MDA Levels Research Articles

The deleterious effect of orally administered aqueous extract of <i>Acalypha wilkesiana</i> (Red Acalypha) on female reproductive organs in Sprague Dawley rats

Acalypha wilkesiana is a herbaceous plant that has been traditionally used to treat and/or manage a variety of illnesses, including respiratory issues, diabetes, jaundice, hypertension, fever, diarrhea, and inflammation of the liver. The effects of taking Acalypha wilkesiana orally on the uterus and ovaries were examined in this study. Twenty (20) adult female Sprague-Dawley rats (165±20g) were purchased and given a two-week period to get used to the laboratory environment. Aqueous extract of Acalypha wilkesiana was given orally for four weeks at concentrations of 0, 100, 200, and 400 mg/kg of BW following acclimatization. Groups A-D provided as the control, low, medium, and high doses, respectively. The rats' weight gain and behavioral patterns were periodically examined. Following their euthanasia, blood was drawn via the ocular sinuses to measure hormonal parameters, and the uterus and ovaries were exercised to examine histology and oxidative stress markers. Significantly lower levels of FSH, LH, estrogen, and progesterone were observed in the treatment groups, while significantly lower levels of SOD and CAT and higher levels of MDA were observed. In both the 40 and 80 mg/kg groups, histological sections of the ovaries and uterus revealed vascular congestion in the ovaries and moderate to severe damage within the uteri. The findings demonstrated that long-term use of Acalypha wilkesiana increased levels of oxidative stress, altered hormone levels, and negatively affected the histoarchitecture of the uterus and ovaries.

Canagliflozin exerts anti-inflammatory and antioxidant effects in the heart and skin tissues: Biochemical and histopathological assessment in a model of accelerated aging induced by D-galactose in mice

Canagliflozin was assessed for its anti-inflammatory and antioxidant effects as an anti-aging drug in animal models. 50 Swiss albino male mice were divided into five groups; all groups received their intervention using gastric gavage; group 1 received normal saline for 14 weeks; group 2 received induction by D-galactose 200 mg/kg/day for seven weeks; and group 3 to 5 received the same induction for seven weeks, followed by another seven weeks of investigated drugs; group 3 received Vitamin C (100 mg/kg/day); group 4 received canagliflozin (3 mg/kg/day); and group 5 received canagliflozin (1 mg/kg/day). At the end of 14 weeks, all animals were euthanasiad, and heart and skin tissue were harvested for further analysis. Canagliflozin at both 1 and 3 mg/kg was successful in reducing the levels of inflammatory mediators (TNF-alpha and IL6), reducing levels of MDA, increasing the levels of SOD, and increasing the levels of collagen-1 and elastin in skin tissue. Additionally, 3 mg/kg Canagliflozin showed a better effect compared to 1 mg/kg regarding its effect on IL6, SOD, and elastin. Histopathologically, treatment with both doses of Canagliflozin attenuates abnormalities induced by D-galactose (bizarre, irregular, and hyperchromatic nuclei). Canagliflozin exhibits potent antioxidant and anti-inflammatory effects in living organisms, effectively prevents cardiac and skin damage generated by D-galactose, and possibly reduces aging.

Capsiate Improves Glucose Metabolism by Improving Insulin Sensitivity in Diabetic Retinopathy Mice

Purpose Capsiate (cap) is a metabolite that affects a number of biological processes, and diabetic retinopathy (DR) is now known to be the primary cause of end-stage eye illness. Methods In order to examine the effects of the cap intervention on body weight, nutritional intake, changes in body weight composition, glucose metabolism levels, retinopathy, and oxidative stress levels, we proposed using a mouse model of diabetic retinopathy caused by STZ. Results Our findings demonstrated that, in addition to increasing lean body mass and lowering fat body mass content, cap intervention significantly improved body weight and dietary consumption in STZ mice. Additionally, our results on glucose metabolism revealed that cap had a significant impact on insulin resistance and the stabilization of OGTT levels. In conclusion, we examined the levels of oxidative stress and retinopathy. We discovered that the cap intervention greatly reduced the levels of MDA and significantly improved the levels of VEGF and retinopathy. In contrast, the STZ group’s levels of SOD, CAT, and GSH were significantly higher. Conclusions According to our research, the Cap intervention improved the damage caused by diabetic retinopathy by reversing the levels of oxidative stress and the disrupted state of glucose metabolism, which in turn decreased the levels of VEGF.

