Electrophysiological, histopathological, and biochemical evaluation of the protective effect of probiotic supplementation against pentylenetetrazole-induced seizures in rats.

BACKGROUND AND PURPOSE: Research on the relationship between the gut microbiome and epilepsy is accumulating. The present study was conducted to evaluate the effect of probiotic supplementation on pentylenetetrazole (PTZ)-induced seizures in rats. METHODS: Twenty-one adult male Wistar albino rats were included. The animals were divided into three groups of seven rats. Group 1 was a control group, whereas Group 2 rats received PTZ treatment and Group 3 rats had PTZ+PB (probiotic) treatment. For 6 weeks, Groups 1 and 2 were given saline (1 ml), whereas Group 3 had probiotic supplement. In the 5th week, tripolar electrodes were attached to the rats. Electrophysiological, behavioral, biochemical, and immunohistochemical evaluations were performed in the 6 weeks after the treatment. RESULTS: PB treatment significantly reduced seizures. In the PTZ group, expression levels of brain-derived neurotrophic factor, nerve growth factor (NGF), and Sox2 (SRY sex-determining region Y-box 2) in rat brains decreased significantly compared to the control group, whereas the expression levels of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), total oxidant status (TOS), and nitric oxide (NO) levels increased. In the PTZ+PB group, NGF expression increased significantly compared to the PTZ group, whereas TNF-α, IL-6, TOS, and NO levels decreased. In histopathological examination, an abundance of necrotic neurons was notable in the PTZ group, which was less in the PTZ+PB group. In addition, body weight of the group supplemented with probiotics decreased after the treatment. CONCLUSIONS: Our results suggest that probiotic supplementation may alleviate seizure severity and exert neuroprotective effects by reducing neuroinflammation and oxidative stress and altering the expression of neurotrophins in epileptogenic brains.

Therapeutic effect of thymoquinone on brain damage caused by nonylphenol exposure in rats.

Nonylphenol (NP), causes various harmful effects such as cognitive impairment and neurotoxicity. Thymoquinone (TQ), has antioxidant, anti-inflammatory, and neuroprotective properties. In this study, our aim is to investigate the effects of TQ on the brain damage caused by NP. Corn oil was applied to the control group. NP (100 mg/kg/day) was administered to the NP and NP + TQ groups for 21 days. TQ (5 mg/kg/day) was administered to the NP + TQ and TQ groups for 7 after 21 days. At the end of the experiment, the new object recognition test was applied to the rats and the rats were killed and their brain tissues were removed. Sections taken from brain tissues were stained with hematoxylin-eosin for histopathological evaluation. In addition, neuronal nuclei (NeuN), glial fibrillary acidic protein (GFAP), Cas-3, and nerve growth factor (NGF) immunoreactivities were evaluated in brain tissue sections. In addition, malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) activities were determined. Comet assay was applied to determine DNA damage in cells. The results of our study showed that NP, caused behavioral disorders and damage to the cerebral cortex in rats. This damage in the form of neuron degeneration seen in the cortex was associated with apoptosis involving Cas-3 activation, increased DNA damage, and free oxygen radicals. NP, SOD, and CAT caused a decrease in enzyme activities. In addition, the cellular protein NeuN was decreased, astrocytosis-associated GFAP was increased, and growth factor NGF was decreased. When all our evaluations are taken together, treatment with TQ showed an ameliorative effect on the behavioral impairment and brain damage caused by NP exposure.

The prolonged effect of Kinesio Taping on joint torque and muscle activity.

