Decreased Lipid Peroxidation Research Articles

The effect of silymarin on ischemia-reperfusion injury in skeletal muscles of rats silymarin and ischemia-reperfusion injury

Aim: Although the precise process is not entirely elucidated, it is well-known that oxidative stress mediators contribute to ischemia-reperfusion (I/R) injury. The impact of silymarin on I/R injury in many different tissues has been examined. For this purpose, we planned to see the effect of silymarin on muscle tissue in rats subjected to lower extremity I/R injury. Material and Methods: We used 18 male Wistar albino rats weighing 225-275 g. Each of the three groups of rats [Control (C), Ischemia-Reperfusion (I/R), and Silymarin-Ischemia/Reperfusion (S-I/R)] consisted of six rats. Silymarin was administered intraperitoneally 30 minutes before the procedure. (100 mg/kg-1) In Group I/R, the infrarenal abdominal aorta was clamped with a microvascular clamp. The clamp was removed after 120 minutes, and reperfusion was achieved for the next 120 minutes. At the end of the reperfusion period, muscle tissue samples were collected, and Malondialdehyde (MDA), catalase (CAT) enzyme activity levels and histopathological parameters were compared. Results: In the histopathological examination, no degeneration was observed in the muscle fibers in the Group C, while findings of striated muscle damage such as muscle atrophy/hypertrophy, muscle degeneration/congestion, internalization of the muscle nucleus/oval/central nucleus, fragmentation/hyalinization and leukocyte cell infiltration were seen in the Group I/R. In Group S-I/R, muscle atrophy /hypertrophy, internalization of the muscle nucleus/oval/central nucleus, fragmentation/hyalinization, and leukocyte cell infiltration were observed to improve these damaged areas compared to Group I/R. MDA levels in the Group I/R were significantly higher compared to Group C and S-I/R. The activity of the CAT enzyme was much higher in Group I/R compared to Group C. Conclusion: Our study revealed that 100 mg/kg-1 silymarin administered by intraperitoneal injection 30 minutes before ischemia effectively decreased lipid peroxidation, oxidative stress, and the injury caused by I/R in muscle histology in rats.

Copper Mitigates Atrazine-Induced Neurotoxicity in Parkinson's Disease Models.

Atrazine (ATR), one of the most prevalent herbicides used worldwide, has been associated with various environmental health concerns, including its potential role in promoting neurodegenerative diseases. Considering the pivotal role of metal homeostasis in the pathophysiology of neurodegenerative disorders, this study investigated the neuroprotective effects of copper supplementation in mitigating the adverse impacts of ATR in Parkinson's disease (PD). Our results reveal that ATR exposure disrupts copper and iron homeostasis within the substantia nigra pars compacta (SNpc), leading to enhanced oxidative stress and dopaminergic neuronal degeneration, which are key features of PD pathology. Remarkably, copper supplementation is able to counteract these neurotoxic effects, as demonstrated by the restoration of metal equilibrium in the SNpc, decreased lipid peroxidation, and improvements in motor function in PD rats. These results highlight the intricate relationship between environmental toxins and metal homeostasis in the genesis of neurodegenerative diseases.

HO-1-Mediated Ferroptosis Regulates Retinal Neovascularization via the COX2/VEGFA Axis