Protective Effects of 17-βE2 on the Primary Hepatocytes of Rainbow Trout (Oncorhynchus mykiss) Under Acute Heat Stress

The rainbow trout (Oncorhynchus mykiss) is a typical cold-water species. However, due to global warming, it has experienced prolonged high-temperature stress. Research indicates that thermotolerance in rainbow trout varies by sex at multiple physiological levels. Specifically, females exhibit higher thermotolerance, which may be attributed to estrogen-mediated signal transduction pathways. This study involved culturing primary hepatocytes from rainbow trout and exposing them to estradiol and estrogen receptor antagonists to assess estradiol’s protective effects. The analysis focused on expression of ER, HSPs genes, hepatocyte viability, and antioxidant indices. Four experimental groups were treated with 17-βE2 at concentrations of 0, 0.1, 1, and 10 μM/mL for durations of 4, 8, 12, 24, and 48 h at 18 °C. 17-βE2 treatment led to increased hepatocyte viability and enhanced SOD, GSH-Px, and CAT levels but decreased MDA levels. hsp70a, hsp90β, era1, and erβ1 levels were notably higher, with the optimal 17-βE2 concentration being 1.0 μM/mL. Following heat stress (24 °C), the addition of 1.0 μM/mL 17-βE2 improved hepatocyte viability and increased SOD, GSH-Px, and CAT levels, while MDA content initially decreased before rising. The gene expression of hsp70a, hsp90β, era1, and erβ1 was significantly elevated compared to controls. Flow cytometry analysis showed increased apoptosis after heat exposure; however, 17-βE2 treatment significantly reduced the heat stress-induced effects (p < 0.05). In conclusion, 17-βE2 and mild heat stress collaboratively enhanced the expression of HSPs and estrogen receptors, thereby providing protection to hepatocytes from heat stress damage, indicating a beneficial protective role of estradiol in rainbow trout hepatocytes.

MsFtsH8 Enhances the Tolerance of PEG-Simulated Drought Stress by Boosting Antioxidant Capacity in Medicago sativa L.

Drought is a major abiotic stress that limits the growth and yield of alfalfa, a vital forage legume. The plant metalloproteinase Filamentation temperature-sensitive H (FtsH) is an ATP- and Zn2+-dependent enzyme that plays a significant character in the plant's response to environmental stress. However, its functional role in drought resistance remains largely unexplored. This study investigates the drought tolerance role of alfalfa MsFtsH8 by analyzing the growth, physiology, and gene expression of overexpressing plants under drought conditions. The results demonstrated that both MsFtsH8-overexpressing Arabidopsis and alfalfa plants exhibited superior growth condition and enhanced membrane stability. The overexpressing alfalfa plants also showed reduced MDA levels, higher proline content, lower H2O2 accumulation, an increased activity of antioxidant-related enzymes (SOD, POD, and CAT) activity, and an elevated expression of antioxidant-related genes. These results indicated that the overexpression of MsFtsH8 enhanced growth, improved osmotic regulation, reduced ROS levels, and increased antioxidative capacity, ultimately leading to greater drought tolerance in alfalfa. Our findings suggest that MsFtsH8 mitigates oxidative damage caused by drought by modulating the plant's antioxidant system, thus improving drought tolerance in alfalfa. This study provides a molecular basis and candidate genes for enhancing drought resistance in alfalfa through genetic engineering.