PURPOSE: Although Kinesio Taping has been extensively used, evidence about the effect of Kinesio Taping is still insufficient. The aim is to determine the effect of Kinesio Taping on elbow joint torque and muscle activity in time and frequency domains. MATERIALS AND METHODS: Thirty-eight healthy subjects were (27 females and 11 males) randomly divided into control and Kinesio Taping groups. Kinesio Taping was applied over biceps brachii muscle in Kinesio Taping group, whereas no taping was applied to control group. Maximum elbow joint torque and electromyography activity in time and frequency domains were assessed during maximum isometric contraction of biceps brachii muscle at baseline, after 10 min, 30 min, and 24 h. Repeated measure ANOVA and mixed ANOVA tests were used for in-group and between-group comparisons, respectively. RESULTS: Elbow joint torques among four assessment sessions were statistically altered in Kinesio Taping group and greater in Kinesio Taping group than in control group (F(3,57)= 3.317, p = 0.026, ηp2 = 0.149; F(3,108)=3.325, p = 0.022, ηp2 = 0.085; respectively). No difference was found in time domain muscle activity among assessment sessions in each group and comparison of groups (p > 0.05). Low-gamma band activity was changed among assessment sessions in Kinesio Taping group (F(3,57)= 6.946, p < 0.001, ηp2 = 0.268) while group × time interaction was not determined. CONCLUSIONS: Kinesio Taping may influence joint torque of elbow more than without Kinesio Taping condition in 24th hour but the interpretation of this effect as a muscle strength enhancement compared with baseline can be arguable. Even if Kinesio Taping could not affect muscle activity in time domain, low-gamma band activity which is closely related to somatosensorial input may reach highest magnitude 24 h after Kinesio Taping.

Probiotic supplementation alleviates absence seizures and anxiety- and depression-like behavior in WAG/Rij rat by increasing neurotrophic factors and decreasing proinflammatory cytokines.

AIM: Epilepsy is one of the most common chronic brain disorders that affect millions of people worldwide. In the present study, we investigated the effects of probiotic supplementation on absence epilepsy and anxiety-and depression-like behavior in WAG/Rij rats. MATERIAL AND METHOD: Fourteen male WAG/Rij rats (absence-epileptic) and seven male Wistar rats (nonepileptic) were used. The effects of probiotic VSL#3 (12.86 bn living bacteria/kg/day for 30 day/gavage) on absence seizures, and related psychiatric comorbidities were evaluated in WAG/Rij rats. Anxiety-like behavior was evaluated by the open-field test and depression-like behavior by the forced swimming test. In addition, the brain tissues of rats were evaluated histopathologically for nerve growth factor [NGF], brain-derived neurotrophic factor [BDNF], SRY sex-determining region Y-box 2 [SOX2] and biochemically for nitric oxide [NO], tumor necrosis factor-alpha [TNF-α] ,and Interleukin-6 [IL-6]. RESULTS: Compared to Wistar rats, WAG/Rij rats exhibited anxiety- and depression-like behavior, and had lower BDNF, NGF and SOX2 immunoreactivity, and higher TNF-α, IL-6 levels in brain tissue. VSL#3 supplementation reduced the duration and number of spike-wave discharges (SWDs) and exhibited anxiolytic or anti-depressive effect. VSL#3 supplement also increased the NGF immunoreactivity while decreasing IL-6, TNF-α and NO levels in WAG/Rij rat brain. CONCLUSION: The findings of the present study showed that neurotrophins, SOX2 deficiency, and pro-inflammatory cytokines may play a role in the pathogenesis of absence epilepsy. Our data support the hypothesis that the probiotics have anti-inflammatory effect. The present study is the first to show the positive effects of probiotic bacteria on absence seizures and anxiety- and depression-like behavior.

Chloroquine attenuates chronic hypoxia-induced testicular damage via suppressing endoplasmic reticulum stress and apoptosis in experimental rat model.

Chronic hypoxia negatively affects male fertility by causing pathological changes in male reproductive system. However, underlying mechanisms of this damage are unknown. Chloroquine (CLQ) is an anti-inflammatory agent that is widely used in the treatment of inflammation-related diseases such as malaria and rheumatoid arthritis. This study aimed to investigate the therapeutic effects of CLQ in the hypoxia-induced testicular damage via assessment of hypoxic response, endoplasmic reticulum stress and apoptosis. For this purpose, 32 Wistar albino rats were divided into 4 groups as control (given 20%-21% O2 , no treatment), CLQ (given 50 mg/kg and 20%-21% O2 for 28 days), hypoxia (HX) (given 10% O2 for 28 days) and HX + CLQ (given 50 mg/kg and 10% O2 for 28 days). After the experiment, blood samples and testicular tissues were taken. Histopathological evaluation was performed on testicular tissues and hypoxia-inducible factor 1-α (HIF1-α), heat shock proteins (HSPs) HSP70, HSP90 and growth arrest and DNA damage-inducible gene 153 (GADD153) expression levels were detected via immunohistochemistry. Moreover, apoptotic cells were detected via terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) staining and serum testosterone levels were determined by enzyme-linked immunosorbent assay (ELISA) assay. Histopathological changes, apoptotic cell numbers and HIF1-α, HSP70, HSP90 and GADD153 expressions significantly increased in HX group (P < .05). Moreover, serum testosterone levels decreased in this group (P > .05). However, CLQ exerted a strong ameliorative effect on all parameters in HX + CLQ group. According to our results, we suggested that CLQ can be considered as an alternative protective agent for eliminating the negative effects of hypoxic conditions on male fertility.

