TOS Levels Research Articles

Acyclovir provides protection against 6-OHDA-induced neurotoxicity in SH-SY5Y cells through the kynurenine pathway

Parkinson's disease is one of the most prevalent neurodegenerative disorders worldwide. The kynurenine pathway associated with oxidative stress and neuroinflammation is recognized to contribute to its pathophysiology, although the exact mechanism is not fully elucidated. In neuroinflammation, IDO-1 catalyzes the conversion of tryptophan to neurotoxic QUIN through the kynurenine pathway. Consequently, QUIN increases oxidative stress via nNOS and NMDA, which causes neurodegeneration. Few studies have reported on the effect of different antiviral drugs in Parkinson's disease; the exact mechanism is still unknown. The antiviral acyclovir has been shown to have neuroprotective properties and can cross the blood-brain barrier. We examined acyclovir's effects and potential mechanisms in the 6-OHDA-induced in vitro model of Parkinson's disease in SH-SY5Y cells using biochemical, immunocytochemical, and in silico methods. MTT assay demonstrated that acyclovir significantly decreased cell mortality induced by the neurotoxic 6-OHDA at dosages of 3.2 µM, 6.4 µM, 12.8 µM, 25.6 µM, and 51.2 µM. In immunocytochemical analysis, acyclovir treatment decreased α-synuclein and TNF-α expressions in cells. In biochemical analyses, while IL-17A and TOS levels decreased depending on varying doses (1.6 µM, 3.2 µM, 6.4 µM, 12.8 µM), TAC levels increased. Using in silico analyses to investigate the mechanism showed that acyclovir docked with TNF-α, IL-17A, IDO-1, nNOS, α-synuclein, and NMDA. The findings demonstrated that acyclovir had neuroprotective effects by modulating the kynurenine pathway and decreasing neurodegeneration via QUIN inhibition in an in vitro Parkinson's disease model. Although the mechanisms of acyclovir's effects in Parkinson's disease are unclear, the results obtained from the experiments are encouraging.

Impact of melamine exposure on apoptotic proteins and oxidative stress markers in mouse hepatic tissue

Most melamine studies have focused on renal toxicity and its effects on the liver are still not well known. We investigated the apoptotic and oxidative effects of melamine on the liver using thirty BALB/c mice, divided into three groups. The control group received saline, while the low-dose melamine (LDM) group was given 400 mg/kg (1/8 LD50) and the high-dose melamine (HDM) group received 1600 mg/kg (1/2 LD50) intragastrically (0.25 ml) for 5 consecutive days. Liver Bcl-2 and caspase-3 expressions were analyzed at the protein level by immunohistochemistry and ELISA, and also at the gene level by quantitative Real-Time PCR. In addition, total antioxidant (TAS), total oxidant (TOS), and oxidative stress index (OSI) levels in liver tissues were measured spectrophotometrically. The immunohistochemical expression of caspase-3 was higher in the LDM and HDM groups compared to the control group (p = 0.002). TOS and OSI levels were increased significantly (P

Effects of quercetin-immobilized albumin cerium oxide nanoparticles on glutamate toxicity: in vitro study.

One aspect of glutamate (Glut) toxicity may be the opening of the blood-brain barrier to albumin (Al), which in itself can cause nerve cell death. Quercetin (Q) is a polyphenolic substance and has a neuroprotective effect. Cerium oxide nanoparticles (Ce2O3NPs) are highly interested in biological applications due to their antioxidant properties. The current study aimed to investigate the impact of Q-immobilized Al+Ce2O3NPs in Glut-induced neurotoxicity, mainly focusing on cell viability and neurobiochemical changes. Hydrothermal synthesis and characterization of Q-immobilized Al+Ce2O3NPs were performed. After preparing the primary neuron culture, it was exposed to Glut to induce neurotoxicity. Then, various doses of Ce2O3NP, Al+Ce2O3NP, and Q+Al+Ce2O3NPs (1, 5, 10, and 25 µg/ml) were applied to the wells and incubated for 24 h. Then, cell viability was determined by MTT analysis. Additionally, oxidative stress parameters were measured. When the obtained data were examined, it was shown that cell viability decreased with Glut concentration but significantly increased with Q+Al+Ce2O3NPs treatment. When oxidative stress markers were considered, Glut treatment increased LDH, AChE, and TOS levels, while TAC and GSH levels decreased. However, the trend changed after Q+Al+Ce2O3NPs treatment, suggesting that damaged neurons were protected against oxidative stress. The results of this study indicate that Q+Al+Ce2O3NP can ameliorate Glut-induced neurotoxicity, especially when used at a dose of 25 µg/ml.

