Stress Markers Research Articles

Osho Dynamic Meditation; Improved Stress Reduction in Farmer Determine by using Serum Cortisol and EEG (A Qualitative Study Review)

A lot of thought should go into how to revitalize agriculture, because rural demand is critical for reviving the manufacturing sector. Agriculture is also significant because it employs 52% of the population and accounts for 17% of GDP. Over the last 17 years, approximately 14 million farmers have committed suicide. Although per capita land availability has decreased, agriculture's share of employment has decreased more slowly. It means that farmer stress is increase day by day. Dynamic meditation is a popular form of active meditation that was introduced in 1970 by an Indian mystic named osho. The impact of osho dynamic meditation on cortisol levels in the serum (cortisol is a stress marker) & therefore to observe whether it has any anti-stress effect. And calculate beta wave (stress wave) calculated by using EEG and observed reduction in waves or not. After study the hole article we can conclude 1. To study the effect of dynamic meditation on mental health. 2. To Study the effect of dynamic meditation on stress by testing serum cortisol. 3. To study the stress level in farmer before dynamic meditation and after dynamic meditation. Using EEG machine and to achieve better results. 4. To promote farmers and other people to do meditation for positive energy and stress-free life.

PAG Masked Protective Physical Exercise-Induced High H2S Levels in 5/6 Nephrectomized Rats

Background: To investigate the mechanisms of exercise therapeutics in preclinical animal models of chronic kidney disease (CKD), PAG (D, L-propargylglycine), an inhibitor of hydrogen sulfide production, was used to examine the protective effects of physical activity on oxidative stress and inflammation levels during CKD. Methods: Male Wistar rats with CKD, induced by the 5/6 nephrectomy procedure and subjected to 8 weeks of exercise training, received injections of PAG, a cystathionine γ-lyase (CSE) inhibitor, at a dose of 19 mg/kg, i.p., twice a week during those 8 weeks. The systolic blood pressure (BP) and renal sympathetic nerve activity (RSNA) were assessed. Additionally, plasma creatinine, BUN, renal hydrogen sulfide (H2S) levels, oxidative stress, and inflammatory markers were evaluated. Results: In the PAG group, inhibition of H2S production significantly reversed the improvements in plasma creatinine, BUN, renal malondialdehyde (MDA) level, superoxide dismutase (SOD) activity, TNF-α, and IL-6 that were achieved by exercise. Additionally, high RSNA and high BP, which were also reversed in the PAG group, compared to the CKD group subjected to exercise training. Conclusions: The results suggest that the improvement in BP, oxidative stress, and inflammation status by exercise in CKD may be at least partially due to CSE/H2S signaling.

Fish oil supplementation during pregnancy decreases liver endocannabinoid system and lipogenic markers in newborn rats exposed to maternal high-fat diet.

Maternal high-fat diet (HF) programs obesity, metabolic dysfunction-associated steatotic liver disease (MASLD), hypertriglyceridemia, and hyperglycemia associated with increased endocannabinoid system (ECS) in the liver of adult male rat offspring. We hypothesized that maternal HF would induce sex specific ECS changes in the liver of newborn rats, prior to obesity onset, and maternal fish oil (FO) supplementation would reprogram the ECS and lipid metabolism markers preventing liver triglycerides (TG) accumulation. Female rats received a control (CT) (10.9% fat) or HF (28.7% fat) diet 8weeks prior to mating and during pregnancy. A subgroup of HF dams received 3% FO supplementation in the HF diet (35.4% fat) during pregnancy (HFFO). Serum hormones and liver TG, ECS, lipid metabolism, oxidative stress and autophagy markers were assessed in male and female newborn offspring. Maternal HF diet increased liver cannabinoid receptor 1 (CB1) in males and decreased CB2 in females, with no effect on liver TG. Maternal FO supplementation reduced liver CB1 regardless of the offspring sex, but reduced TG liver content only in females. FO reduced the liver content of the endocannabinoid anandamide in males, and the content of 2-arachidonoylglycerol in both sexes. Maternal HF increased lipogenic and decreased lipid oxidation markers, and FO induced the opposite regulation in the liver of offspring. Prenatal HF and FO differentially modulate liver ECS in the offspring before obesity and MASLD development. These results suggest that maternal nutrition at critical stages of development can modulate the offspring's ECS, predisposing or preventing the onset of metabolic diseases.

