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Aims and Objectives: Honey possesses specific anti-inflammatory properties. We evaluated the effects of oral honey supplementation on skeletal muscle-related inflammatory markers among military graduates after overtraining., Methods: This randomized double-blind controlled trial was conducted on 42 overtrained military graduates who were randomly assigned to receive either honey supplementation (5 mL of 12% honey solution twice daily for 6 weeks) or a placebo for 6 weeks. In our study, we utilized Milk Vetch Sahand honey as the intervention. Serum levels of C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), aldolase A, and creatine kinase (CK) were evaluated using the enzyme-linked immunosorbent assay method before and after the intervention., Results: A total of 21 male participants with a mean age of 20.75 years were included in each group. No significant differences were found between the groups in the pre-intervention assessment of inflammatory biomarkers. However, in the post-intervention assessment, participants who received honey exhibited significantly smaller increases in CRP ( p  < 0.001), TNF-α ( p  = 0.001), aldolase A ( p  < 0.001), and CK levels ( p  < 0.001) compared to the controls. The mean changes in these biomarkers were notably lower in the honey group indicating a potential anti-inflammatory effect of honey., Conclusion: This study demonstrates that honey supplementation significantly reduces inflammatory biomarkers such as TNF-α, CRP, aldolase A, and CK in military graduates experiencing overtraining, underscoring its potential to alleviate inflammation associated with intense physical training. To confirm and extend these findings, further research with larger sample sizes and longer follow-up periods is recommended., Competing Interests: All authors contributed to the writing and reviewing of this paper. No conflicts of interest are detected., (© 2025 The Author(s). Health Science Reports published by Wiley Periodicals LLC.)

Introduction: Migraine, a common disorder marked by severe and repetitive headaches, has been linked to the involvement of the NMDA receptor (NMDAR), a receptor responsible for glutamate signaling. Moringa oleifera (M. oleifera), recognized for its anti-inflammatory properties and therapeutic potential in various conditions, has been investigated. This study aims to assess the efficacy and precise mechanisms of M. oleifera for the treatment of migraine, for which evidence is limited., Methods: Rats were stratified into four distinct groups. The control group did not undergo the migraine-induction protocol. Post-induction, the "sumatriptan" group was administered sumatriptan injections, the "treatment" group received oral M. oleifera extract, and the "vehicle" group was provided with oral solvent treatment. Behavioral evaluations encompassing Von Frey's and hot plate assessments, in addition to qPCR analysis targeting Nr2a, Nr2b, Bax, Bcl-2, and Caspase-3, were conducted., Results: Von Fery's and hot plate tests revealed a notable decrease in triggering pressure and temperature within the vehicle group when compared to the other groups (both ps < 0.001). The Nr2a expression levels in both the vehicle and treatment cohorts exhibited significantly higher values than those observed in the control group (p < 0.001, p = 0.001) and the sumatriptan group (p < 0.001, p = 0.002). Conversely, no substantial alterations in Nr2b or Bcl-2 expression levels were observed across the study groups (p = 0.404, p = 0.976). Notably, heightened expressions of Caspase-3 and Bax were evident in the vehicle group relative to the other groups (p = 0.013, p = 0.010)., Conclusions: Moringa oleifera extract appears to mitigate symptoms of migraine by inhibiting apoptosis, suggesting potential efficacy in migraine treatment; however, additional research investigating a wider range of pathways is necessary., Clinical Trial Number: Not applicable., Competing Interests: Declarations. Ethics approval and consent to participate: The entire experimental protocol adhered to the guidelines set forth by the National Institutes of Health (NIH) [22] and was approved by the Ethics Committee of AJA University of Medical Sciences (Ethics code: IR.AJAUMS.REC.1401.040). We confirm that the animals used in this study were not privately owned by another institution, individual, or farm. They were obtained from an established laboratory animal facility for research purposes Consent for publication: All authors declare their consent for the publication of the current manuscript in the journal BMC Neuroscience Competing interests: The authors declare no competing interests., (© 2025. The Author(s).)