Mitochondrial Oxidative Stress and Cardiac Dysfunction in TERT Knockout Mice

Abstract Background Heart failure (HF) is a major cause of hospitalization in the elderly, with its incidence increasing due to aging and associated risk factors like hypertension, diabetes, and myocardial fibrosis. Aging-related myocardial fibrosis, characterized by alterations in the extracellular matrix and myocardial structure, impairs cardiac function. Mitochondrial oxidative stress plays a pivotal role in cardiac electrical and structural remodeling, necessitating a deeper understanding of its involvement in aging-related heart failure. Purpose The purpose of this study is to investigate the mechanisms of aging-related ventricular electrical and structural remodeling by constructing an aging mouse model. This research aims to provide potential therapeutic targets for heart failure associated with aging. Methods We developed a third-generation homozygous telomerase reverse transcriptase (TERT) knockout mouse model. Comparing third-generation homozygous TERT knockout mice (F3 group) with age-matched wild-type males (WT group). The study encompassed blood pressure measurement, electrocardiographic analysis, echocardiography, ELISA for cardiac biomarkers, ventricular tissue electrophysiology, fibrosis assessment through staining, transcriptomic profiling via RNA-seq, and electron microscopy of ventricular mitochondria. Results Compared to the WT group, the F3 group demonstrated increased P53 and P16 protein expression. Decreased LVEF and FS, along with increased interventricular septum thickness, left ventricular diameter, and left ventricular volume. Elevated serum NT-pro-BNP and troponin I (cTnI) levels, with prolonged QRS duration. Decreased left and right ventricular conduction velocity, accompanied by increased conduction dispersion. Notable elevation in COLI, TGFβ, and α-SMA gene transcription and protein expression in ventricular tissue. Significant differences in mitochondrial oxidative stress signal pathways via RNA-seq analysis. Elevated serum MDA levels and decreased SOD levels, with up-regulated Mn-SOD gene transcription and protein expression, and down-regulated MFN2 and Drp1 gene transcription and protein expression in ventricular tissue. Electron microscopy revealed mitochondrial abnormalities such as loose arrangement, decreased number, swelling, vacuolation, and myofilament disintegration or breakage in the F3 group. Conclusion Third-generation TERT-/- senescent mice exhibit notable cardiac impairments, including electrical remodeling, structural changes, and mitochondrial dysfunction. These findings suggest a potential link between mitochondrial oxidative stress and aging-related heart failure, indicating novel therapeutic opportunities targeting mitochondrial dysfunction for managing such conditions.

Accumulation of coumaric acid is a key factor in tobacco continuous cropping obstacles.

Phenolic acids are believed to play a significant role in tobacco continuous cropping obstacles, but the strength and potential mechanisms of different phenolic acids remain unclear. This study evaluated the allelopathic effects of six phenolic acids that exhibited cumulative effects in our previous research. Different concentrations of phenolic acids with the strongest allelopathic effects were added to potting soil to explore their impacts on tobacco growth and physiological characteristics, as well as on soil chemical properties and microbial community structure. The results showed that coumaric acid exhibited the strongest direct allelopathic effect. Exogenous coumaric acid significantly reduced soil pH and shifted the soil microbial community from bacteria-dominated to fungi-dominated. Simultaneously, the abundance of bacteria related to nutrient utilization (e.g., Flavisolibacter, Methylobacterium) and fungi related to disease resistance (e.g., Fusicolla, Clonostachys) gradually decreased, along with a reduction in soil catalase, urease, invertase, and acid phosphatase activities. Leaf MDA levels increased continuously with higher concentrations of coumaric acid, while the root resistance hormone (jasmonic acid and the jasmonate-isoleucine complex) levels show the opposite trend. Coumaric acid may inhibit tobacco growth by influencing the physiological processes in tobacco plants directly and the broader soil microecological balance indirectly. This study provides theoretical guidance for precise mitigation of continuous cropping obstacles in future tobacco cultivation.

Impact of Vitamin C and Hydroxyurea on the Reproductive System Health in Male Rats

Hydroxyurea (HU) is a medication used to treat various diseases and is also being studied for its effects on spermatogenesis. Vitamin C (VC), an antioxidant, has been shown to protect sperm cells from oxidative stress, potentially improving fertility and sperm quality. In a study involving twenty-four adult male albino rats divided into four groups, Group 1 served as the control, Group 2 received 5 mg of vitamin C, Group 3 received 100 mg of hydroxyurea per body weight, and Group 4 received a combination of vitamin C and hydroxyurea to assess essential functions of the reproductive system, including hormone levels, antioxidant markers, oxidative stress indicators, histopathology, and identification of DNA damage. The study found that hydroxyurea significantly reduced testicular weight, SOD, CAT, and GSH while increasing FSH and MDA levels and causing abnormalities in sperm morphology. Hydroxyurea also caused apparent alterations in the histological structure of the testes and comet parameters. Rats treated with vitamin C showed a significant increase in absolute and relative epididymis weight compared to the control group. Moreover, vitamin C intervention reversed the adverse effects observed in rats fed hydroxyurea, indicating that low doses of vitamin C can protect against testicular damage.