Thymoquinone attenuates doxorubicin-cardiotoxicity in rats.

Contrary to the fact that doxorubicin is a powerful chemotherapeutic agent for the treatment of neoplastic diseases, cardiotoxicity is too important to be ignored. Thymoquinone serves as a powerful free radical scavenger. In the study, the effects of thymoquinone against doxorubicin-cardiotoxicity will be evaluated. Forty rats were divided into five groups. Group I: control group (n = 8); group II: olive oil group (n = 8); group III: thymoquinone group (n = 8); given 10 mg/kg thymoquinone intraperitoneally per day throughout the experiment; group IV: doxorubicin group (n = 8); injected with a single dose of 15 mg/kg ip doxorubicin on the 7th day of the experiment; group V: doxorubicin + thymoquinone group (n = 8); administered with 10 mg/kg thymoquinone per day during the experiment and 15 mg/kg doxorubicin ip on the 7th day. The experiment was planned for 14 days. Immunohistochemically, heat shock protein (HSP) 70 and HSP90, glucose-regulated protein 78 (GRP78), caspase-3 were stained. We made terminal deoxynucleotidyl transferase dUTP nick end labeling for apoptotic evaluation. Total oxidant status (TOS) levels and total antioxidant status (TAS) were measured in the heart tissue. Atrial natriuretic peptide (ANP) and pro-B type natriuretic peptide (proBNP) were evaluated. In the study, HSP70, HSP90, GRP78, and caspase-3 levels increased in group IV. TOS and TAS levels were significant compared to group I. Doxorubicin significantly increased ANP and NT-proBNP levels. Thymoquinone revealed significant differences in these values. Thymoquinone can be an important cardioprotective agent against doxorubicin-cardiotoxicity.

Thymoquinone has a neuroprotective effect against inflammation, oxidative stress, and endoplasmic reticulum stress in the brain cortex, medulla, and hippocampus due to doxorubicin.

Although doxorubicin (DOX) is used in many cancer treatments, it causes neurotoxicity. In this study, the effect of thymoquinone (THQ), a powerful antioxidant, on DOX-induced neurotoxicity was evaluated. In total, 40 rats were used and 5 groups were formed. Group I: control group (n = 8); Group II: olive oil group (n = 8); Group III: the THQ group (n = 8); THQ 10 mg/kg per day was given intraperitoneally (i.p.) throughout the experiment; group IV: DOX group (n = 8); On Day 7 of the experiment, a single dose of 15 mg/kg intraperitoneally DOX injected; group V: DOX + THQ group (n = 8); Throughout the experiment, 10 mg/kg THQ per day and intraperitoneally 15 mg/kg DOX on Day 7 were injected. Immunohistochemically, tumor necrosis factor-α (TNF-α), interleukin-17 (IL-17), hypoxia-inducible factor 1α (HIF1-α), glucose regulatory protein 78 (GRP78), and the gene inducible by growth arrest and DNA damage 153 (GADD153) proteins were evaluated in the brain cortex, medulla, and hippocampus regions. Total oxidant status (TOS) levels and total antioxidant status (TAS) in the brain tissue were measured. TNF-α, IL-17, HIF1-α, GRP78, and GADD153 immunoreactivities significantly increased in the DOX group in the study. THQ significantly reduced these values. THQ increased the TAS level significantly and decreased the TOS level significantly compared to the DOX group. THQ may play a role as a neuroprotective agent in DOX-induced neurotoxicity in the cortex, medulla, and hippocampus regions of the brain.