Retinal neovascularization (RNV) is a key pathological process in many blinding disorders. This study aims to investigate the potential mechanisms of heme oxygenase-1 (HO-1) on ferroptosis during RNV. Through bioinformatics analysis, differentially expressed ferroptosis-related genes were identified in the oxygen-induced retinopathy (OIR) mouse model. Ferroptosis was assessed in the OIR model and the human retinal microvascular endothelial cells (HRECs) with the treatment of H2O2. The mRNA and protein levels were measured through RT-qPCR and western blot. Lipid peroxidation was assessed through C11-BODIPY staining. HO-1 expression was knocked down by intravitreal injection with a self-complementary adeno-associated virus in the OIR model and small interfering RNA in HRECs. The pathological neovascular area and avascular area were assessed through immunofluorescent staining. The cellular functions of HRECs were evaluated with migration and tube formation assays. Our results demonstrate that HO-1 was significantly upregulated in the OIR model. 4-HNE upregulation and GPX4 downregulation were observed in the OIR model. The H2O2-induced oxidative stress resulted in lipid peroxidation, GPX4 downregulation, and mitochondrial morphology changes in HRECs. HO-1 knockdown induced GPX4 upregulation, and decreased lipid peroxidation in vitro and in vivo. Furthermore, HO-1 inhibition reduced pathological RNV in the OIR model and attenuated migration and tube formation in HRECs. Treatment with 6-OHDA restored the decrease of VEGFA, migration, and tube formation caused by HO-1 knockdown in HRECs. Overall, HO-1-mediated ferroptosis can regulate RNV through the COX2/VEGFA signal axis. These findings suggest that targeting HO-1 may serve as a promising approach for treating retinal neovascular diseases.

Lactiplantibacillus plantarum 1008 Enhances Testicular Function and Spermatogenesis via the Modulation of Gut Microbiota in Male Mice with High-Fat-Diet-Induced Obesity

Our study was designed to investigate the Lactiplantibacillus plantarum 1008 (LP1008) on testicular antioxidant capacity, spermatogenesis, apoptosis, autophagy, and metabolic function in male mice with high-fat-diet-induced obesity. A total of thirty-six male C57BL/6 mice were fed a normal diet (denoted as the NC group) or a high-fat control diet (denoted as the HFC group) for 16 weeks, then half of the HFC group was randomly chosen and subsequently fed with LP1008 for the final 8 weeks (high-fat diet + LP1008; denoted as the HFP group). The HFP group expressed improved blood cholesterol, insulin resistance, hepatic function, and lipopolysaccharide (LPS) levels compared to the HFC group. Meanwhile, the HFC group displayed decreased testicular testosterone levels, sperm quality, and 17β-HSD protein expression, which were rescued after LP1008 treatment. Moreover, the HFC group had lower superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX) enzyme activities. After LP1008 treatment, enhanced antioxidative activities and decreased lipid peroxidation were observed. The HFC group also exhibited aggravated apoptosis, inflammation, and autophagy proteins in the testis, which were ameliorated by LP1008 supplementation. Furthermore, the gut microbiota analysis results revealed that the Firmicutes/Bacteroidetes ratio was significantly elevated in the HFC and HFP groups compared to the NC group and that LP1008 treatment diminished Ruminococcaceae and enhanced Bifidobacteriaceae diversity. In summary, LP1008 treatment strengthened antioxidative enzyme levels and regulated microbiota-ameliorated HFC-induced oxidative stress, apoptosis, inflammation, and autophagy, and thus improved testicular function and semen quality.

Growth performance, serum metabolites, plasma protein fraction, meat lipid profile and antioxidant activities of breast meat of broiler chicken fed diets containing Cinnamomum ceylon powder, Zingiber officinale powder and Moringa oleifera leafmeal supplem

An experiment was conducted to determine growth performance, serum metabolites, plasma protein fraction, meat lipid profile and antioxidant activities of meat of broilers as affected by Cinnamomium ceylon, Zingiber officinale and Moringa oleifera supplementation. A total of 112 day old chicks were allotted into four treatments replicated four times with seven birds per replicate in a completely randomized design (CRD). Basal diets were formulated for broiler starters (0-28days) and finisher phase (29-56) days. The basal diets were divided into 4 diets : diet 1- control diet without supplementation; diet 2- contained 0.2% Cinnamomum ceylon supplementation (CCS); diet 3- contained 0.2% Zingiber officinale supplementation (ZOS), diet 4-contained 0.2% Moringa oleifera leafmeal (MOLM) supplementation. The experiment lasted for 56 days. Results showed an improvement in final liveweight, weight gain, feed intake and feed conversion ratio of birds on 0.2% MOLM. Birds on phytogenic feed additives have lower values of urea, cholesterol, glucose, high density lipoprotein and low density lipoprotein. Birds administered phytogenic supplements exhibited much greater plasma albumin levels. Low levels of meat cholesterol, triglycerides and low density lipoprotein were found in birds fed phytogenic feed additives while high levels of high density lipoprotein were recorded for birds on phytogenic feed additives. The supplementation of broilers diets with phytogenic feed additives increased the glutathione peroxidase and superoxide dismutase and decreased lipid peroxidation. It was concluded that supplementation of broiler diets with Moringa oleifera leaf meal enhanced body weight gain, antioxidant activities also reduced cholesterol level in both serum metabolites and meat.