Supplementation of Chlorogenic Acid Alleviates the Effects of H2O2-Induced Oxidative Stress on Laying Performance, Egg Quality, Antioxidant Capacity, Hepatic Inflammation, Mitochondrial Dysfunction, and Lipid Accumulation in Laying Hens

This research examined the impact of chlorogenic acid (CGA) on laying performance, antioxidant capacity, egg quality, hepatic inflammation, mitochondrial function, and lipid metabolism in hens subjected to hydrogen peroxide (H2O2)-induced oxidative stress (OS). Three hundred sixty healthy 43-wk-old Hy-Line brown hens were randomly assigned to six treatments: a basal diet + 0 (control and H2O2), 600 (600 mg/kg CGA and 600 mg/kg CGA + H2O2), and 800 (800 mg/kg CGA and 800 mg/kg CGA + H2O2) mg/kg CGA for 84 d. On the 64th and 78th days of the trial, hens in groups H2O2, 600 mg/kg CGA + H2O2, and 800 mg/kg CGA + H2O2 were injected intraperitoneally with 10% H2O2. The results demonstrated that 600 and 800 mg/kg CGA significantly improved the egg production rate (EPR) and egg quality and reduced lipid peroxidation compared to the control group. The 800 mg/kg CGA showed greater improvements in the EPR and average egg weight (AEW) compared to the 600 mg/kg dose. Conversely, H2O2 exposure significantly decreased the EPR, AEW, and egg quality and increased feed conversion rate and average daily feed intake. H2O2 exposure significantly decreased serum T-AOC and increased serum MDA levels while reducing hepatic T-SOD, GSH-Px, and CAT activities. Meanwhile, H2O2 exposure significantly elevated liver reactive oxygen species levels, pathological damage, and NF-κB, TNFα, and IL-1β gene expression. Additionally, H2O2 treatment disrupted hepatocyte mitochondrial structure and significantly increased the expression of VDAC1 protein, and IP3R, GRP75, MCU, Fis1, and MFF genes, while downregulating the expression of MFN2 protein and PGC1α gene. Oil Red O staining demonstrated that H2O2 induced significant lipid accumulation in hepatocytes. Concurrently, H2O2 significantly increased serum triglycerides, total cholesterol, and liver triglycerides levels while decreasing serum hepatic lipase activity. This was primarily attributed to the significant upregulation of liver SREBP1, FASN, and ACC genes and the downregulation of the liver CPT1 gene induced by H2O2. Furthermore, CGA pretreatment effectively prevented the degeneration in laying performance and egg quality, as well as OS, liver inflammation, pathological damage, and mitochondrial dysfunction induced by H2O2. CGA inhibited H2O2-induced hepatic lipid accumulation by upregulating fatty acid oxidation-related gene expression and downregulating fatty acid synthesis-related gene expression. These findings indicate that the dietary addition of 800 mg/kg of CGA is the optimum supplementation dose. CGA can enhance laying performance and egg quality while alleviating OS, hepatic inflammation, mitochondrial dysfunction, and lipid accumulation in H2O2-challenged laying hens.

Puerarin Ameliorates Ferroptosis in Neuronal Injury Through the PI3K/AKT Signaling Pathway

Ferroptosis plays an important role in the pathogenesis of neuronal damage, generally mediated by iron and lipid peroxidation. In the present study, we measured the protective effects of puerarin against corticosterone-induced neuronal injury via PI3K/AKT-mediated activation of nuclear factor erythroid 2-related factor 2 (Nrf2). After exposing corticosterone-treated PC12 cells to indicated compounds, we measured the key regulators of ferroptosis (ferritin, SLC7A11, and Ptgs2), ferroptosis events (levels of iron, ROS, MDA, and GSH), and the PI3K/AKT/Nrf2 axis. Corticosterone induced ferroptosis in PC12 cells, evidenced by reduced levels of ferritin, SLC7A11, and GSH and increased levels of iron, ROS, and MDA. These effects were reversed by inhibiting ferroptosis with ferrostatin-1. Puerarin-mediated activation of Nrf2 repressed ferroptosis in corticosterone-treated PC12 cells by upregulating ferritin and SLC7A11 expression. Moreover, the protective effects of puerarin on ferroptosis in corticosterone-treated cells relied on the activation of the PI3K/AKT pathway though the upregulation of nuclear Nrf2. These findings indicate that ferroptosis plays an essential role in corticosterone-induced neuronal damage, and puerarin protects against ferroptosis in corticosterone-treated cells via PI3K/AKT-mediated activation of Nrf2.