Assessment of the protective and therapeutic effect of melatonin against thioacetamide-induced acute liver damage.

Acute or chronic damage to the liver may occur through alcohol, drugs, viruses, genetic disorders, and toxicity. In this study, we planned to investigate the protective and therapeutic effects of melatonin (Mel) by causing damage to the liver with thioacetamide (TAA). Thirty-five rats were used. Group I: control group (seven pieces), group II: Mel group (seven pieces) the single dose on the first day of the experiment was 10 mg/kg, group III: TAA (seven pieces) 300 mg/kg with 24-hour intervals, two doses, group IV: Mel + TAA group (seven pieces) 10 mg/kg single dose Mel was applied 24 hours before TAA application, group V: TAA + Mel group (seven pieces) single dose (24th hour) of 10 mg/kg Mel was administered after TAA (300 mg/kg) two doses. The liver histology was evaluated. Apoptosis, autophagy, and necrosis markers in tissue were determined by immunohistochemistry. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP) levels in blood serum samples and transforming growth factor-ß (TGF-ß) and tumor necrosis factor-α (TNF-α) levels were determined in liver tissue. TAA affected histologically the classical lobule structure both in cell cords and sinusoids. Caspase-3, RIP3, and LC3 levels were increased in group III compared with the control group. TAA did not cause a statistically significant change in TNF-α level but decreased the TGF-ß level significantly. AST and ALT levels were statistically significant in group II and V compared with group I, the ALP level was significant in group IV compared with group II. The results of this study showed that TAA caused significant damage to tissues and increased cell death, Mel was found to have more therapeutic than the protective effect on tissues.

Direct Validation of Model-Predicted Muscle Forces in the Cat Hindlimb During Locomotion.

Various methods are available for simulating the movement patterns of musculoskeletal systems and determining individual muscle forces, but the results obtained from these methods have not been rigorously validated against experiment. The aim of this study was to compare model predictions of muscle force derived for a cat hindlimb during locomotion against direct measurements of muscle force obtained in vivo. The cat hindlimb was represented as a 5-segment, 13-degrees-of-freedom (DOF), articulated linkage actuated by 25 Hill-type muscle-tendon units (MTUs). Individual muscle forces were determined by combining gait data with two widely used computational methods-static optimization and computed muscle control (CMC)-available in opensim, an open-source musculoskeletal modeling and simulation environment. The forces developed by the soleus, medial gastrocnemius (MG), and tibialis anterior muscles during free locomotion were measured using buckle transducers attached to the tendons. Muscle electromyographic activity and MTU length changes were also measured and compared against the corresponding data predicted by the model. Model-predicted muscle forces, activation levels, and MTU length changes were consistent with the corresponding quantities obtained from experiment. The calculated values of muscle force obtained from static optimization agreed more closely with experiment than those derived from CMC.

Investigation of the effect of Myricetin on Cisplatin-induced liver hepatotoxicity.

OBJECTIVE: Cisplatin, a widely used anticancer agent, induces hepatotoxicity alongside organ damage. Understanding Cisplatin's toxicity mechanism and developing preventive measures are crucial. Our study explores Myricetin, a flavonoid, for its protective effects against Cisplatin-induced hepatotoxicity. METHODS: In our study, a total of 32 Wistar albino male rats were utilized, which were categorized into four distinct groups: Control, Myricetin, Cisplatin, and Myricetin+Cisplatin. For the histological assessment of hepatic tissues, hematoxylin-eosin and periodic acid Schiff staining were employed, alongside immunohistochemical measurements of TNF-α, interleukin-17, and interleukin-6 immunoreactivity. Additionally, aspartate transaminase and alanine transaminase values were examined by biochemical analysis. RESULTS: In the histological evaluation of the tissues, a normal healthy cell structure and a strong periodic acid Schiff (+) reaction were observed in the hepatocyte cells in the tissues of the Control and Myricetin groups, while intense eosinophilia, minimal vacuolization, congestion, and sinusoidal expansions were observed in the hematoxylin-eosin stainings, and a decrease in the positive reaction in the periodic acid Schiff staining was observed in the Cisplatin group. Consistent with these histological findings, an increase in TNF-α, interleukin-17, and interleukin-6 expressions (p<0.0001) and a concomitant increase in aspartate transaminase and alanine transaminase values were observed in the Cisplatin group. In the group protected by Myricetin, a significant improvement was observed in all these histological and biochemical values. CONCLUSION: Cisplatin induces notable histopathological alterations in the liver. In this context, Myricetin exhibits the potential to alleviate Cisplatin-induced damage by modulating histological parameters and biochemical processes.