The link between amyloid β and ferroptosis pathway in Alzheimer’s disease progression

Alzheimer’s disease (AD) affects millions of people worldwide and represents the most prevalent form of dementia. Treatment strategies aiming to interfere with the formation of amyloid β (Aβ) plaques and neurofibrillary tangles (NFTs), the two major AD hallmarks, have shown modest or no effect. Recent evidence suggests that ferroptosis, a type of programmed cell death caused by iron accumulation and lipid peroxidation, contributes to AD pathogenesis. The existing link between ferroptosis and AD has been largely based on cell culture and animal studies, while evidence from human brain tissue is limited. Here we evaluate if Aβ is associated with ferroptosis pathways in post-mortem human brain tissue and whether ferroptosis inhibition could attenuate Aβ-related effects in human brain organoids. Performing positive pixel density scoring on immunohistochemically stained post-mortem Brodmann Area 17 sections revealed that the progression of AD pathology was accompanied by decreased expression of nuclear receptor co-activator 4 and glutathione peroxidase 4 in the grey matter. Differentiating between white and grey matter, allowed for a more precise understanding of the disease’s impact on different brain regions. In addition, ferroptosis inhibition prevented Aβ pathology, decreased lipid peroxidation and restored iron storage in human AD iPSCs-derived brain cortical organoids at day 50 of differentiation. Differential gene expression analysis of RNAseq of AD organoids compared to isogenic controls indicated activation of the ferroptotic pathway. This was also supported by results from untargeted proteomic analysis revealing significant changes between AD and isogenic brain organoids. Determining the causality between the development of Aβ plaques and the deregulation of molecular pathways involved in ferroptosis is crucial for developing potential therapeutic interventions.

Reduced glutathione attenuates pediatric sepsis-associated encephalopathy by inhibiting inflammatory cytokine release and mitigating lipid peroxidation-induced brain injury.

Sepsis-associated encephalopathy (SAE) is a severe complication of sepsis. Reduced glutathione (GSH) has antioxidant properties and is used as a neuroprotective agent in some studies. However, research on the application of exogenous GSH in the treatment of SAE is limited. This study aimed to determine the effects of exogenous GSH in pediatric SAE patients and mice. We evaluated clinical parameters, inflammatory factors, and oxidative stress before and after GSH treatment. The clinical trials demonstrated that GSH treatment improved brain damage markers (S-100 beta protein, brain fatty acid-binding protein), increased neurological status scores (Glasgow coma scale), and reduced Pediatric Risk of Mortality III scores in children with SAE. GSH treatment also significantly reduced the levels of inflammatory factors (interleukin-6, tumor necrosis factor-α) and decreased lipid peroxidation (superoxide dismutase). Additionally, GSH reduced lipid peroxidation resulting from abnormal lipid metabolism, as indicated by the levels of acyl-CoA synthetase long-chain family member 4, lysophosphatidylcholine acyltransferase 3, and glutathione peroxidase 4. In-vivo experiments showed that the neuroprotective effect of GSH was dose-dependent, with better effects observed at medium and high doses. Furthermore, GSH alleviated brain damage, suppressed the release of inflammatory factors, and inhibited lipid peroxidation in SAE mice. The animal experiments also showed that GSH reduces lipid peroxidation through the 15-lipoxygenase/phosphatidylethanolamine binding protein 1/glutathione peroxidase 4 pathway. Our study suggests that exogenous GSH has neuroprotective effects in pediatric SAE. These findings provide a basis for the potential use of GSH as a therapeutic method for SAE.