Alleviating effects of Gracilaria verrucosa supplement on non-specific immunity, antioxidant capacity and immune-related genes of pacific white shrimp (Litopenaeus vannamei) provoked with white spot syndrome virus

Our work evaluated the possible underlying roles of dietary dried seaweed (Gracilaria verrucosa; GV) on the inherent immune response, antioxidant capacity, immune-related gene expression, and protection of whiteleg shrimp (Litopenaeus vannamei) contra white spot syndrome virus (WSSV). Three hundred and sixty healthy L. vannamei (15.26 g ± 1.29 g) were graded into four supplemental groups ( Triplicate/group) and fed with diets including 0 (control), 2, 4, and 8 g GV (kg diet) −1 for 21 days. Following the feeding period, each group of shrimp received an intramuscular WSSV injection (1.4 × 106 copies/ml). Hemolymph and gills samples were collected before and after the challenge with WSSV. Notably, the administration of dietary GV significantly enhanced the innate immune parameters of pacific white shrimp including total hemocyte count (THC), phagocytosis, phenoloxidase activity, reactive oxygen species (ROS) production, and lysozyme activity before and after challenge with WSSV. Additionally, dietary supplementation of 4, and 8 g of GV (kg diet)−1 remarkably elevated ACP, AKP, SOD, GPx, and catalase activities along with a decrease in the MDA level in gills of shrimp before and post-WSSV challenge. In response to the GV supplement, significant upregulation of expression of ALF1, CRU1, PEN4, and CTL with downregulation of TRAF6, STAT, TLR1, and NOS genes was recorded in the gills tissue before and post-challenge with WSSV, especially at a dose of 8.0 GV g kg − 1. Dietary inoculated shrimp with GV revealed notably higher survival percentages after being challenged with WSSV. Conclusively, these data indicate that Gracilaria verrucosa can be recommended as a valuable supplemented seaweed to stimulate the innate immunity and enhance the health of Litopenaeus vannamei against viral infection.

Screening of active components of melastoma dodecandrum lour. against diabetic osteoporosis using cell membrane chromatography-mass spectrometry.

Melastoma dodecandrum Lour. (MD), a traditional botanical drug known for its hypoglycemic, antioxidant, and anti-inflammatory properties, is commonly used to treat diabetes, osteoarthritis, and osteoporosis. However, its specific active components against diabetic osteoporosis remain unclear. This study aimed to identify the key active components in MD using cell membrane chromatography coupled with mass spectrometry and validate their effects in vitro. An AGEs-induced osteoblast injury model was established. MTT assays measured cell viability, and ALP activity was assessed using a biochemical kit. Western blotting was employed to detect the expression levels of osteoblast-related proteins OCN and RUNX2 and the AGE receptor protein RAGE. ELISA was used to determine the levels of SOD, MDA, CAT, and GPx. PCR quantified TNF-α expression to evaluate the protective effects and potential mechanisms of MD. The AGEs-induced osteoblast cell membrane chromatography-mass spectrometry method facilitated the rapid identification of potentially active compounds based on their affinity for the osteoblast cell membrane. Cell experiments further validated the activity of the characteristic component isovitexin. MD significantly improved cell viability in AGEs-damaged osteoblasts, enhanced ALP, SOD, CAT, and GPx activities, reduced MDA levels, increased OCN and RUNX2 protein expression, and decreased TNF-α mRNA and RAGE protein expression. Cell membrane chromatography identified 20 chemical constituents, including 13 flavonoids, 4 organic acids, 1 phenylpropanoids, 1 terpenoids, and 1 alkaloid. Cell experiments have confirmed that isovitexin has significant protective activity against osteoblasts and can inhibit the expression of specific receptor RAGE on the osteoblast membrane, consistent with the effect of MD. MD and its active component, isovitexin, provide protective effects against AGEs-induced osteoblast injury, offering a basis for subsequent drug development.

GhGME31D identified to regulate AsA activation in response to alkali stress from GME gene family implications in cotton

Vitamin C, also referred to as ascorbic acid (AsA), is recognized for its capacity to cure and avert scurvy, and it is crucial for regular human growth and development. In various crops, AsA participates in stress response mechanisms mediated by abscisic acid and has been discovered to have a crucial function in the morphogenesis, growth, development, and production of male gametes in plants. GDP-D-mannose 3′,5′-epimerase (GME) is essential in the synthesis of vitamin C. Our research identified 91, 83, 51, and 46 genes, respectively, found in G. barbadense (GbGMEs), G. hirsutum (GhGMEs), G. arboretum (GaGMEs), and G. raimondii (GrGMEs). Plants resulting from VIGS infection with GhGME31D clearly showed yellowing, water loss and wilting of leaves and black spots on stems. Measurement of MDA and AsA levels indicated that the plants were more damaged. This indicates that AsA has a substantial impact on plant growth and development.