The effect of papaverine on tendon healing and adhesion in rats following Achilles tendon repair.

OBJECTIVES: The study aimed to examine the histopathological and biomechanical effects of papaverine administered intraperitoneally and locally on Achilles tendon healing in a rat model. MATERIALS AND METHODS: Forty-eight adult male Sprague-Dawley rats (range, 300 to 400 g) were used in this study conducted between October and November 2022. The rats were divided into three groups, with each group further subdivided into two for sacrifice on either the 15th (early period) or 30th (late period) day after surgery. The first (control) group received no treatment following Achilles tendon repair, while papaverine was intraperitoneally administered every other day for 10 days in the second group and locally in the third group after surgery. On the 15th and 30th days, the rats were sacrificed, and their Achilles tendons were subjected to biomechanical testing and histopathological evaluation. RESULTS: Histopathologically, there were no significant differences among the groups on the 15th day. However, on the 30th day, the locally applied papaverine group exhibited superior histopathological outcomes compared to the control group (p<0.05). Concerning the highest tensile strength values before rupture, the biomechanical assessment showed that the group receiving local papaverine treatment in the early period and both the group with systemic papaverine treatment and the one with local papaverine treatment in the late period displayed a statistically significant advantage compared to the control group (p<0.05). CONCLUSION: Locally administered papaverine has positive biomechanical effects in the early period and exhibits a positive correlation both histopathologically and biomechanically in the late period. Novel therapeutic options may be provided for patients through these findings.

Effect of vitamin B12 on methotrexate-induced cardiotoxicity in rats.

Objectives: Methotrexate (MTX) is a drug with anti-inflammatory and immunosuppressive effects and is also a folic acid antagonist. Our aim in this study is to determine the molecular mechanisms of cardiotoxicity caused by MTX, a chemotherapeutic drug, and to evaluate the protective effects of vitamin B12 on this toxicity. Materials and Methods: A total of 32 rats were used in our study and 4 groups were formed. Control group, Vit B12 group (3 µg/kg B12 for 15 days, IP), MTX group (20 mg/kg MTX single dose on day 8 of the experiment, IP), MTX +Vit B12 group (3 µg/kg, IP ), Vit B12 throughout the 15 days, and a single dose of 20 mg/kg MTX (IP) on day 8 of the experiment. Immunohistochemically, expressions of hypoxia-inducible factor 1α (HIF1-α), vascular endothelial growth factor receptor-2 (VEGFR-2), erythropoietin (EPO), and interleukin-6 (IL-6) were evaluated in the heart tissue. Total catalase (CAT), superoxide dismutase (SOD), and malondialdehyde (MDA) levels were measured in the heart tissue. At the same time, ANP and NT-proBNP levels were measured in the blood serum. Results: In the study, the expression of HIF1-α and VEGFR-2 increased significantly in the MTX group, while IL-6 and EPO significantly decreased. At the same time, CAT and SOD levels were significantly decreased and MDA levels increased significantly in the MTX group. While vitamin B12 significantly corrected all these values, it also greatly reduced the increases in ANP and NT-proBNP levels caused by MTX. Conclusion: It is important to use Vit B12 before and after MTX administration to replace the folate that MTX has reduced.

Diffusion tensor imaging: survival analysis prediction in breast cancer patients.