Nitric Oxide-Dependent Regulation of Oxygen-Related Processes in a Rat Model of Lead Neurotoxicity: Influence of the Hypoxia Resistance Factor

Background/Aims: Lead exposure is known to induce oxidative stress and neurotoxicity. Nitric oxide (NO) plays an important role in modulating oxidative stress, with L-arginine as a precursor of NO and Nω-nitro-L-arginine (L-NNA) as an inhibitor of NO synthase, an enzyme that catalyses the production of nitric oxide (NO) from L-arginine. Methods: This study investigated the differential effects of L-arginine and L-NNA on markers of oxidative stress and biochemical changes in brain tissue from rats with different levels of resistance to hypoxia exposed to lead nitrate. Rats with either low or high resistance to hypoxia were exposed to lead nitrate (oral 3.6 mg lead nitrate/kg b.w. per day for 30 days) and treated with L-arginine (600 mg/kg b.w., i.p., 30 min before and after exposure to lead nitrate) or L-NNA (35 mg/kg b.w., i.p., 30 min before and after exposure to lead nitrate). Brain tissue samples were analysed for lipid peroxidation, oxidative modification of proteins, and activity of antioxidant enzymes, including superoxide dismutase, catalase, glutathione reductase, and peroxidase, and total antioxidant status (TAS). We also examined the biomarkers of biochemical pathways involving the activity of alanine and aspartate aminotransferases, succinate dehydrogenase (SDH), and α-ketoglutarate dehydrogenase (KGDH). In addition, the trend observed was supported by assessments of the acetylcholine levels and acetylcholinesterase activity (ACh-AChE system) in brain tissue. Results: In rats with low resistance to hypoxia, the L-arginine treatment significantly reduced lipid peroxidation and oxidative protein modification but increased antioxidant enzyme activity, suggesting a protective effect against lead-induced oxidative stress. Conversely, in rats with high resistance to hypoxia, L-NNA had a protective effect, reducing lead-induced oxidative damage and decreasing lipid peroxidation, whereas L-arginine exacerbated oxidative stress and impaired antioxidant defences. These findings were supported by corresponding changes in the acetylcholine-acetylcholinesterase system, reflecting the observed patterns of lead-induced oxidative stress and neurotoxicity. The study shows that L-arginine exerts a protective effect by reducing lead-induced oxidative damage via an improvement in TAS. Our study shows that lead nitrate exposure significantly increases ala-nine and aspartate aminotransferase activity in brain tissue, with L-arginine exacerbating and L-NNA reversing this effect. The lead nitrate exposure also affected the activities of SDH and KGDH, which are important for cellular energy production and hypoxia resistance, with L-arginine altering SDH activity depending on the level of resistance and L-NNA enhancing both SDH and KGDH activities. These trends were further validated by alterations in the ACh-AChE system, highlighting the differential role of NO-dependent mechanisms in modulating lead-induced neurotoxicity based on hypoxia resistance. Conclusion: These findings suggest potential targeted therapeutic strategies based on the oxidative stress profile and highlight the potential of nitric oxide system modulators in counteracting lead-induced biochemical alterations and the dynamics of the ACh-AChE system depending on the individual physiological reactivity of organisms.

Lactic acid bacteria supplementation: A bioprotective approach to mitigating cadmium-induced toxicity and modulating gene expression in murine models

This study aimed to assess the effects of different strains of lactic acid bacteria, namely LeviLactobacillus brevis (AC10), Lacticaseibacillus rhamnosus (AC11), and Pediococcus acidilactici (AC15), on mice exposed to cadmium-induced oxidative stress. The study assessed weight gain, liver enzymes, antioxidant enzymes, immunoglobulin factors, lipid peroxidation, and gene expression in liver and brain of mice. The findings revealed that the AC10 and AC11 strains had a higher ability to absorb Cd as compared to AC15. The in vivo analysis demonstrated that the dietary dual supplementation of AC10 and AC11 resulted in significant (p < 0.05) improvements, including increased body weight and food intake, reduced cadmium tissue deposition, decreased lipid peroxidation, enhanced cellular antioxidant redox potential, suppressed inflammation genes in the liver and brain tissues, and improved morpho-characteristics of the jejunum in mice challenged by cadmium-induced toxicity. The multiple mechanisms of action, including heavy metal sequestration, antioxidant enhancement, and maintenance of intestinal integrity, highlight the potential of these probiotics’ intervention as a viable approach to counteract the deleterious effects of cadmium exposure.