Association between Sexual Abuse Experience and Salivary Stress Biomarkers among Transgender and Gender Non-Conforming Individuals in Chennai – A Cross-Sectional Study

Introduction: Gender-nonconforming people undergo unimaginable sexual and physical abuse. This leads to stress and other stress-related disorders which can be easily determined by salivary stress biomarkers. Early life stress has an association with the immune system linked with stress. Transgenders and gender nonconforming people are prone to sexual abuse in early life more compared to normal people. This study aims to know about the association between sexual and physical abuse experience and salivary stress biomarkers in Transgender and gender-nonconforming individuals. Materials and Methods: This study was a cross-sectional epidemiological study. A snowball sampling design was adopted. The study was conducted in various places in Thozhi Shelter for Transgenders, Chetpet, Chennai among Gender non-conforming individuals and Transgenders. This study was conducted in April 2022. MDA and IL-6 levels were determined from their saliva using the passive drool method. Result: Interleukin L 6 and MDA levels were significantly higher in the GNC Group than in the control group. 63.64% of Transgender and gender non-conforming individuals experienced sexual abuse whereas 73% of them have experienced physical abuse in their lifetime. Conclusion: Transgender and gender non-conforming individuals who experienced physical/sexual abuse have increased IL 6 levels and decreased MDA levels in saliva when compared to the non-transgender individuals.

Alleviating effect of whey protein supplementation on oxidative stress in hypothyroidism.

Hypothyroidism is one of the most prevalent thyroid pathologies, which causes oxidative stress by disrupting antioxidant mechanisms. In mammals, the thyroid glands regulate metabolism, development, and growth. Dysfunction of the thyroid gland can result in hypothyroidism, hyperthyroidism, thyroiditis, and thyroid cancer. Whey protein is a widely consumed protein supplement containing abundant sulphur-containing amino acids and bioactive peptides. Here, we analysed the effect of whey protein on oxidative stress in hypothyroidism. In vivo studies were conducted in two phases for 30 and 90 days, respectively. Hypothyroidism was induced in Wistar albino rats by administering 0.05% propylthiouracil (PTU) through drinking water. Five hypothyroid groups and the normal control group were maintained in the first 30 day phase of the study. Among these, one group served as the induced control group, three groups received whey protein at different concentrations (100, 300, and 500 mg per kg body weight), and the last group received L-thyroxine (2 μg per 100 g body weight) as a positive medication. The activities of antioxidant enzymes, such as superoxide dismutase, catalase, glutathione peroxidase, and glutathione-S-transferase, were analysed, and the levels of total antioxidants, glutathione, and malondialdehyde were determined. Ca2+ ATPase and Na+/K+ ATPase activities were detected by estimating the inorganic phosphate content. Histopathological analysis was carried out on the thyroid and liver tissues of all groups. Antioxidant activity was notably increased for higher doses of whey protein compared to that in the diseased control group (p < 0.05). From this initial study, the dose that achieved the desired therapeutic effect was 500 mg kg-1, which was considered for the next 90 day phase of the study. The 90 day phase of the study was conducted with five groups: normal, whey protein-supplemented, hypothyroid, whey protein-supplemented hypothyroid, and levothyroxine-supplemented hypothyroid. All the PTU-treated groups showed degenerative alterations in thyroid histology. Whey protein supplementation causes a considerable decrease in MDA levels with an increase in the major antioxidant enzyme and ATPase activities, with p < 0.05. As a nutritional supplement, whey protein, at a 500 mg kg-1 dose, effectively boosts antioxidant activity without causing any toxicological concerns in long-term use.