Oxidative Stress Assessment in Colorectal Cancer Patients

Colorectal cancer (CRC), a global health challenge, exhibits rising incidence in low-income nations due to lifestyle changes. Oxidative stress, indicated by reactive oxygen species imbalance and Malondialdehyde (MDA), is linked to CRC. This study investigates oxidative stress markers, antioxidant enzymes, genetic markers, cellular regulation markers, and Vitamin E in CRC patients in Erbil. Ninety CRC patients and 30 healthy controls provided blood samples, processed and stored at –20°C. Enzyme-linked immunosorbent assay kits quantified oxidative stress, antioxidant markers, and Vitamin E. Oxidative stress markers showed significant differences, with elevated MDA and 8-hydroxy-2’-deoxyguanosine levels in patients. Nitrotyrosine exhibited lower expression in patients. Antioxidant enzymes glutathione peroxidase and superoxide dismutase were enhanced in patients, while glutathione (GSH), glutathione reductase and catalase levels were significantly lower in patients. The genetic marker KRAS showed a substantial decrease in patients (<0.0001) but both adenomatous polyposis coli (APC) and CRC antigen (CCA) were higher. Serum vitamin E levels were significantly lower in patients (71.78 ± 6.368) compared to controls (142.3 ± 4.828, p < 0.0001). Elevated oxidative stress, altered enzymatic activity, significantly lower expression of KRAS, and higher expression of APC and CCA in the patient group. Furthermore, reduced Vitamin E levels were observed in the patient group, highlighting potential challenges in antioxidant defense.

Curcumin in the treatment of inflammation and oxidative stress responses in traumatic brain injury: a systematic review and meta-analysis

Background and aimTraumatic brain injury (TBI), a leading cause of high morbidity and mortality, represents a significant global public health challenge. Currently, no effective treatment for TBI exists. Curcumin, an active compound extracted from the root of Curcuma longa, has demonstrated neuroprotective properties both in vitro and in vivo. Notably, it has shown potential in reducing oxidative stress and inflammation and enhancing redox balance. This paper conducts a systematic review and meta-analysis to explore curcumin’s role in TBI animal models extensively. The findings offer valuable insights for future human clinical trials evaluating curcumin as a therapeutic supplement or nutraceutical in TBI management.MethodsComprehensive literature searches were conducted across MEDLINE, Embase, Cochrane, Web of Science, and Google Scholar databases. These searches aimed to identify relevant manuscripts in all languages, utilizing the keywords “curcumin” and “traumatic brain injury.”ResultsThe final quantitative analysis included 18 eligible articles corresponding to animal studies. The analysis revealed that curcumin significantly reduced inflammatory cytokines, including IL-1β (p = 0.000), IL-6 (p = 0.002), and TNF-α (p = 0.000), across various concentrations, time points, and administration routes. Additionally, curcumin markedly enhanced the activity of oxidative stress markers such as SOD (p = 0.000), Sir2 (p = 0.000), GPx (p = 0.000), and Nrf2 (p = 0.000), while reducing MDA (p = 0.000), 4-HNE (p = 0.001), and oxyprotein levels (p = 0.024). Furthermore, curcumin improved cerebral edema (p = 0.000) and upregulated neuroprotective factors like synapsin I (p = 0.019), BDNF (p = 0.000), and CREB (p = 0.000), without reducing mNSS (p = 0.144). About autophagy and apoptosis, curcumin increased the activity of Beclin-1 (p = 0.000) and Bcl-2 (p = 0.000), while decreasing caspase-3 (p = 0.000), the apoptosis index (p = 0.000), and P62 (p = 0.002).ConclusionCurcumin supplementation positively affects traumatic brain injury (TBI) by alleviating oxidative stress and inflammatory responses and promoting neuroprotection. It holds potential as a therapeutic agent for human TBI. However, this conclusion necessitates further substantiation through high-quality literature and additional randomized controlled trials (RCTs).Systematic Review Registrationhttps://www.crd.york.ac.uk/prospero/. The registration number of PROSPERO: CRD42023452685.

Increasing the radiation-induced cytotoxicity by silver nanoparticles and docetaxel in prostate cancer cells.