Genistein Enhances the Beneficial Effects of Exercise on Antioxidant and Anti-Inflammatory Balance and Cardiomyopathy in Ovariectomized Diabetic Rats.

This study aimed to investigate the effects of genistein, swimming exercise, and their co-treatment on heart oxidative stress, inflammation, and cardiomyopathy in ovariectomized diabetic rats. It is well-established that diabetes is a major risk factor for cardiovascular disease in both young and postmenopausal women. Genistein is a natural phytoestrogen that has estrogenic effects. Studies have shown that genistein has a positive impact on menopause, cardiovascular dis-ease, and diabetes in women. However, the impact of genistein treatment alone and in combination with exercise training on the management of cardiac disease in diabetic women after ovarian hor-mone deprivation has not been fully explored. The objective of this study was to evaluate the effect of genistein alone or in combination with exercise training on the cardiac expression of oxidative/inflammation biomarkers (MDA, OSI, TOS, TNF- α, and NF-κB) and miRNA-133, IGF-1, and Bcl-2 in the diabetic ovariectomized rats. A group of Wistar rats were randomly divided into seven groups, with eight rats in each group. The groups were named control, sham, ovariectomized group (OVX), OVX +diabetes (OD), OD+ genistein (1 mg/kg, eight weeks; daily SC), OD+exercise (eight weeks), and OD+ genistein+exercise (eight weeks). The rats were given a high-fat diet and low-dose streptozotocin injection to induce diabetes. After eight weeks, the rats were anesthetized, and their hearts were removed. The study assessed the effects of treatment by measuring the expression of miRNA-133 using Real-time Polymerase Chain Reaction (PCR) and the protein levels of Bcl-2, Bax, and IGF-1 using Western blotting. The study also evaluated the levels of inflammation and oxidative stress markers using ELISA. Pathological changes were also assessed using periodic acid Schiff and he-matoxylin & eosin. After ovariectomy, the levels of cardiac miRNA-133, IGF-1, and Bcl-2 expression were down-regulated, and the levels of MDA, OSI, TOS, TNF-α, and NF-κB were increased, with a reduced total antioxidant capacity. Diabetes had an additive effect on these factors. Genistein was found to have a positive impact on oxidative and inflammation levels, and it also increased the expression of miRNA-133, Bcl-2, and IGF-1 in rats with OD. Furthermore, the combination of genistein and exercise had a positive effect on miRNA-133, Bcl-2, and IGF-1 expression in the heart, leading to a decrease in Bax levels. The combined intervention showed a noticeable improve-ment in oxidative and inflammation conditions. Histological examination revealed some abnormal-ities in cardiac tissue, which were found to be improved with genistein and/or exercise treatments. Genistein or/and exercise as a natural replacement therapy could improve diabetic-induced cardiac complications in ovariectomized rats' hearts.

Investigation of Apoptotic and Anticancer Effects of 2-substituted Benzothiazoles in Breast Cancer Cell Lines: EGFR Modulation and Mechanistic Insights.

Benzothiazole derivatives, a class of heterocyclic compounds, exhibited diverse biological activities influenced by substituents in the thiazole ring. This study aimed to synthesize these compounds with two functional groups to investigate their potential as anticancer agents, particularly against breast cancer. While previous research demonstrated the efficacy of 2-substituted benzothiazoles against glioma and cervical and pancreatic cancer cells, there is a gap in studies targeting breast cancer. The synthesized compounds were tested in vitro using MCF-7, MDA-MB-231, and MCF-10A cell lines, with Doxorubicin as the positive control. Various assays were conducted, including Annexin V/PI, cell cycle analysis, wound healing, and measurement of mitochondrial membrane potential. Protein expression of EGFR and transcription levels of apoptosis-related genes (Bax and Bcl-xL) and cancer progression-related genes (JAK, STAT3, ERK, AKT, mTOR) were analyzed. Additionally, the balance between antioxidants and oxidants was evaluated by measuring TAS and TOS levels. Our findings revealed that benzothiazole compounds significantly inhibited breast cancer cell growth by reducing cell motility, disrupting mitochondrial membrane potential, and inducing cell cycle arrest in the sub-G1 phase. These compounds increased reactive oxygen species accumulation, leading to cell death. Furthermore, they decreased EGFR protein levels, increased Bax gene transcription, and downregulated the expression of genes such as JAK, STAT3, ERK, AKT, and mTOR. In conclusion, benzothiazole derivatives exhibited potent inhibitory effects on breast cancer in vitro by promoting apoptosis, downregulating EGFR activity, and modulating key signaling pathways, including JAK/STAT, ERK/MAPK, and PI3K/Akt/mTOR. These results highlighted the potential of benzothiazole derivatives as novel therapeutic agents for breast cancer treatment.