Is castration leading to biological aging in dogs? Assessment of lipid peroxidation, inflammation, telomere length, mitochondrial DNA copy number, and expression of telomerase and age-related genes

BackgroundBiological aging is a complex process influenced by various factors, including reproductive status and castration. This study aimed to evaluate the impact of castration on biological aging in dogs.MethodFifteen male crossbred dogs were randomly divided into a sham-operation control group (n = 5) and a castrated group (n = 10). Blood samples were collected at weeks 0, 4, 8, 12, 16, and 18 post-surgery. Malondialdehyde (MDA as indicator of Lipid peroxidation), C-reactive protein (as an indicator of inflammation), telomere length, mitochondrial DNA (mtDNA) copy number, and the expression of age-related (P16, P21, TBX2) and telomerase-related (TERT) genes were assessed in blood samples.ResultsPlasma MDA levels were higher in the control group at weeks 16 and 18, while CRP levels were higher only at week 18. Telomere length and mtDNA copy number were lower in the control group at week 18. Gene expression analysis showed that P16 was lower in the control group at weeks 8 and 12, P21 and TERT were lower at weeks 16 and 18, and TBX2 was lower at weeks 16 and 18. The TBX2/P16 ratio was lower in the control group at weeks 16 and 18 but higher at week 12, while the TBX2/P21 ratio did not differ between groups.ConclusionCastration appears to have a protective effect against biological aging in dogs, as evidenced by lower lipid peroxidation, inflammation, and age-related changes in telomere length, mtDNA copy number, and gene expression.

Unraveling the Ferroptosis-inducing Potential of Methanol Leaves Extract of Prosopis Juliflora Via Downregulation of SLC7A11 and GPX4 mRNA Expression in A549 Lung Cancer Cells.

Prosopis juliflora has been employed in many traditional treatments. As evidenced by our earlier research, Prosopis juliflora leaf methanol extract (PJME) has a promising future in the fight against lung cancer. It may also be used in conjunction with other treatments to effectively manage lung cancer. The main objective of this study was to explore the potential of PJME to inhibit lung cancer in A549 cells, along with its underlying mechanisms of action. The antiproliferative effects were determined using MTT and LDH tests. Apoptosis- inducing capacity was evaluated using the DAPI staining, caspase-3 test, cytochrome C assay, PARP cleavage, and qRT-PCR. To investigate the mechanism of action of PJME in lung cancer, the levels of ROS, MMP, GSH, MDA, and specific ferroptosis indicators were measured. The experimental data of the current study indicated that exposure of A549 cells to PJME reduced cell viability and increased cellular cytotoxicity. The apoptosis-inducing ability of PJME in A549 cells was validated by enhanced nuclear condensation, level of the caspase- 3, cytochrome C, and PARP release. In addition, qRT-PCR investigations verified that the administration of PJME led to a decrease in the expression of anti-apoptotic gene Bcl2 while enhancing the mRNA level of pro-apoptotic genes, such as Bax and caspase-3, in A549 cells. The study also found that PJME has the ability to activate ferroptosis pathways, as evidenced by elevated reactive oxygen species (ROS) generation, changes in the levels of antioxidant markers (MDA and GSH), and decreased expression of SLC7A11 and GPX4. The results of the present study clearly showed that PJME inhibited the proliferation of A549 cells and induced ferroptosis by reducing the expression of the important targets SLC7A11 and GPX4. Further research is necessary to fully understand the clinical efficacy of PJME before it can be investigated as supplemental or adjuvant therapy for lung cancer.

Poliumoside inhibits apoptosis, oxidative stress and neuro-inflammation to prevent intracerebroventricular Streptozotocin-induced cognitive dysfunction in Sprague-Dawley Rats: in in-vivo, in-vitro and in-silico study.

Alzheimer's disease (AD) is a severe neurological illness causes cognitive decline and mortality if not treated early. However, the current therapeutic modalities are inefficient to manage the cognitive dysfunction of AD. Therefore, in the present manuscript, we have enumerated the pharmacological benefit of Poliumoside in the Streptozotocin-induced cognitive dysfunction in Sprague-Dawley (SD) rats. Initially, the cognitive dysfunction in rats was induced by the intracerebroventricular administration of Streptozotocin, then rats received PMD (5 mg and 10 mg/kg body weight) was given. Various behavioural analysis, such as Morris water maze (MWM), and object recognition tests (ORT), and locomotor analysis was conducted in PMD treated group. Various biochemical analysis was conducted to analyze the effect of PMD on hippocampus oxidative-nitrosative stress and pro-inflammatory cytokines. MTT assay and annexin V/PI staining was performed to analyse the effect of PMD on the cell viability and neuronal toxicity of PC12 cells, respectively. Molecular docking analysis was also conducted with crystal structure of human AChE. PMD treatment improved cognitive capacity in rats in MWM and ORT. Compared to STZ rats, PMD-treated rats had significantly higher locomotor activity and lower AChE activity. PMD also restores dopamine, 5-HT, and NE levels and reduces metabolic their deactivation as evidenced by increased levels of DOPAC, HVA, 5-HIAA. Nitrite, MDA, SOD, CAT, and GSH levels were restored near normal in PMD-treated rats, reducing hippocampus oxidative-nitrosative stress. Pro-inflammatory cytokines were similarly lowered in PMD-treated rats. In in-vitro studies, PMD did not affect PC12 cell survival at the maximal dose of 10 µM. In addition, PMD concentration-dependently prevents H₂O₂-induced neuronal death in PC12 cells. The in-silico docking analysis showed that the PMD fit snugly into the active site of human AChE by engaging with the anionic domain and the catalytic triad of Trp86, Tyr337, Phe338, and Gly121 residues. In conclusion, our study demonstrated that PMD have significant impact on AD by inhibiting ACheE and restoring neurotransmitter levels, which enhances Ach levels in rats and improves cognitive impairment in STZ rats.