Radiation therapy is utilized for treatment of localized prostate cancer. Nevertheless, cancerous cells frequently develop radiation resistance. While higher radiation doses have not always been effective, radiosensitizers have been extensively studied for their ability to enhance the cytotoxic effects of radiation.So, this study aims to evaluate the possible radiosensitization effects of docetaxel (DTX) and silver nanoparticles (SNP) in LNCaP cells. The cytotoxic effects of DTX, SNP and2Gy of X-Ray radiation treatments were assessed in human LNCaP cell line using the MTT test after 24 h. Moreover, the effects of DTX, SNP and radiation on Epidermal growth factor (EGF), Caspase 3, inducible nitric oxide synthase and E-cadherin gene expression were analyzed using the Real-time PCR method. The level of Hydrogen peroxide (H2O2), an oxidative stress marker, was also detected 24h after various single and combined treatments. The combinations of SNP (in low toxic concentration) and/or DTX (0.25× IC50 and 0.5 × IC50 concentrations for triple and double combinations respectively) with radiation induced significant cytotoxicity in LNCaP cells in comparison to monotherapies. These cytotoxic effects were associated with the downregulation of EGF mRNA. Additionally, H2O2 levels increased after Radiation + SNP + DTX triple combination and double combinations including Radiation + SNP and Radiation + DTX versus single treatments. The triple combination treatment also increased Caspase 3 and and E-cadherin mRNA levels in compared to single treatments in LNCaP cells. Our results indicate that the combination of SNP and DTX with radiation induces significant anti-cancer effects. Upregulation of Caspase 3 and E-cadherin gene expression, and decreased mRNA expression level of EGF may be exerted specifically by use of this combination versus single treatments.

Microelements, Fatty Acid Profile, and Selected Biomarkers in Grass Carp (Ctenopharyngodon idella) Muscle Tissue: Seasonal Variations and Health Risk Assessment

AbstractThe study assesses associations between microelement levels, fatty acid composition, and oxidative stress markers in grass carp muscle in the summer and autumn seasons. Additionally, various factors were considered, including the estimated daily intake (EDI), target hazard quotient (THQ), total THQ (TTHQ), and metal pollution index (MPI), to evaluate potential health risks for consumers. The microelements (Al, As, Ba, Cd, Co, Cr, Cu, Fe, Hg, Li, Mn, Ni, Pb, Se, Sr, and Zn) were determined using inductively coupled plasma optical emission spectrometry (ICP-OES), and total mercury was determined using cold-vapor atomic absorption spectroscopy (CV-AAS). Fatty acid profiling was realized using gas chromatography (GC) detection with a flame ionization detector (FID). The overall tendency of microelement levels was as follows: Fe > Zn > Al > Sr > Ba > Ni > Se > Cr> Cu > Mn > Pb > As > Li > Hg; <LOQ (below limit of quantification): Cd, and Co. The correlation analysis between concentrations of trace elements (Al, Ba, Cr, Cu, Mn, Li, Sr, Zn, and Hg) and the fatty acids (C16:0, C16:1, C18:1n9c, C18:2n6c, C20:4n6c, EPA, and DHA), as well as between Al, Ba, Fe, or Hg and oxidative stress markers (superoxide dismutase—SOD, glutathione peroxidase—GPx, or total antioxidant status—TAS), revealed statistically significant interactions in different seasons. THQ values were lower than 1; TTHQ values ranged from 0.27 to 0.76. The main toxic elements forming TTHQ were Hg and Ni (49%). The calculated health risk assessment indices indicate a low concentration of observed elements and low risks associated with the consumption of grass carp muscle from the tested location, although concentrations and THQ of mercury and nickel may be of slight concern.

Towards a natural treatment for mania: red onion husk extract modulates neuronal resilience, redox signalling, and glial activation

BackgroundRed onion husk, a readily available agricultural waste material, contains diverse bioactive compounds with potential health benefits. This study aimed to assess the safety and therapeutic potential of red onion husk extract in managing manic-like symptoms and associated neurochemical dysfunctions.MethodsAcute and repeated oral dose studies were conducted in mice and rats to evaluate the safety profile of the extract. FT-IR analysis identified functional groups in the extract, while GC-MS analysis identified specific bioactive compounds in the flavonoid-rich fraction. A ketamine-induced manic behaviour model in Wistar rats was employed to assess the extract’s efficacy in attenuating manic-like symptoms. Behavioural and neurochemical analyses were performed to further investigate the extract’s effects.ResultsThe extract demonstrated a favourable safety profile in both acute and repeated dose studies. FT-IR analysis revealed a complex mixture of organic compounds, including hydroxyl groups, alkynes/nitriles, aromatic and non-aromatic C = C bonds, amines, and polysaccharides. GC-MS analysis identified 17 bioactive compounds, including five-methyl-2-phenylindolizine, methadone N-oxide, and 3-phenylthiane, S-oxide. Ketamine administration significantly increased oxidative stress markers, TBARS, and suppressed antioxidant enzyme activities (SOD, GPx, CAT) in both the cerebral cortex and hippocampus, alongside elevated acetylcholinesterase (AchE) activity, indicating enhanced neuronal excitability. Pre-treatment with FRF (25 mg/kg) effectively mitigated ketamine-induced oxidative stress, as evidenced by reduced TBARS levels and partially restored SOD and GPx activities. Interestingly, FRF significantly increased CAT activity (p < 0.001), potentially suggesting an additional compensatory mechanism. Notably, FRF pre-treatment also counteracted ketamine-upregulated AchE activity, offering neuroprotection against heightened neuronal excitability.ConclusionRed onion husk extract exhibits a favourable safety profile and exerts potent antioxidant and neuroprotective effects, possibly through modulating Nrf2 signalling pathways. Its ability to counteract ketamine-induced oxidative stress and neuronal hyperactivity highlights its potential as a complementary therapeutic strategy for managing manic episodes in bipolar disorder. Further research is warranted to elucidate the precise molecular mechanisms underlying FRF’s action and explore its clinical efficacy in human studies.