Naringenin and caffeic acid increase ethanol production in yeast cells by reducing very high gravity fermentation-related oxidative stress.

Very high gravity (VHG) fermentation is an industrial-scale process utilizing a sugar concentration above 250g/L to attain a significant ethanol concentration, with the advantages of decreased labor, production costs, water usage, bacterial contamination, and energy consumption. Saccharomyces cerevisiae is one of the most extensively employed organisms in ethanol fermentation through VHG technology. Conversely, high glucose exposure leads to numerous stress factors that negatively impact the ethanol production efficiency of this organism. Here, the impact of various phytochemicals added to the VHG medium on viability, glucose consumption, ethanol production efficiency, total antioxidant-oxidant status (TAS and TOS), and the response of the enzymatic antioxidant system of yeast were investigated. 2.0 mM naringenin and caffeic acid increased ethanol production by 2.453 ± 0.198 and 1.261 ± 0.138-fold, respectively. The glucose consumption rate exhibited a direct relationship with ethanol production in the naringenin-supplemented group. The highest TAS was determined as 0.734 ± 0.044 mmol Trolox Eq./L in the same group. Furthermore, both phytochemical compounds exhibited robust positive correlations with TAS (rnaringenin = 0.9986; rcaffeic acid = 0.9553) and TOS levels (rnaringenin = -0.9824; rcaffeic acid = -0.9791). While naringenin caused statistically significant increases in glutathione reductase (GR) and thioredoxin reductase (TrxR) activities, caffeic acid significantly increased TrxR and superoxide dismutase (SOD). Both phytochemicals seem to impact the ethanol production ability by regulating the redox status of the cells. We believe that the incorporation of particularly cost-effective antioxidants into the fermentation medium may serve as an alternative way to enhance the efficiency of bioethanol production using VHG technology.

Expiratory muscle strength training reduces oxidative stress and systemic inflammation in men with obstructive sleep apnea syndrome: a double-blinded, randomized parallel trial

Abstract Study Objectives This study aimed to evaluate and compare the effects of high and low-intensity expiratory muscle strength training (EMST) on disease severity, systemic inflammation, oxidative stress, respiratory muscle strength, exercise capacity, symptoms, daytime sleepiness, fatigue severity, and sleep quality in male patients with obstructive sleep apnea syndrome (OSAS). Methods Thirty-one male patients diagnosed with moderate OSAS were included in this double-blind, randomized, parallel study. Patients were randomized into two groups: High-EMST and Low-EMST groups. EMST was used at home 7 days/week, once a day, for 25 breaths, 12 weeks. Respiratory muscle strength was measured using a mouth pressure device. Disease severity (Apnea–Hypopnea Index [AHI]) and, respiratory sleep events by polysomnography, total oxidant level(TOS), total antioxidant level(TAS), oxidative stress index (OSI), C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-10 (IL-10) levels by blood serum were evaluated. Results The percentage of AHI change in the high-EMST group(50.8%) was significantly higher than in the low-EMST group(6.3%; p = .002, d = 1.31). In general, as MEP increased by one unit, AHI decreased by 0.149 points (b = −0.149; CR = −3.065; p = .002), and as AHI increased by one unit, ODI increased by 0.746 points (b = 0.746; CR = 10.604; p < .001). TOS, OSI, TNF-α and IL-6 levels decreased at similar rates in both groups. Conclusions EMST significantly reduces systemic inflammation and oxidative stress while improving expiratory muscle strength in male patients with moderate OSAS. High-EMST is more effective in enhancing the severity of disease than low-EMST. EMST is a practical, effective, and promising treatment for pulmonary rehabilitation in patients with moderate OSAS. Clinical Trials Effect of EMST systemic inflammation and oxidative stress in patients with moderate OSAS, https://clinicaltrials.gov/study/NCT05242406, with the number NCT05242406.