PURPOSE: We aimed to explore the performance of diffusion-tensor imaging (DTI) and apparent diffusion coefficient (ADC) parameters in evaluating disease-free survival (DFS) and overall survival (OS) in patients with invasive breast cancer. MATERIAL AND METHODS: A total of 49 women with invasive breast cancer who were diagnosed between 2017 and 2022 were included. All patients underwent breast magnetic resonance imaging (MRI) with DTI and diffusion-weighted imaging (DWI) features, with examiners blinded to the clinical data. Volume anisotropy (VA), fractional anisotropy (FA), and ADC values were measured to assess intratumoral measured heterogeneity. Correlations and differences in diffusion metrics according to OS and DFS status of the cases were analyzed. The discriminative ability of the quantitative findings was assessed by receiver operating characteristic (ROC) curve analyses and validated in the independent cohort. RESULTS: We evaluated patients with metastases (n = 13, 36.5%) and those without metastases (n = 36, 73.5%). Differences in the ADC, FA, and VA values were observed. The results of Cox regression survival analysis for all the patients included in the survival analysis revealed that DTI metrics contributed to the prediction of overall survival (OS) in the emerging models (p < 0.05). Both FA and VA were associated with OS (p = 0.037 and p = 0.038, respectively). However, ADC was not associated with OS (p = 0.177) or DFS (p = 0.252). CONCLUSION: To the best of our knowledge, this is the first study to assess the prognostic value of DTI-MRI in breast cancer with statistical survival analysis techniques. We believe that DTI measurements can be used as a biomarker for OS analysis in breast cancer given the available data.

Gastric Teratoma in an Adult Female Patient: A Case Report.

BACKGROUND: Gastric teratoma (GT) occurs as a rule in infancy and is an extremely unusual gastric tumor in adult patients. CASE PRESENTATION: In this paper, we present the clinical and imaging findings of a 56-year-old female patient with a GT. The patient's main symptoms were increasing abdominal discomfort and pain. After the physical examination, she underwent ultrasound (US) and computed tomography (CT), which showed a large mass at the posterior wall of the stomach, and a teratoma was initially considered. After surgery, pathology confirmed the diagnosis of GT. The patient recovered after surgery and was discharged in good health. To the best of our knowledge, this study is the first reported case of gastric teratoma in an adult woman in the literature. CONCLUSION: Gastric teratoma of the adult period is a rare benign neoplasm that may have several complications; therefore, imaging is crucial for diagnosis and accurate treatment management. The aim of this study is to emphasize the value of US and CT in the diagnosis and treatment monitoring of mature gastric teratomas.

Machine learning-based prediction of joint moments based on kinematics in patients with cerebral palsy.

Joint moments during gait provide valuable information for clinical decision-making in patients with cerebral palsy (CP). Joint moments are calculated based on ground reaction forces (GRF) using inverse dynamics models. Obtaining GRF from patients with CP is challenging. Typically developed (TD) individuals' joint moments were predicted from joint angles using machine learning, but no such study has been conducted on patients with CP. Accordingly, we aimed to predict the dorsi-plantar flexion, knee flexion-extension, hip flexion-extension, and hip adduction-abduction moments based on the trunk, pelvis, hip, knee, and ankle kinematics during gait in patients with CP and TD individuals using one-dimensional convolutional neural networks (CNN). The anonymized retrospective gait data of 329 TD (26 years ± 14, mass: 70 kg ± 15, height: 167 cm ± 89) and 917 CP (17 years ± 9, mass:47 kg ± 19, height:153 cm ± 36) individuals were evaluated and after applying inclusion-exclusion criteria, 132 TD and 622 CP patients with spastic diplegia were selected. We trained specific CNN models and evaluated their performance using isolated test subject groups based on normalized root mean square error (nRMSE) and Pearson correlation coefficient (PCC). Joint moments were predicted with nRMSE between 18.02% and 13.58% for the CP and between 12.55% and 8.58% for the TD groups, whereas with PCC between 0.85 and 0.93 for the CP and between 0.94 and 0.98 for the TD groups. Machine learning-based joint moment prediction from kinematics could replace conventional moment calculation in CP patients in the future, but the current level of prediction errors restricts its use for clinical decision-making today.

Quinoa (Chenopodium quinoa Willd.) supplemented cafeteria diet ameliorates glucose intolerance in rats.