Herniarin ameliorates acrylamide-induced neurotoxicity in rat: involvement of neuro-inflammation and acetylcholinesterase

This study aimed to investigate the protective effects of herniarin against acrylamide neuro-toxicity. Rats were administered 50 mg/kg of acrylamide (Acr) along with oral doses of herniarin at 50, 100, and 200 mg/kg for 11 days. After treatment, the animals were sacrificed and biochemical markers including superoxide dismutase (SOD), catalase activity, malondialdehyde (MDA), nitric oxide (NO), thiols and acetylcholine esterase (AChE) level were evaluated. Moreover, mRNA expression of neuro-inflammatory cytokines including TNF-α, IL-1β, and IL-6 were measured using qRT-PCR method. As results, Acr increased MDA with subsequent reduction in SOD, catalase, and thiols content. In contrast, administration of herniarin remarkably normalised the antioxidants and decreased lipid peroxidation. Furthermore, it downregulated mRNA expression of TNF-α, IL-1β, and IL-6 (p < 0.001) as well as decreased NO (p < 0.01) and AchE levels (p < 0.001) in the Acr-injured brains. Herniarin ameliorated Acr-induced brain injury via modulating redox hemostasis, cholinergic function, as well as inhibiting neuro-inflammation in rats.

Investigating the Hepatic Response to Orlistat and White Tea in Rats on a High-Fat Diet.

High-fat diets have detrimental health impacts that increase the likelihood of developing obesity and metabolic syndrome. This study aimed to examine the potential antioxidant and anti-inflammatory effects of orlistat and white tea in rats fed a high-fat diet. Thirty-two rats were randomized into four groups: control (standard diet), HFD (high-fat diet), HFD+Orlistat (high-fat diet+orlistat), and HFD+WT (high-fat diet+white tea extract). A significant increase in malondialdehyde (MDA) levels and a decrease in total thiol (TT) levels were detected in the HFD group (p < 0.001). On the other hand, a decrease in the MDA level (p < 0.001) and an increase in the TT level were observed in the orlistat and white tea groups compared with those in the HFD group (p < 0.001). Histopathological examinations revealed that, compared with the HFD alone, orlistat and white tea reduced fat accumulation, prevented degenerative changes in hepatocytes, and decreased the histopathological damage score (p = 0.001). Immunohistochemical examinations of nuclear factor-kappa B (NF-kB/p65) revealed that compared with the HFD, orlistat and white tea reduced immunopositivity (p = 0.001). White tea decreases lipid peroxidation and oxidative stress. Both white tea and orlistat decreased fat formation and inflammation in the liver and regulated inflammation by reducing Nf-kB positivity. Nevertheless, further research is needed to assess their impact on human subjects.

Taming hemoglobin chemistry—a new hemoglobin-based oxygen carrier engineered with both decreased rates of nitric oxide scavenging and lipid oxidation

The clinical utility of hemoglobin-based oxygen carriers (HBOC) is limited by adverse heme oxidative chemistry. A variety of tyrosine residues were inserted on the surface of the γ subunit of recombinant fetal hemoglobin to create novel electron transport pathways. This enhanced the ability of the physiological antioxidant ascorbate to reduce ferryl heme and decrease lipid peroxidation. The γL96Y mutation presented the best profile of oxidative protection unaccompanied by loss of protein stability and function. N-terminal deletions were constructed to facilitate the production of recombinant hemoglobin by fermentation and phenylalanine insertions in the heme pocket to decrease the rate of NO dioxygenation. The resultant mutant (αV1del. αL29F, γG1del. γV67F, γL96Y) significantly decreased NO scavenging and lipid peroxidation in vitro. Unlike native hemoglobin or a recombinant control (αV1del, γG1del), this mutation showed no increase in blood pressure immediately following infusion in a rat model of reperfusion injury, suggesting that it was also able to prevent NO scavenging in vivo. Infusion of the mutant also resulted in no meaningful adverse physiological effects apart from diuresis, and no increase in oxidative stress, as measured by urinary isoprostane levels. Following PEGylation via the Euro-PEG-Hb method to increase vascular retention, this novel protein construct was compared with saline in a severe rat reperfusion injury model (45% blood volume removal for 90 minutes followed by reinfusion to twice the volume of shed blood). Blood pressure and survival were followed for 4 h post-reperfusion. While there was no difference in blood pressure, the PEGylated Hb mutant significantly increased survival.