Investigation of Oxidative Stress Parameters and Pro-Inflammatory Cytokines in a Neuropathy Model Created with Taraxacum Officinale L. Leaf Extract and Cisplatin

The aim of this study was to investigate the effect of Taraxacum officinale leaf extract, a plant known for its potent antioxidant and anti-inflammatory properties, on cisplatin-induced neurotoxicity. Cancer treatment has demonstrated platinum drugs, particularly cisplatin, as among the most effective treatments. However, the drug comes with serious side effects. The use of cisplatin is limited due to its cytotoxic effects, potentially preventing patients from benefiting optimally from anticancer agents. Taraxacum officinale has been used for various diseases for years, observed clinically in conditions such as dyspepsia, liver, gallbladder, and urinary disorders. Nowadays, Taraxacum officinale has entered our lives in various forms as a dietary supplement. However, this plant possesses many bioactivities, particularly potent anti-inflammatory, antioxidant, and hepatoprotective properties.In this study, chronic cisplatin administration was used to induce a peripheral neuropathy model, administered intraperitoneally (i.p) once a week for 5 weeks at a dose of 3 mg/kg. Taraxacum officinale leaf extract was administered intragastrically once daily at a dose of 500mg/kg for the same duration to determine its potential effects on cisplatin neuropathy. After drug administration, motor performance was evaluated using the rotarod test, while sensory transmission status was assessed using tail withdrawal and hot/cold plate tests. Oxidative stress parameters and proinflammatory cytokine markers were analyzed biochemically. In animals exposed to cisplatin, thermal hypoalgesia and cold hypoalgesia were observed (p<0.001), motor coordination balance was prolonged with the rotarod test (p<0.001), and tail withdrawal time was extended (p<0.001). Biochemically, oxidative stress parameters TOS (p<0.05), OSI (p<0.05), and MDA (p<0.05) levels significantly increased compared to the cisplatin control group. TAS levels provided a statistically significant increase compared to the cisplatin-administered group (p<0.05). Proinflammatory cytokine markers TNF-α (p<0.05), IL-6 (p<0.001), and NFKB (p<0.05) levels were found to be higher compared to the cisplatin control group. It was determined that Taraxacum officinale improved these side effects induced by cisplatin both behaviorally and biochemically. In conclusion, Taraxacum officinale leaf extract is a plant with potent antioxidant and anti-inflammatory activity.

Anti-Cataract Effect of the Traditional Aqueous Extract of Yerba Mate (Ilex paraguariensis A. St.-Hil.): An In Ovo Perspective.

The therapeutic effect of different doses of the traditional aqueous extract of dried leaves of yerba mate (Ilex paraguariensis A. St.-Hil.) was investigated in an experimental cataract model in chicken embryos. LC-MS/MS analysis allowed the identification and quantification of 53 metabolites. In the hydrocortisone-induced cataract model, lenses were examined morphologically after treatment and parameters related to oxidative stress (total antioxidant/oxidant status (TAS/TOS), glutathione (GSH), and malondialdehyde (MDA)) were evaluated. Antiproliferative cell nuclear antigen (PCNA) and caspase-3 H-scores were determined and crystallin alpha A (CRYAA) gene expression in the lenses was measured by RT-PCR. The degree of cataract decreased in all treatment groups. While there was no significant difference in TAS levels compared to the negative control, TOS, GSH, and MDA levels were dose-dependently regulated. Treatment groups other than the high-dose group regulated the decrease in PCNA and the increase in caspase-3. CRYAA gene expression increased significantly only at the lowest dose. YM, which is becoming increasingly popular as a traditional tea, showed a therapeutic effect on hydrocortisone-induced cataracts in chicken embryos at relatively low doses.

Protective Action of Curcumin and Alpha-lipoic Acid, Against Experimental Ultraviolet-A/B Induced Dermal-injury in Rats.

The objective of this study was to examine the therapeutic efficacy of curcumin (CUR) and α-lipoic acid (ALA) in mitigating UV-A and UV-B-induced damage (UVAB) in rat dorsal skin. This was achieved through the utilisation of immunohistochemical (TUNEL), biochemical and stereological techniques. The rats in the UVAB, UVAB + CUR, and UVAB + ALA groups were subjected to UVAB irradiation for a period of two hours per day over the course of one month. The UVAB + CUR and UVAB + ALA groups were administered 100 mg/kg/day of curcumin and 100 mg/kg/day of α-lipoic acid via gavage 30 min prior to UVAB irradiation. The CUR group was administered 100 mg/kg/day of curcumin via gavage, while the ALA group received the same dose of α-lipoic acid. A significant change in the volume ratio of the dorsal skin epidermis and dermis was observed in the stereological findings of the rats in the UVAB group. These changes exhibited a favourable progression as a consequence of the CUR and ALA applications. In the UVAB group, TOS and OSI were significantly elevated as a consequence of the rise in oxidative stress. Conversely, the treatment groups demonstrated a notable reduction in TOS and OSI levels. The study also revealed a substantial increase in the number of apoptotic cells within the UVAB group. However, the treatment groups exhibited a significant decline in apoptotic cells. In conclusion, the findings suggest that CUR and ALA possess a protective effect against UVAB-induced skin damage.