Beta vulgaris L. beetroot protects against iron-induced liver injury by restoring antioxidant pathways and regulating cellular functions

Beta vulgaris L. is a root vegetable that is consumed mainly as a food additive. This study aimed to describe the protective effect of B. vulgaris on Fe2+-mediated oxidative liver damage through in vitro, ex vivo, and in silico studies to establish a strong rationale for its protective effect. To induce oxidative damage, we incubated the livers of healthy male rats with 0.1 mM FeSO4 to induce oxidative injury and coincubated them with an aqueous extract of B. vulgaris root (BVFE) (15–240 µg/mL). Induction of liver damage significantly (p < .05) decreased the levels of GSH, SOD, CAT, and ENTPDase activities, with a corresponding increase in MDA and NO levels and Na+/K+ ATPase, G6 Pase, and F-1,6-BPase enzyme activities. BVFE treatment (p < .05) reduced these levels and activities to almost normal levels, with the most prominent effects observed at 240 µg/mL BVFE. An HPLC investigation revealed sixteen compounds in BVFE, with quercetin being the most abundant. Chlorogenic acid and iso-orientation showed the highest binding affinities for G6 Pase and Na+/K + ATPase, respectively. These findings suggest that B. vulgaris can protect against Fe2+-mediated liver damage by suppressing oxidative stress and cholinergic and purinergic activities while regulating gluconeogenesis. Overall, the hepatoprotective activity of this extract might be driven by the synergistic effect of the identified compounds and their probable interactions with target proteins.

Evaluation of Some Antioxidant Parameters (Vitamin E &amp; C), MDA and Hemoglobin Levels, in Women of Reproductive Age, Based on Mode of Child Delivery, in Owerri, Imo State, Nigeria

Childbirth indicates the positive outcome of pregnancy in humans, in which mode of child delivery, which is either by vaginal delivery (VD) or cesarean-section delivery (CS) is considered critical in maintaining maternal health. Antioxidants delay or inhibit cellular damage, mainly through their free radical-scavenging property. Changes in vitamin E and vitamin C antioxidants, lipid peroxidation (MDA) and hemoglobin (Hb) can lead to complications, forming reactive oxygen species (ROS) and cellular imbalance, bringing about oxidative stress (OS). These parameters remove the ROS efficiently and protect the body from the adverse effects of oxidative stress. The purpose of our study was to evaluate the effect of mode of child delivery on maternal VE, VC, MDA and Hb status, in women of reproductive age in Owerri, Imo state, Nigeria. It involved 200 pregnant women, within the reproductive ages of 20 to 39 years, with 100 subjects being those who gave birth through VD and 100 being those who gave birth through CS. Data were analyzed using SPSS version 23, with results expressed as mean ± standard deviation and presented in tables. Independent t-tests and ANOVA were used for comparisons, with p≤0.05 considered significant. The results from this study showed that, women who gave birth through VD had significantly lower VE (p&lt;0.001) and VC (p&lt;0.001) levels compared to those who had CS. Similarly, the levels of MDA were significantly (p&lt;0.001) reduced in women who gave birth through VD compared to those who had CS. The antepartum Hb of VD women was significantly higher than postpartum levels, while the antepartum Hb of CS women was significantly lower compared to the postpartum levels. The results indicate that women who gave birth through VD had significantly reduced VE, VC, MDA and Hb levels, after childbirth, compared to births of CS delivery. It is recommended that antioxidant parameters (Vitamin E &amp; C), MDA and hemoglobin (Hb) levels, be assessed in women during childbirth in order to help in the management of their postpartum conditions.