Targeting the Labile Iron Pool with Engineered DFO Nanosheets to Inhibit Ferroptosis for Parkinson's Disease Therapy.

Ferroptosis in neurons is considered one of the key factors that induces Parkinson's disease (PD), which is caused by excessive iron accumulation in the intracellular labile iron pool (LIP). The iron ions released from the LIP lead to the aberrant generation of reactive oxygen species (ROS) to trigger ferroptosis and exacerbate PD progression. Herein, a pioneering design of multifunctional nanoregulator deferoxamine (DFO)-integrated nanosheets (BDPR NSs) is presented that target the LIP to restrict ferroptosis and protect against PD. The BDPR NSs are constructed by incorporating a brain-targeting peptide and DFO into polydopamine-modified black phosphorus nanosheets. These BDPR NSs can sequester free iron ions, thereby ameliorating LIP overload and regulating iron metabolism. Furthermore, the BDPR NSs can decrease lipid peroxidation generation by mitigating ROS accumulation. More importantly, BDPR NSs can specifically accumulate in the mitochondria to suppress ROS generation and decrease mitochondrial iron accumulation. In vivo experiments demonstrated that the BDPR NSs highly efficiently mitigated dopaminergic neuronloss and its associated behavioral disorders by modulating the LIP and inhibiting ferroptosis. Thus, the BDPR-based nanovectors holds promise as a potential avenue for advancing PD therapy.

Extract from Falcaria vulgaris loaded with exosomes for the treatment of hypertension in pregnant mice: In vitro and In vivo investigations.

Hypertensive disorders during pregnancy pose significant risks to both maternal and fetal health, necessitating safe and effective therapeutic interventions. This study aimed to investigate the potential of an extract derived from Falcaria vulgaris (FV), loaded with exosomes to form the Exo/FV complex, as a novel therapeutic agent for the management of hypertension in pregnant mice: antioxidants, antimicrobials, and phenolic compounds present in FV lower blood pressure. The isolation of exosomes was done by ultracentrifugation methods and the FV was loaded into the exosomes by electroporation method. The Exo/FV was found to be spherical with diameter ranges from 20 to 30nm and they were tested for biocompatibility in NHI 3T3 cell lines and found to be effective. This research investigated invivo hypertension in mice induced by L-NAME and treated with FV and Exo/FV and found that AChE and MAO determine mice's redox state tends to reduce blood pressure. Increased non-protein thiol (NP-SH) and decreased lipid peroxidation were also found, and PDE-5, ACE, Arginase, and MDA activity has also been tested. This analysis showed that Exo/FV effectively treated hypertension during pregnancy.

Chlamydomonas sp. extract meliorates the growth and physiological responses of 'Camarosa' strawberry (Fragaria × ananassa Duch) under salinity stress.