Cannabidiol ameliorates lipopolysaccharide-induced cardiovascular toxicity by its antioxidant and anti-inflammatory activity via regulating IL-6, Hif1α, STAT3, eNOS pathway.

Systemic inflammation causes several organ damage by activating the intracellular signaling mechanisms. Heart and aorta tissues are the structures mostly affected by this situation. By examining underlying processes, this study sought to determine whether cannabidiol (CBD) may have protective effects against the cardiovascular damage brought on by lipopolysaccharide (LPS). A total of 32 female rats were randomly allocated to one of four groups: control, lipopolysaccharide (LPS) (5mg/kg, i.p., single dose), LPS + CBD (5mg/kg, i.p., single dose), and CBD groups. The rats were killed six hours after receiving LPS, and tissues from the heart and aorta were taken. Histopathological and immunohistochemical analyzes were performed. Oxidative stress was evaluated biochemically by spectrophotometric method. Expression levels of genes were studied by RT-qPCR method. Histopathological analysis of the LPS group showed moderate hyperemia, hemorrhages, edema, inflammation, and myocardial cell damage. There was a slight to moderate increase in Cox-1, G-CSF, and IL-3 immunoexpressions, along with enhanced expressions of IL-6, Hif1α, and STAT3 genes, and decreased expressions of eNOS genes. Additionally, there were increased levels of TOS and decreased TAS levels observed biochemically. CBD treatment effectively reversed and improved all of these observed changes. CBD protects the heart and aorta against systemic inflammation through its antioxidant and anti-inflammatory activity via regulating IL-6, Hif1α, STAT3, and eNOS intracellular pathways.

Evaluation of oxidative stress and inflammation in patients with polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is a heterogeneous endocrine and metabolic disorder characterized by hyperandrogenism, hyperinsulinemia, and insulin resistance. The prevalence of PCOS is increasing worldwide. Although the etiology of this disease is currently unknown, it is thought to be closely related to inflammation and oxidative stress. Our study aimed to compare patients have PCOS to healthy volunteers and assess the changes in oxidative stress and inflammatory parameters in these patients. Thirty patients between the ages of 18-45 diagnosed with PCOS and 30 healthy volunteers with the same demographic characteristics were included in this study. Clinical parameters were measured using immunoassays. Oxidative stress biomarkers, total oxidant (TOS), total antioxidant (TAS), total thiol (TT), and native thiol (NT) levels were measured using photometric methods according to Erel's method. The dynamic disulfide level (DIS) and oxidative stress index (OSI) were calculated using mathematical equations. Among the inflammatory parameters, values for interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α) were measured photometrically using commercially purchased kits. Moreover, TT and NT levels were lower in patients with PCOS compared to those in the healthy group statistically significantly (P<0.001). In addition, TAS, TOS, OSI, DIS, IL-1β, IL-6, and TNF-α levels were identified to be significantly higher in the patients with PCOS than those in the healthy group (P<0.001). Evaluation of oxidative stress and clinical parameters used in the follow-up may be beneficial for the disease.

Role of curcumin on beta-amyloid protein, tau protein, and biochemical and oxidative changes in streptozotocin-induced diabetic rats