Anti-fatigue activity of methyl dihydrojasmonate and linalool in a rat model evaluated by a novel index for neuro-immune and oxidative stress interactions

Avoiding fatigue is a long-standing challenge in both healthy and diseased individuals. Establishing objective standard markers of fatigue is essential to evaluate conditions in spatiotemporally different locations and individuals and identify agents to fight against fatigue. Herein, we introduced a novel method for evaluating fatigue using nervous system markers (including dopamine, adrenaline, and noradrenaline), various cytokine levels (such as interleukin [IL]-1β, tumor necrosis factor [TNF]-α, IL-10, IL-2, IL-5 and IL-17A), and oxidative stress markers (such as diacron-reactive oxygen metabolites [d-ROMs] and biological antioxidant potential [BAP]) in a rat fatigue model. Using this method, the anti-fatigue effects of methyl dihydrojasmonate (MDJ) and linalool, the fragrance/flavor compounds used in various products, were assessed. Our method evaluated the anti-fatigue effects of the aforementioned compounds based on the changes in levels of the nerves system markers, cytokines, and oxidative stress markers. MDJ exerted more potent anti-fatigue effects than linalool. In conclusion, the reported method could serve as a useful tool for fatigue studies and these compounds may act as effective therapeutic agents for abrogating fatigue symptoms.

Dexmedetomidine attenuates ferroptosis byKeap1-Nrf2/HO-1 pathway inLPS-induced acute kidney injury.

Previous research has demonstrated that Dexmedetomidine (DEX), an α2 adrenergic agonist commonly used for its sedative and analgesic properties, can attenuate lipopolysaccharide (LPS)-induced acute kidney injury (AKI). This study explores the possibility that DEX's protective effects in LPS-induced AKI are mediated through the inhibition of ferroptosis, a form of regulated cell death characterized by iron-dependent lipid peroxidation, and the activation of the antioxidant response through the Keap1/Nrf2/HO-1 signaling pathway. We induced AKI in 42 mice using LPS and divided them into six groups: saline control, LPS, LPS + DEX, LPS + Ferrostatin-1 (LPS + Fer-1; a ferroptosis inhibitor), LPS + DEX with α2-receptor antagonist Altipamizole (LPS + DEX + ATI), and LPS + DEX with Nrf2 inhibitor ML385 (LPS + DEX + ML385). After 24h, we analyzed blood and kidney tissues. LPS exposure resulted in AKI, with increased serum creatinine, BUN, and cystatin C, and tubular damage, which DEX and Fer-1 ameliorated. However, Altipamizole and ML385 negated these improvements. The LPS group exhibited elevated oxidative stress markers and mitochondrial damage, reduced by DEX and Fer-1, but not when α2-adrenergic or Nrf2 pathways were blocked. Nrf2 and HO-1 expression declined in the LPS group, rebounded with LPS + DEX and LPS + Fer-1, and fell again with inhibitors; inversely, Keap1 expression varied. Our results demonstrate that DEX may protect against LPS-induced AKI, at least partially by regulating ferroptosis and the α2-adrenergic receptor/Keap1/Nrf2/HO-1 pathway, suggesting a potential therapeutic role for DEX in AKI management by modulating cell death and antioxidant defenses.