Microalgae like Chlamydomonas are beneficial organisms employed as biological stimulants to improve plants' growth, fruit quality, and stress tolerance. In the current study, the effects of Chlamydomonas sp. foliar spraying (0, 20, and 40 ml L-1) were assayed on Camarosa strawberry plants under salinity stress (0, 40, and 80 mM NaCl). The results showed that the foliar application of Chlamydomonas extract influenced strawberry's morphological, physiological, and biochemical characteristics under salinity stress. Foliar treatment of Chlamydomonas extract with and without salinity stress increased the leaf number and leaf area, the leaf relative water content, and photosynthetic pigments content. Moreover, the foliar application of Chlamydomonas extract decreased lipid peroxidation and hydrogen peroxide content and, on the other hand, enhanced the antioxidant enzymes activity (superoxide dismutase, guaiacol peroxidase, and peroxidase), phenolics, flavonoids, and anthocyanins content under salinity stress. For instance, the highest total antioxidant capacity was found in the plants foliar treated with 40 ml L-1of Chlamydomonas algae extract under 80 mM salinity stress, which increased by 102.4% compared to the controls, as well as the highest total phenolic compounds and anthocyanin's content were 30.22, and 7.2% more than the control plants, respectively. Overall, the foliar application of Chlamydomonas algae extracts, especially at a concentration of 20 ml L-1enhanced the strawberry's growth, yield, and physiological traits under saline conditions. The results with more detailed evaluations will be advisable for the pioneer farmers and extension section.

Artichoke leaf hydroethanolic extract reduces neuropathic pain in a rat model of chronic constriction injury via attenuating the sciatic nerve oxidative stress

Neuropathic pain, a nerve damage consequence, presents symptoms such as dysesthesia, hyperalgesia, and allodynia. This study aimed to evaluate the alleviating potential of artichoke leaf extract in neuropathic pain induced by chronic constriction injury (CCI) of the sciatic nerve in male rats. The hydroethanolic extract of artichoke leaf was administered via gavage at doses of 200, 400, and 800 mg/kg for 21 days. Behavioural tests were conducted on days 1, 4, 7, 14, and 21 post-surgeries. Only the dose of 800 mg/kg significantly reduced thermal hyperalgesia and allodynia from day 14 and mechanical allodynia from day 7, and the other doses did not affect behaviours. Biochemical analysis showed that artichoke extract decreased lipid peroxidation and restored antioxidant enzyme activities (SOD and GPx) in the sciatic nerve tissue. In conclusion, artichoke leaf extract administration diminishes neuropathic pain-related behaviours by enhancing antioxidant capacity and reducing oxidative stress in the rats’ sciatic nerve.

Novel insights into famotidine as a GSK-3β inhibitor: An explorative study in aluminium chloride-induced Alzheimer’s disease rat model

Alzheimer's disease (AD), a chronic neurodegenerative disease, presents a substantial global health challenge. This study explored the potential therapeutic role of famotidine, a histamine (H2) receptor antagonist, as a glycogen synthase kinase-3β (GSK-3β) inhibitor in the context of AD induced by aluminium chloride (AlCl3) in a rat model. The intricate relationship between GSK-3β dysregulation and AD pathogenesis, particularly in amyloid-β (Aβ) production, formed the basis for investigating famotidine's efficacy. Molecular modelling revealed famotidine's efficient binding to GSK-3β, suggesting inhibitory potential. In behavioural assessments, famotidine-treated groups exhibited dose-dependent improvements in Morris Water Maze, Novel Object Recognition, and Y-Maze tests, comparable to the standard Rivastigmine tartrate group. Biochemical analyses showed that famotidine inhibits acetylcholinesterase, decreases lipid peroxidation, increases antioxidant activity, and mitigates oxidative stress. Moreover, famotidine significantly lowered the levels of GSK-3β, IL-6, and Aβ(1−42). The neuroprotective effects of famotidine were further supported by histopathological analysis. This comprehensive investigation underscores famotidine's potential as a GSK-3β inhibitor, providing insights into its therapeutic impact on AD induced by AlCl3. The study offers a promising avenue for repurposing famotidine due to its established safety profile and widespread availability, highlighting its potential in addressing the formidable challenge of AD.