Diabetes is one of the most common endocrine metabolic diseases and is associated with the accumulation of beta-amyloid plaques in the brain. Amyloid beta (Aβ) and abnormal tau proteins are effective in the development of Alzheimer’s disease. The aim of this study is to investigate the therapeutic and protective effects of curcumin on beta-amyloid (Aβ) accumulation and tau protein expression levels, as well as biochemical and oxidative changes in streptozotocin-induced diabetes in rats. The study comprised five groups, each consisting of eight rats: control, diabetic, curcumin, curcumin during diabetic induction, and curcumin post-diabetic induction. Groups 2 and 4 were administered a single dose of 45 mg/kg streptozotocin on day 1, while group 5 received it on day 28. Curcumin was orally administered via gavage at a dose of 100 mg/kg/day for 35 days to the third, fourth, and fifth groups. At the end of the trial (day 35), blood sugar levels and insulin resistance were similar between the control and curcumin-treated groups but significantly higher in the diabetic groups (P < 0.05). The protective effect of curcumin is tested during induction and active diabetes. The results indicated that diabetic rats displayed increased levels of Aβ, tau protein, and total oxidant capacity (TOS) compared to the curcumin-treated groups. Additionally, the total antioxidant capacity (TAS) levels were lower in the diabetic rats (P < 0.05). Aβ protein levels are lower in both the serum and brain of rats with active diabetes and treated with curcumin compared to control rats (P > 0.05). In addition, serum TAS levels were higher in rats treated with curcumin following the induction of diabetes than pre-induction of diabetes (P > 0.05). The TOS levels in the serum were higher in the rats treated with curcumin during active diabetes compared to the rats treated prior to the induction of diabetes (P < 0.05). However, no significant difference was observed in the brain. The above results show that curcumin has an effect on reducing oxidative stress caused by diabetes and increasing antioxidant activity.

Altered blood parameters in “major depression” patients receiving repetitive transcranial magnetic stimulation (rTMS) therapy: a randomized case-control study

Major depressive disorder (MDD) is a debilitating illness that includes depressive mood. Repetitive Transcranial Magnetic Stimulation (rTMS) is a therapy method used in the treatment of MDD. The purpose of this study was to assess neurotrophic factors, and oxidative stress levels in MDD patients and evaluate the changes in these parameters as a result of rTMS therapy. Twenty-five patients with MDD and twenty-six healthy volunteers with the same demographic characteristics were included in the study. Brain-derived neurotrophic factors were measured photometrically with commercial kits. Oxidative stress parameters were measured by the photometric method. Oxidative stress index (OSI) and disulfide (DIS) levels were calculated with mathematical formulas. In this study, total antioxidant status (TAS), total thiol (TT), and native thiol (NT) antioxidant parameters and brain-derived neurotrophic factor (BDNF), glial cell line-derived neurotrophic factor (GDNF), and allopregnanolone (ALLO) levels were reduced in pre-rTMS with regard to the healthy control group; TOS, OSI, DIS, and S100 calcium-binding protein B (S100B) levels were increased statistically significantly (p < 0.01). Moreover, owing to TMS treatment; TAS, TT, NT, BDNF, GDNF, and ALLO levels were increased compared to pre-rTMS, while DIS, TOS, OSI, and S100B levels were decreased significantly (p < 0.01). The rTMS treatment reduces oxidative stress and restores thiol-disulfide balance in MDD patients. Additionally, rTMS modulates neurotrophic factors and neuroactive steroids, suggesting its potential as an antidepressant therapy. The changes in the biomarkers evaluated may help determine a more specific approach to treating MDD with rTMS therapy.

The impact of sericin on inflammation, oxidative stress, and lipid metabolism in female rats with experimental knee osteoarthritis.

This study investigated the effects of sericin on inflammation, oxidative stress, and lipid metabolism in female rats with experimental knee osteoarthritis (KOA), focusing on evaluating its effectiveness via the sterol regulatory protein (SREBP)-1C and SREBP-2 pathways. The rats were randomly assigned to three experimental groups: the C group (control), the KOA group (KOA control), and the sericin group (KOA + sericin). The KOA model was created by injecting monosodium iodoacetate (MIA) into the knee joint. Sericin was administered intra-articularly to rats on days 1, 7, 14, and 21 (0.8g/kg/mL, 50 µL). After 21days, the rats were sacrificed, and serum samples were analyzed using an ELISA to measure tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), IL-10, SREBP-1c, SREBP-2, acetyl-CoA carboxylase (ACC), fatty acid synthase (FAS), cholesterol, triglyceride, and total oxidant-antioxidant status (TOS-TAS) levels. The KOA group exhibited higher serum TNF-α, IL-1β, TOS, SREBP-1C, ACC, FAS, triglyceride, SREBP-2, and cholesterol levels than the C group (P < 0.05). However, the levels of these cytokines, except cholesterol, were significantly lower in the sericin group than in the KOA group. The KOA group exhibited significantly lower serum TAS and IL-10 levels than the C group (P < 0.05). In the sericin group, there was a statistically significant increase (P < 0.05). Sericin shows promising potential for reducing inflammation, oxidative stress, and lipid metabolism in experimental models of KOA in rats. However, further clinical research is necessary to validate the potential of sericin as a therapeutic agent for treating KOA. Key Points • Sericin can reduce knee osteoarthritis (KOA) symptoms in an experimental rat model. • In particular, in the serum of an experimental KOA rat model, sericin specifically reduces the levels of proinflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α) and interleukin-1beta (IL-1β), and increases the levels of anti-inflammatory cytokines, such as IL-10. • Sericin reduced lipid metabolism via the sterol regulatory protein (SREBP)-1C and SREBP-2 pathways and oxidative stress in the serum of the experimental KOA rat model. • The intra-articular administration of sericin has been shown to significantly reduce lipid metabolism, oxidative stress, and inflammation, as supported by biochemical analysis. These findings suggest its promising potential as an alternative treatment option for KOA.