Essential oils combat Botrytis cinerea in apples: unveiling sugar, vitamin, and antioxidant dynamics

AbstractThis study investigated the effects of individual and combination applications of EOCs against Botrytis Cinerea in apple fruits, with a focus on sugar, vitamin, and antioxidant enzyme dynamics. In protective and curative treatments, sucrose content varied between 18.9 and 87.9 g.L-1, with the “CT” group exhibiting significantly higher sucrose levels (87.9 g.L-1). Glucose content ranged from 6.2 g.L-1 (“CT” and “C + F”) to 35.5 g.L-1 (“T + C + E + F”). Fructose content varied significantly, with the “F + T + C + E” treatment showing the highest (11.4 g.L-1) and the “CT” group the lowest (2.5 g.L-1). Rhamnose content in the curative treatment reached 14.9 g.L-1 (“F + T”) and in the protective treatment, the “C + E + F” group had the highest (3.3 g.L-1). Galactose content ranged from 0.1 to 13.0 g.L-1. Xylose content in curative treatment ranged from 12.1 to 13.6 g.L-1, with the combination “F + T” displaying the highest. In preventive treatment, arabinose content ranged from 0.7 to 3.0 g.L-1, with the “T + C + F” group having the highest. In terms of vitamins, the combination “T + F” showed the highest B1 (25.4 mg.100 g-1) and B2 (24.6 mg.100 g-1) content. Vitamin A, B1, and B2 increased in the “F + T” group, and vitamin C increased in the “F + T + C” group (33.4 mg.100 g-1). The quantification of oxidative stress markers and antioxidant enzymes revealed significant reductions in H2O2, MDA, and proline levels in EOC applications. In preventive treatment, the combination “T + C + E + F” exhibited the most effective improvement in SOD activity (556.5 EU mg-1 ), CAT activity increased significantly in the “T + C + F” group (189.3 EU mg-1), and APX activity saw the highest increase in the “T + C + E + F” group (185.6 EU mg-1). Contrastingly, curative treatments showed higher H2O2, MDA, and proline levels. The most significant decrease in H2O2 level occurred in the “T + C + E + F” group (36.7 nmol.g-1), and a significant decrease in MDA level was noted in the same group. Notable changes were observed in the activities of antioxidant enzymes, with the “F + T + C + E” group displaying the highest SOD activity (440.7 EU mg-1), and the “F + T” group showing the highest GST activity (542.0 EU mg-1). This research provided comprehensive insights into the biochemical responses of apple fruits to EOC treatments, offering potential strategies for effective fungal management in agriculture.

Black Chokeberry (Aronia melanocarpa) Juice Supplementation Improves Oxidative Stress and Aging Markers in Testis of Aged Rats

Spermatogenesis is a process that continues until the end of an individual’s life, although with reduced activity with advancing age. Inflammation, oxidation, and apoptosis are events considered as predictors of pathogenesis and the development of age-related diseases observed in aged testes. The use of natural compounds with antioxidant and anti-inflammatory properties has a beneficial effect on the inflammatory and oxidative status of the aged testis. The aim of this study was to determine the effect of supplementation with antioxidant-rich black chokeberry (Aronia melanocarpa) juice on several markers of oxidative stress and aging in rat testis. In total, 24 male Wistar rats were divided into three experimental groups: young controls aged 2 months, old controls aged 27 months, and 27-month-old rats supplemented with black chokeberry juice at a dose of 10 mL/kg for 3 months. A. melanocarpa juice supplementation led to reduced oxidative stress, manifested by increased immunoexpression of nNOS, eNOS, and MAS1 in the seminiferous tubules and in the Leydig cells. The morphometrically determined tubule structure data showed no significant differences between the three groups. However, the intensity of the immunoreaction for TRK-C and NT3 in Leydig cells was demonstrably higher in the supplemented old animals compared with the old controls. There was a significantly higher number of blood vessels around the seminiferous tubules in the supplemented animals compared to the old controls. These data indicate that supplementation with A. melanocarpa juice slows down aging processes in the testis and preserves the functional activity of Leydig cells.

Taxifolin alleviate metabolic and neurochemical alterations in the hippocampus and cortex of rats with rotenone-induced toxicity: In vivo and in silico insight

IntroductionExposure to rotenone could directly affects the function of mitochondrial which leads to neurodegeneration. This study evaluated the therapeutic potential of taxifolin (Huāqí sōng dài; 花旗松甙) to alleviate metabolic and neurochemical alterations in the hippocampal and cortical region of brain of rotenone-toxified rats. MethodsMale Wistar rats were subcutaneously administered 1.5 mg/kg rotenone for 10 days, followed by post-treatment with varying doses of taxifolin (0.25, 0.5 and 1.0 mg/kg) for 3 days through the same route. Activities of mitochondrial complex I, membrane ion pump and lactate dehydrogenase (LDH) were evaluated in the hippocampus and cortex of the brain of rotenone-toxified rats. Markers of neurotransmitter metabolism and oxidative stress were also biochemically estimated and molecular interaction between taxifolin and tyrosine hydroxylase, monoamine oxidase, glutamine synthetase and Na+/K+ATPase was determined by in silico simulation. ResultsTaxifolin attenuated dysfunction of mitochondrial, Na+/K+ATPase, LDH and modulate neurotransmitter metabolism. Also, the elicited oxidative stress was mitigated by taxifolin in the hippocampus and cortex of the brain of rotenone-toxified rats. Furthermore, taxifolin showed excellent interactions with targeted enzymes in silico. The highest binding affinity was recorded in taxifolin-tyrosine hydroxylase complex. Hydrogen bond and hydrophobic interactions were the two key molecular interaction between the taxifolin and targeted enzymes. DiscussionTaxifolin alleviates metabolic and neurochemical aberrations in rotenone-induced neurotoxicity model in rats in vivo and exhibits promising interactions with specific target enzymes that are key to neurotransmission in silico.

