.

Protective Effect of Prunella vulgaris L. Whole Plant or Spicas Water Extracts on Hyperthyroidism with Liver-yang Hyperactivity Syndrome

Background: Prunella vulgaris L. (Lamiaceae) is a perennial medicinal plant commonly used to treat thyroid dysfunction, infectious hepatitis, and mastitis in north-east Asia and Europe. In China, there has been a historical change in the medicinal use of P. vulgaris from the use of whole plants to the use of the spicas. Purpose: This study aimed to evaluate the protective effects of whole plant P. vulgaris water extracts and spicas on hyperthyroidism with liver-yang hyperactivity syndrome and to preliminarily explain the mechanism of action of these water extracts. Methods: Rats were induced with aconite decoction and levothyroxine and treated with P. vulgaris whole plant and spicas water extract for 28 days at the same time. Body weight, food intake, and rectal temperature were monitored. The serum thyroid function indicators thyroid stimulating hormone (TSH), thyroid hormone-free triiodothyronine (FT3) and free thyroxine (FT4), liver function index alanine aminotransferase (ALT) and aspartate aminotransferase (AST), oxidative damage index malondialdehyde (MDA), and superoxide dismutase (SOD) were detected. Liver and thyroid tissues were taken for sectioning and observation. The liver inflammatory factors human tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were detected by immunohistochemistry, and the expression levels of the apoptotic proteins caspase-3 and B-cell lymphoma-2 (Bcl-2) were detected. Results: Both P. vulgaris whole plant and spica water extract groups exhibited markedly reduced FT3 and FT4 contents, increased the TSH content, and decreased ALT and AST activities. Furthermore, these agents improve thyroid and liver lesion tissue; reduce MDA content; increase SOD activity; reduce IL-6, TNF-α, and caspase-3 expression; and increase Bcl-2 expression. Conclusion: The whole plant and spicas water extracts of P. vulgaris have obvious protective effects on hyperthyroidism and hyperactivity in liver yang, and the protective effect of the water extract of spicas is greater than that of the whole plant water extract.