Potential neuroprotective effects of 2-hydroxypropyl-β cyclodextrin against amyloid β (1-42)-induced neurotoxicity on the rat hippocampus

The neurodegenerative mechanisms of Alzheimer’s disease (AD) are not fully understood, but it is believed that amyloid beta (Aβ) peptide causes oxidative stress, neuroinflammation, and disrupts metabotropic glutamate receptor 5 (mGluR5) signaling by interacting with cholesterol and caveolin-1 (Cav-1) in pathogenic lipid rafts. This study examined the effect of 2-hydroxypropyl-β-cyclodextrin (HP-CD) on cholesterol, oxidative stress (total oxidant status), neuroinflammation (TNF-α), and mGluR5 signaling molecules such as PKCβ1, PKCβ2, ERK1/2, CREB, BDNF, and NGF in Aβ (1-42)-induced neurotoxicity. The Sprague-Dawley rats were divided into four groups: control (saline), Aβ (1-42), HP-CD (100 mg/kg), and Aβ (1-42) + HP-CD (100 mg/kg). All groups received bilateral stereotaxic injections of Aβ (1–42) or saline into the hippocampus. After surgery, HP-CD was administered intraperitoneally (ip) for 7 days. Cholesterol, TNF-α, and TOS levels were measured in synaptosomes isolated from hippocampus tissue using spectrophotometry, fluorometry, and enzyme immunoassay, respectively. The gene expressions of Cav-1, mGluR5, PKCβ1, PKCβ2, ERK1/2, CREB, BDNF, and NGF in hippocampus tissue were evaluated using reverse transcription PCR after real-time PCR analysis. Treatment with Aβ (1-42) significantly elevated cholesterol, TOS, TNF-α, Cav-1, PKCβ2, and ERK1/2 levels. Additionally, mGluR5, CREB, and BDNF levels were shown to be lowered. HP-CD reduced cholesterol, TOS, and TNF-α levels while increasing mGluR5, CREB, and BDNF in response to Aβ (1–42) treatment. These findings indicate that HP-CD may have neuroprotective activity due to the decreased levels of cholesterol, oxidative stress, and neuroinflammation, as well as upregulated levels of mGluR5, CREB, and BDNF.

Effect of Gallic Acid on PTZ-induced Neurotoxıcıty, Oxidative Stress and Inflammation in SH-SY5Y Neuroblastoma Cells

Aim: Human neuroblastoma cell lines are widely used to elucidate the cellular and molecular mechanisms of neurotoxicants and to facilitate the prioritization of in vivo testing. Pentylenetetrazole (PTZ) is a tetrazole derivative. Although PTZ is the most commonly used chemical to create an in vivo and in vitro epilepsy (EP) model, its mechanism of action in neuronal cells has not been fully elucidated. Gallic acid (GA) has broad biological properties such as antioxidant, anti-microbial, and anti-inflammatory activities. This study aimed to investigate the effect of GA on PTZ-induced neurotoxicity in neuroblastoma cells. Methods: For the study, four groups were formed from SH-SY5Y neuroblastoma cells as control (C), GA (100 μM), PTZ (30 μM), and PTZ+GA. In the study, total antioxidant and oxidant status (TAS and TOS), inflammatory cytokines (TNF α, IL 1β, and IL 6), lipid peroxidation levels as malondialdehyde (MDA), glutathione peroxidase (GSHPx), and glutathione (GSH) levels in the SH-SY5Y neuroblastoma cells were determined. Results: The results showed that PTZ treatment caused neurotoxicity in the neuroblastoma cell line and increased TOS, TNF α, IL 1β, IL 6, and MDA levels while decreasing TAS, GSH, and GSHPx levels. This situation improved with GA treatment. Conclusion: As a result, it was determined that GA treatment showed a protective effect in the PTZ-induced neural toxicity model in SH-SY5Y human neuroblastoma cell lines.