Enrichment of Bioactive Lipids in Urinary Extracellular Vesicles and Evidence of Apoptosis in Kidneys of Hypertensive Diabetic Cathepsin B Knockout Mice after Streptozotocin Treatment

Cathepsin B (CtsB) is a ubiquitously expressed cysteine protease that plays important roles in health and disease. Urinary extracellular vesicles (uEVs) are released from cells associated with urinary organs. The antibiotic streptozotocin (STZ) is known to induce pancreatic islet beta cell destruction, diabetic nephropathy, and hypertension. We hypothesized that streptozotocin-induced diabetic kidney disease and hypertension result in the release of bioactive lipids from kidney cells that induce oxidative stress and renal cell death. Lipidomics was performed on uEVs isolated from CtsB knockout mice treated with or without STZ, and their kidneys were used to investigate changes in proteins associated with cell death. Lysophosphatidylethanolamine (LPE) (18:1), lysophosphatidylserine (LPS) (22:6), and lysophosphatidylglycerol (LPG) (22:5) were among the bioactive lipids enriched in uEVs from CtsB knockout mice treated with STZ compared to untreated CtsB mice (n = 3 uEV preparations per group). Anti-oxidant programming was activated in the kidneys of the CtsB knockout mice treated with STZ, as indicated by increased expression of glutathione peroxidase 4 (GPX4) and the cystine/glutamate antiporter SLC7A11 (XCT) (n = 4 mice per group), which was supported by a higher reactivity to 4-hydroxy-2-nonenal (4-HNE), a marker for oxidative stress (n = 3 mice per group). Apoptosis but not ferroptosis was the ongoing form of cell death in these kidneys as cleaved caspase-3 levels were significantly elevated in the STZ-treated CtsB knockout mice (n = 4 mice per group). There were no appreciable differences in the pro-ferroptosis enzyme acyl-CoA synthetase long-chain family member 4 (ACSL4) or the inflammatory marker CD93 in the kidneys (n = 3 mice per group), which further supports apoptosis as the prevalent mechanism of pathology. These data suggest that STZ treatment leads to oxidative stress, inducing apoptotic injury in the kidneys during the development of diabetic kidney disease and hypertension.

Effects of Cranberry Extract (Vaccinium macrocarpon) Supplementation on Lipid Peroxidation and Inflammation in Patients with Chronic Kidney Disease (Stages 3-4): A Randomized Controlled Trial

Background. Growing evidence suggests that bioactive compounds in berry fruits may mitigate inflammation in patients with chronic kidney disease (CKD). Objectives. To evaluate cranberry (Vaccinium macrocarpon) supplementation effects on modulation of transcription factors involved in inflammation and oxidative stress in nondialysis (stages 3 and 4) patients with CKD. Design/Participants. A randomized, double-blind, placebo-controlled study was performed with 30 patients to receive capsules containing cranberry extract (1000 mg/day) or placebo (1000 mg/day of corn starch) for two months. Measurements. The mRNA expression of nuclear factor-erythroid 2-related factor-2 (Nrf2) and nuclear factor-kB (NF-kB) was evaluated in peripheral blood mononuclear cells (PBMCs) by quantitative real-time polymerase chain reaction. Thiobarbituric acid reactive substances (TBARS) were measured in the plasma to assess oxidative stress. Interleukin-6 (IL-6) plasma levels were assessed by enzyme-linked immunosorbent assay and C-reactive protein (CRP) by immunoturbidimetric method. Results. Twenty-five patients completed the study: 12 in the cranberry group (56.7 ± 7.5 years and body mass index (BMI) of 29.6 ± 5.5 kg/m2) and 13 in the placebo group (58.8 ± 5.1 years and BMI 29.8 ± 5.4 kg/m2). There were no differences in NF-kB or Nrf2 mRNA expressions (p=0.99 and p=0.89) or TBARS, CRP, and IL-6 plasma levels after cranberry supplementation. Conclusions. The cranberry extract administration (1000 mg/day) did not affect Nrf2 and NF-kB mRNA expression, oxidative stress, or inflammatory markers levels in nondialysis CKD patients. This trial is registered with NCT04377919.