Quinoa (Chenopodium quinoa Willd.) is a pseudocereal with rich nutritional composition, gluten free, and organoleptic. The primary aim of this study was to elucidate the possible protective roles of quinoa in glucose homeostasis in a model of cafeteria diet-induced obesity. Male Wistar rats (3 weeks of age) were randomly allocated to be fed by; control chow (CON; n = 6), quinoa (QUI; n = 6), cafeteria (CAF; n = 6), or quinoa and cafeteria (CAFQ; n = 6) for 15 weeks. CAFQ resulted in decreased saturated fat, sugar, and sodium intake in comparison with CAF. Compared to CON, CAF increased body weight gain, plasma insulin, plasma glucose, decreased liver IRS-1, AMPK mRNA expressions, and pancreatic ß-cell insulin immunoreactivity, and developed hepatocyte degeneration and microvesicular steatosis. Compared to CAF, QUI lowered body weight, plasma glucose, and plasma insulin, increased liver IRS-1 and AMPK mRNA expressions, and pancreatic ß-cell insulin immunoreactivity. Compared to CAF, CAFQ lowered plasma glucose, increased liver IRS-1 mRNA expressions, increased pancreatic ß-cell insulin immunoreactivity, and lowered hepatocyte degeneration and microvesicular steatosis. Dietary treatments did not influence IRS-2, AKT2, and INSR mRNA expressions. HOMA-IR, HOMA-ß, and QUICKI were also similar between groups. Restoration of insulin in CAFQ islets was as well as that of CON and QUI groups. In conclusion, as a functional food, quinoa may be useful in the prevention of obesity and associated metabolic outcomes such as glucose intolerance, disrupted pancreatic ß-cell function, hepatic insulin resistance, and lipid accumulation.

Evaluation of histologic, antiapoptotic and antioxidant effects of melatonin against the acute ocular toxicity of Cisplatin.

This study aimed to investigate the protective effect of melatonin against the acute toxicity of cisplatin in ocular tissues. The eyes of 40 rats were divided into 4 groups: Control group (10 rats), Melatonin (Mel) group (10 rats), Cisplatin (Cis) group (10 rats), Melatonin (Mel) + Cisplatin (Cis) group (10 rats). Retina, cornea, and ciliary body tissues were examined after hematoxylin-eosin staining of sections obtained from the eyes and were scored for disorganization and degeneration. Apoptotic cells were counted for the retina, cornea, and ciliary body with the TUNEL (Terminal deoxynucleotidyl transferase dUTP nick end labeling) method. The total antioxidant status (TAS) / total oxidant status (TOS) of homogenized eye tissues were measured. While apoptotic cells were found to increase in the cornea of the Cisplatin (Cis) group, no difference was found regarding the retina and ciliary body cell count. An increased number of apoptotic cells in the cornea of the Cis group was found while there was a decrease in the group where Cisplatin and Melatonin were administered together (Mel+Cis group). There was no statistically significant difference amongst groups for TOS or TAS. Melatonin had a partial protective effect against histological damage.

Thymoquinone regulates nitric oxide synthase enzymes and receptor-interacting serine-threonine kinases in isoproterenol-induced myocardial infarcted rats.

This study aims to investigate the protective effects of thymoquinone (THQ) in isoproterenol (ISO)-induced myocardial infarction (MI) in rats. Thirty-two rats were divided into four equal groups. Control, THQ; Intragastric(ig) by dissolved 20 mg/kg in 500 µl olive oil at 24-h intervals for 7 days, ISO; On the 6th and 7th days of the experiment, it was dissolved in 1 ml distilled water, 100 mg/kg, subcutaneously(sb), THQ + ISO; THQ was given 20 mg/kg at 24-h intervals for 7 days, 100 mg/kg was given on days 6 and 7 of the ISO experiment. At the end of the experiment, blood and heart tissues were taken and histological, Western blot and biochemical analyzes were performed. In the ISO group, cardiomyocyte damage and large necrotic areas were observed. While neuronal nitric oxide synthase (nNOS) decreased, inducible NOS (iNOS) and endothelial NOS (eNOS) expression increased. Receptor-interacting serine-threonine kinase (RIP/RIPK) RIP1 and RIP3 protein levels were increased. Lactate dehydrogenase (LDH), creatin-kinase (CK-MB) and cardiac troponin I (cTn-I) levels were increased. Atrial natriuretic peptide (ANP) and N-terminal pro-brain natriuretic peptide (NT-proBNP) levels were decreased. THQ caused the reduction of necrotic areas caused by ISO. NOS regulated enzyme levels. Increased ISO-induced decreased RIP1 and RIP3 expressions. THQ regulated the biochemical parameter levels. ISO triggers MI-induced necrosis through NOS enzymes by causing severe histological changes in heart tissue. THQ, on the other hand, reveals that it can be an important antinecrotic agent in the prevention of MI-induced damage by regulating both NOS enzyme levels and necrosis markers.