Serum testosterone levels and oxidative stress in type 1 diabetes, type 2 diabetes, and obesity.

Obesity, type 1 diabetes mellitus (T1DM), and type 2 diabetes mellitus (T2DM) are metabolic diseases that continue to be a global problem. Testosterone levels in men are affected by several factors, including obesity and DM. Although the relationship between diabetes and testosterone is not fully understood, oxidative stress is thought to play a major role. The aim of this study was to compare serum testosterone levels and oxidative stress markers [total antioxidant status (TAS), total oxidant capacity (TOS), oxidative stress index (OSI), and ischaemic modified albumin (IMA)] among the control group and experimentally induced obese, T1DM, and T2DM rats. The study included 28 male Sprague-Dawley rats divided into 4 groups: the obesity group were fed a high-fat diet (HFD), the T2DM group received a HFD plus a single dose of streptozocin (STZ), the T1DM group received only STZ, and there was a control group. Serum testosterone, TAS, TOS, OSI, and IMA were analysed. Serum testosterone levels were lower in the T1DM and T2DM groups compared to the control and obesity groups. The TOS levels were highest in the T2DM group, followed by the T1DM group, the obesity group, and finally the control group. No significant difference was found between the obesity group and the control group in terms of TOS levels. Regarding TAS levels, the order observed was control group > obesity group > T2DM > T1DM. Testosterone was positively correlated with TAS and negatively correlated with TOS and OSI. Increased oxidative stress in diabetes may be an important factor that decreases serum testosterone levels.

Oxidative Stress Markers and Histopathological Changes in Selected Organs of Mice Infected with Murine Norovirus 1 (MNV-1).

This paper describes the effects of murine norovirus (MNV) infection on oxidative stress and histopathological changes in mice. This study uses histopathological assays, enzymatic and non-enzymatic antioxidant markers, and total oxidative status and capacity (TOS, TAC). The results suggest that MNV infection can lead to significant changes with respect to the above-mentioned parameters in various organs. Specifically, reduced superoxide dismutase (SOD), Mn superoxide dismutase (MnSOD), catalase (CAT), and glutathione reductase (GR) activities were observed in liver tissues, while higher MnSOD activity was observed in kidney tissues of MNV-infected mice when compared to the control. GR activity was lower in all tissues of MNV-infected mice tested, with the exception of lung tissue. This study also showed that norovirus infection led to increased TOS levels in the brain and liver and TAC levels in the brain, while TOS levels were significantly reduced in the kidneys. These changes may be due to the production of reactive oxygen species (ROS) caused by the viral infection. ROS can damage cells and contribute to oxidative stress. These studies help us to understand the pathogenesis of MNV infection and its potential effects on oxidative stress and histopathological changes in mice, and pave the way for further studies of the long-term effects of MNV infection.

Effects of edaravone on testicular torsion-detorsion injury in rats.

This study aimed to assess the protective ability of edaravone on testicular torsion-detorsion injury in rats. Eighteen adult male Sprague-Dawley rats were randomly divided into three groups: Sham group (control, n=6); testicular torsion/detorsion (T/D group, n=6) and T/D+edaravone (T/D+E group, n=6). The spermatic cords of rats of the T/D group and the T/D+E group were rotated 720° in a clockwise direction and maintained for 120min in this torsion position. Around 90min after the torsion, edaravone at a dose of 10mg/kg dissolved in saline was administered IP to the T/D+E group. The testicle was counter-rotated to its normal position to allow reperfusion for 4h. Left testes of each animal were excised 240min after beginning of reperfusion. Oxidative stress markers (TAS, TOS, SOD, and MDA) and apoptotic pathways (Caspase 3, Caspase 8, Caspase 9, Bcl-2, and Bax,) were assessed by ELISA methods. Also, testicles were subjected to the histopathologic and ultrasound examinations. Ultrasound imaging showed that edaravone reduced the surface area and increased vascularization in testicles with T/D (p<0.0001, p<0.05, respectively). Edaravone pretreatment markedly decreased the levels of MDA, TOS, Bcl-2, Bax, Caspase 3, Caspase 8, and Caspase 9 (p<0.0001). Also, it increased significantly TAS levels (p<0.0001) and reduced insignificantly SOD activity. Histopathologic examinations demonstrated that edaravone significantly attenuated the histological damage caused by T/D in testicles. Taken together, the findings indicate that pretreatment of edaravone has protective effect against testicular T/D injury.