Brain-targeted nasal chrysin microemulsion for reducing oxidative stress in Parkinson's disease: Pharmacodynamic, biochemical evaluation and brain distribution studies

Chrysin, a flavone reported to treat Parkinson's, has limited oral bioavailability due to poor solubility and extensive pre-systemic metabolism. Therefore, a chrysin microemulsion (Chy-ME) was developed to improve bioavailability and brain targeting for treating Parkinson's disease via the nasal route. Chy-ME was prepared using the phase titration method and characterized for physicochemical parameters, nasociliotoxicity, and anti-Parkinson activities in a rotenone-induced experimental rat model. Chy-ME showed spherical globules with a size of 365.03 nm ± 6.8, a PDI of 0.107 ± 0.0316 and a zeta potential of −24.86 mV ± 2.286. It was non-irritant to the nasal mucosa and had in vitro and ex vivo drug release of 90.52 % and 68.67 %, respectively at 24 h. The in vivo study showed significantly improved locomotor activity and catalepsy score in the Chy-ME treated group than in oral or nasal chrysin suspension groups in rats. Chy-ME treatment showed elevated dopamine levels than the other two groups. Also, enhanced oxidative stress markers, i.e., SOD, GSH, and catalase levels, indicated the antioxidant potential of Chy-ME linked with preventing neuronal damage in Parkinson's. The maximum chrysin amount was estimated in the Chy-ME group (8.3212 ± 1.8125 μg/mL) than in oral (4.1364 ± 1.1095 μg/mL) or nasal (5.0879 ± 0.0058 μg/mL) suspension groups in the brain distribution study. In vivo studies revealed the brain-targeting potential of Chy-ME, evidenced by a substantial alleviation of Parkinson's symptoms, increased dopamine levels, improved oxidative stress markers and higher chrysin content in the brain. Therefore, nasal delivery of chrysin could overcome poor oral bioavailability and be explored for treating Parkinson-related symptoms as a brain-targeted approach.

Inhibiting the SARM1-NAD+ axis reduces oxidative stress-induced damage to retinal and nerve cells

Retinal neurodegenerative diseases are a category of refractory blinding eye conditions closely associated with oxidative stress induced by mitochondrial dysfunction in retinal cells. SARM1, a core driver molecule leading to axonal degeneration, possesses NAD+ enzyme (NADase) activity. However, the role of the SARM1-NAD+ axis in oxidative stress-induced retinal cell death remains unclear. Here, we employed the SARM1 NADase inhibitor DSRM-3716 and established a glucose oxidase (GOx)-induced oxidative stress cell model. We found that compared to the GOx group, the DSRM-3716 pre-treated group reduced the hydrolysis of NAD+, inhibited the elevation of oxidative stress markers induced by GOx, decreased mitochondrial dysfunction, lowered the phosphorylation level of JNK, and attenuated the occurrence of pyroptosis in retinal and nerve cells, thereby providing protection for neurite growth. Further utilization of the JNK activator Anisomycin activated JNK, revealed that the JNK/c-Jun pathway down-regulated NMNAT2 expression. Consequently, it reduced cellular NAD+ synthesis, exacerbated mitochondrial dysfunction and cell pyroptosis, and reversed the protective effect of DSRM-3716 on cells. In summary, the inhibition of SARM1 NADase activity substantially mitigates oxidative damage to retinal cells and mitochondrial damage. Additionally, JNK simultaneously serves as both an upstream and downstream regulator in the SARM1-NAD+ axis, regulating retinal cell pyroptosis and neurite injury. Thus, this study provides new insights into the pathological processes of retinal cell oxidative stress and identifies potential therapeutic targets for retinal neurodegenerative diseases.

Anti-arthritic and immunomodulatory efficacy of Micromeria biflora Benth extract and its fractions in rats by restoring oxidative stress, metalloproteinases, pro-inflammatory and anti-inflammatory cytokines network.