Thymoquinone alleviates doxorubicin induced acute kidney injury by decreasing endoplasmic reticulum stress, inflammation and apoptosis.

Doxorubicin (DOX) is used as an anticancer drug despite its many side effects. Thymoquinone (THQ) is a plant-derived substance that exhibits antioxidant and anti-inflammatory properties. We investigated the protective effects of THQ on DOX induced nephrotoxicity in rats. Rats were divided into five groups of eight: group 1, untreated control; group 2, olive oil group given olive oil intraperitoneally (i.p.) for 14 days; group 3, THQ group given 10 mg/kg THQ i.p. for 14 days; group 4, DOX group given a single dose of 15 mg/kg DOX i.p. on day 7 of experiment; group 5, DOX + THQ given 10 mg/kg THQ i.p. for 14 days and 15 mg/kg DOX i.p. on day 7. Kidney tissues were evaluated for histopathology. Caspase-3, IL-17, GRP78 and TNF-α immunostaining was used to determine the expression levels of these proteins among the groups. The TUNEL method was used to determine the apoptotic index. Total antioxidant status (TAS), total oxidant status (TOS), and TNF-α and TGF-ß1 levels in kidney tissue were measured using ELISA assay. Histopathologic damage, caspase-3, IL-17, GRP78 and TNF-α immunoreactivity, TUNEL positive cells, TOS, TNF-α and TGF-ß1 levels were increased in group 4 compared to group 1. The TAS of group 4 decreased compared to group 1. We found decreased caspase-3, IL-17, GRP78 and TNF-α expressions and TUNEL positive cells in group 5 compared to group 4. In rats given DOX, THQ reduced kidney damage by suppressing endoplasmic reticulum stress, inflammation and apoptosis pathways.

Effects of probiotic supplementation on very low dose AFB1-induced neurotoxicity in adult male rats.

AIMS: Aflatoxin B1 (AFB1) is the most toxic and common form of AF found in food and feed. Although AFB1 exposure has toxic effects on many organs, studies on the brain are limited. Moreover, to the best of our knowledge, there is no study on the effect of probiotics on AFB1-induced neurotoxicity. Therefore, we aimed to evaluate the possible effects of probiotics on AFB1-induced neurotoxicity in the brain. MAIN METHODS: Thirty-two adult male Wistar rats were divided into four groups: Vehicle (VEH), Probiotic (PRO) (2.5 × 1010 CFU/day VSL#3, orally), Aflatoxin B1 (AFB1) (25 µg/kg/week AFB1, orally), and Aflatoxin B1 + Probiotic (AFB1 + PRO) (2.5 × 1010 CFU/day VSL#3 + 25 µg/kg/week AFB1, orally). At the end of eight weeks, rats were behaviorally evaluated by the open field test, novel object recognition test, and forced swim test. Then, oxidative stress and inflammatory markers in brain tissues were analyzed. Next, brain sections were processed for Hematoxylin&Eosin staining and NeuN and GFAP immunostaining. KEY FINDINGS: Probiotic supplementation tended to decrease oxidative stress and inflammatory markers compared to the AFB1 group. Besides, brain tissues had more normal histological structures in VEH, PRO, and AFB1 + PRO groups than in the AFB1 group. Moreover, in probiotic groups, GFAP immunoreactivity intensity was decreased, while NeuN-positive cell number increased in brain tissues compared to the AFB1 group. SIGNIFICANCE: Probiotics seem to be effective at reducing the neurotoxic effects of AFB1. Thus, our study suggested that especially Bifidobacterium and Lactobacillus species can improve AFB1-induced neurotoxicity with their antioxidant and anti-inflammatory effects.