Glucose-responsive carboxymethyl chitosan/ sodium alginate film protects against mechanical wound on postharvest blueberry

Fresh fruits and vegetables, particularly berries, are highly susceptible to mechanical damage, which results in nutrient loss, reduced quality, and increased decay from microbial infections, ultimately leading to significant losses. Here, a biodegradable polysaccharide film was employed to encapsulate glucose oxidase (Gox), thereby creating a glucose/wounding-responsive active package that reduced fruit respiration, promoted healing and protected blueberry wounds from mold infection. The combination of carboxymethyl chitosan and sodium alginate resulted in the formation of the polysaccharides film CSF that effectively restricted the permeation of oxygen, water, and carbon dioxide around the surface of the fruit. The encapsulation of Gox in the CSF film (CSFG) reduced glucose levels through enzymatic reaction in surface wounds of the fruit, thereby competing for glucose to establish a starvation-like microenvironment for the pathogenic fungus Botrytis cinerea. The enzymatic reaction also facilitated the production of hydrogen peroxide, which functioned as a fungicide that inhibits the growth of B. cinerea and served as a secondary messenger in fruit immunity. The CSFG film increased beta-glucanase activity, and decreased lipid peroxidation in wounds of blueberries. Therefore, this glucose-responsive CSFG barrier significantly reduced the decay rates of gray mold, caused by B. cinerea in wounded blueberries, by 66.7% compared to the control at 6 d of storage. Taken together, the glucose-responsive active packaging film provides an alternative package for safeguarding blueberries against mechanical damage.

Volcanic ash in the water column: Cellular, physiological and anatomical implications for the gastropod suspension-feeder Crepipatella peruviana (Lamarck, 1822)

The influx of volcanic ash into seawater alters particle composition with implications for the cellular, physiological and anatomical response of suspension-feeding organisms. Adult females of Crepipatella peruviana were exposed to three diets consisting of a fixed concentration of 50,000 cells ml−1 of the microalga Isochrysis galbana plus different concentrations of ash particles (30, 90 and 150 mg L−1). The objective was to determine the cellular, physiological and anatomical responses. Mortality increased with ash concentrations, while feeding and respiration rates, tissue weight, and condition index decreased. The gills showed severe degradation of cilia and the presence of large mucous aggregates of cilia and ash. An increase in ash resulted in decreased lipid peroxidation and protein carbonyls, but increased total antioxidant capacity and phenols. Thus, volcanic ash particles may exert a high impact at both cellular and physiological levels for C. peruviana, where inhibition of gill function reduces the ability to acquire food.

Biomarkers of oxidative stress, biochemical changes, and the activity of lysosomal enzymes in the livers of rainbow trout (Oncorhynchus mykiss Walbaum) vaccinated against yersiniosis before a Yersinia ruckeri challenge

Abstract Introduction This study aimed to evaluate biomarkers of oxidative stress (2-thiobarbituric acid reactive substances, aldehyde and ketone derivatives of oxidatively modified proteins and total antioxidant capacity), the activity of antioxidant enzymes (superoxide dismutase, catalase, glutathione reductase and glutathione peroxidase), that of lysosomal enzymes (alanyl aminopeptidase, leucyl aminopeptidase, β-N-acetylglucosaminidase and acid phosphatase) and changes in biochemical parameters (alanine aminotransferase, aspartate aminotransferase, de Ritis ratio, lactate dehydrogenase activity, lactate and pyruvate levels and their ratio) in the liver tissue of fish that were vaccinated against enteric redmouth disease and challenged with its causative agent, the bacterium Yersinia ruckeri. Material and Methods The vaccine was administered orally to trout, some of which were challenged with Y. ruckeri 61 days later. For comparison, unvaccinated and unchallenged trout and unvaccinated and challenged trout were also evaluated. Results In the unvaccinated fish, infection with Y. ruckeri disrupted the pro-oxidant/antioxidant balance, led to a significant increase in lipid peroxidation and oxidative modification of proteins, decreased total antioxidant capacity and significantly increased the activity of lysosomal enzymes. In vaccinated fish, the Y. ruckeri challenge increased the activity of glutathione-related enzymes and decreased lipid peroxidation, anaerobic metabolism and the activity of lysosomal enzymes in fish livers relative to the unvaccinated and challenged group. In contrast, these parameters increased after the Y. ruckeri challenge in unvaccinated trout relative to those in the untreated group. Conclusion Vaccination exerted a protective effect during the Y. ruckeri challenge and had no adverse effect on fish livers.