Micromeria biflora (M.B) Benth has proven anti-inflammatory efficacy, thereby, the goal of the current investigation was to assess the anti-arthritic potential of M.B ethanolic extract and fractions as well as to investigate the likely mechanism of action. The effectiveness of M.B against acute arthritic manifestations was assessed using an arthritic model prompted by formaldehyde, whereas a chronic model was developed using an adjuvant called Complete Freund's in Sprague-Dawley rats. Weekly evaluations were conducted for parameters involving paw volume, body weight, and arthritic score; at the completion of the CFA model, hematological, biochemical and oxidative stress parameters as well as the level of various mediators (PGE2, IL-1β, TNFα, IL6, MMP2, 3, 9, VEGF, NF-ĸB, IL-10, and IL-4) were evaluated. The results demonstrated the plant's ability to treat arthritis by showing a significant decrease in paw volume, arthritic score, and histological characteristics. The levels of NF-ĸB, MMP2, 3, 9, IL6, IL1β, TNFα, and VEGF were all significantly reduced after treatment with plant extract and fractions. Plant extract and its fractions substantially preserved body weight loss, oxidative stress markers and levels of IL-4 and 1L-10. PGE2 levels were also shown to be reduced in the treatment groups, supporting the M.B immunomodulatory ability. Hematological and biochemical indicators were also normalized after M.B administration. Outcomes of the study validated the anti-arthritic and immunomodulatory attributes of M.B probably through modulating oxidative stress, inflammatory, pro-inflammatory and anti-inflammatory biomarkers.

STUDY OF PHYSIOLOGICAL AND BIOCHEMICAL VARIATIONS IN POPULATION GROUPS UNDERGOING ACUTE OR CHRONIC STRESS

Objective: Stress arises from derangements of personal and professional activities. The basic reason is changes in lifestyle and psychosocial adaptations. Life becomes demanding, complicated, mechanical, and devoid of health. In today’s modern world, occupational stress has become the major factor for loss of health and peacefulness of mind. Methods: This is an observational descriptive study which was conducted in a group of 84 people between 25 and 60 years of age to study the association of acute stress on salivary amylase level and effect of chronic stress on lipid profile, glycosylated hemoglobin and certain inflammatory markers in people representing different forms of stress. Three groups of the population were studied. Group 1 (n=20) - Patients undergoing any elective surgery (abdominal/genitourinary) or an invasive diagnostic procedure (upper GI endoscopy, lymph node biopsy) Group 2 (n=32) – High/middle socio-economic male or female working for ≥8 h/day with or without stress. Group 3 (n=32) – Low socioeconomic male or female earning &lt;100 Rs/day with or without stress. Salivary alpha-amylase and chromogranin A (CgA) levels are good markers of stress. Results: There was increased levels of cortisol (p&lt;0.0001), alpha amylase (p&lt;0.01), and decreased levels of CgA (p&lt;0.001) pre-procedure period as a marker of acute stress. In the chronic stress group of low income as well as high-income status, glycosylated hemoglobin, and blood lipid profile in both males and females were significantly deranged. Plasma malondialdehyde (MDA) levels and interleukin (IL)-1 and IL-2 were significantly raised in both groups. Serum ferritin level was low in the low socioeconomic group but normal in the high socioeconomic group. Conclusion: Salivary amylase level was raised in acute stress and there is a direct correlation of chronic stress with high low-density lipoprotein/ high-density lipoprotein ratio, raised glycosylated Hemoglobin, serum MDA, IL-1, 2 levels irrespective of economic group.

Strength Training Protects High-Fat-Fed Ovariectomized Mice against Insulin Resistance and Hepatic Steatosis

Menopause is characterized by a reduction in sex hormones in women and is associated with metabolic changes, including fatty liver and insulin resistance. Lifestyle changes, including a balanced diet and physical exercise, are necessary to prevent these undesirable changes. Strength training (ST) has been widely used because of the muscle and metabolic benefits it provides. Our study aims to evaluate the effects of ST on hepatic steatosis and insulin resistance in ovariectomized mice fed a high-fat diet (HFD) divided into four groups as follows: simulated sedentary surgery (SHAM-SED), trained simulated surgery (SHAM-EXE), sedentary ovariectomy (OVX-SED), and trained ovariectomy (OVX-EXE). They were fed an HFD for 9 weeks. ST was performed thrice a week. ST efficiently reduced body weight and fat percentage and increased lean mass in OVX mice. Furthermore, ST reduced the accumulation of ectopic hepatic lipids, increased AMPK phosphorylation, and inhibited the de novo lipogenesis pathway. OVX-EXE mice also showed a better glycemic profile, associated with greater insulin sensitivity identified by the euglycemic–hyperinsulinemic clamp, and reduced markers of hepatic oxidative stress compared with sedentary animals. Our data support the idea that ST can be indicated as a non-pharmacological treatment approach to mitigate metabolic changes resulting from menopause.