Background : Aluminum phosphide (AlP) poisoning is prevalent in numerous countries, resulting in high mortality rates. Phosphine gas, the primary agent responsible for AlP poisoning, exerts detrimental effects on various organs, notably the heart, liver and kidneys. Numerous studies have documented the advantageous impact of Coenzyme Q 10 (CoQ 10 ) in mitigating hepatic injuries. The objective of this investigation is to explore the potential protective efficacy of CoQ 10 against hepatic toxicity arising from AlP poisoning. Method : The study encompassed distinct groups receiving almond oil, normal saline, exclusive CoQ 10 (at a dosage of 100 mg/kg), AlP at 12 mg/kg; LD 50 (lethal dose for 50%), and four groups subjected to AlP along with CoQ 10 administration (post-AlP gavage). CoQ 10 was administered at 10, 50, and 100 mg/kg doses via Intraparietal (ip) injections. After 24 h, liver tissue specimens were scrutinized for mitochondrial complex activities, oxidative stress parameters, and apoptosis as well as biomarkers such as aspartate transaminase (AST) and alanine transaminase (ALT). Results : AlP induced a significant decrease in the activity of mitochondrial complexes I and IV, as well as a reduction in catalase activity, Ferric Reducing Antioxidant Power (FRAP), and Thiol levels. Additionally, AlP significantly elevated oxidative stress levels, indicated by elevated reactive oxygen species (ROS) production, and resulted in the increment of hepatic biomarkers such as AST and ALT. Administration of CoQ 10 led to a substantial improvement in the aforementioned biochemical markers. Furthermore, phosphine exposure resulted in a significant reduction in viable hepatocytes and an increase in apoptosis. Co-treatment with CoQ 10 exhibited a dose-dependent reversal of these observed alterations. Conclusion : CoQ 10 preserved mitochondrial function, consequently mitigating oxidative damage. This preventive action impeded the progression of heart cells toward apoptosis., Competing Interests: Declaration of conflicting interestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Botulinum toxin (Botox) is widely used in beauty industry and its long-term consequences can be a matter of concern. The hippocampal cholinergic system plays a significant role in memory and learning that could be affected by Botulinum toxin. However, to date, the effect of Botox on memory system has been controversial. This survey aimed to examine the effects of Botox on spatial memory, and biochemical and histological parameters of the hippocampus in male rats by using Rivastigmine (R) as a cholinesterase inhibitor that is more selective for the central nervous system (CNS). Thirty-five male Wistar rats (200-250 g) were distributed into seven groups: Sham, Botox A (3, 6, and 15 IU intramascularly) and Botox A (3, 6, and 15 IU) plus Rivastigmine (1 mg/kg intraperitoneally). Spatial memory was assessed in the Morris Water Maze (MWM) 4 weeks later. Moreover, the hippocampal tissue was removed for histopathological and biochemical analyses. Botox significantly impaired memory performance in MWM by increasing escape latency and swim distance and decreasing the time spent in the target zone. Furthermore, in the Botox groups, the level of acetylcholine decreased, while the level of the acetylcholinesterase enzyme increased significantly in the hippocampus. Also, local lesions were observed in the form of degeneration and loss of pyramidal neurons, as well as a decrease in the volume and shrinkage of the cell body and an increase in microglia in the damaged area. Rivastigmine administration alleviated biochemical and histological parameters and partially ameliorated Botox-induced impairments. In summary, rivastigmine could be a suitable protective approach for side effects of Botox in the hippocampus., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)

This study aimed to consider the expression of Nrf2, NLRP3 and caspase 1 genes, as well as oxidative stress, and the protective role of N-acetyl cysteine (NAC) in the liver of rats treated with cadmium (Cd). Male rats were randomly divided into five groups including G1 (control), G2 (single dose of Cd), G3 (continuous dose of Cd), G4 (single dose of Cd + NAC), and G5 (continuous dose of Cd + NAC). Levels of malondialdehyde (MDA) and total antioxidant capacity (TAC) were measured. Expression of Nrf2, NLRP3 and caspase 1 genes was considered using RT-PCR. NAC treatments significantly improved TAC, but decreased MDA values in rats that exposed to continuous dose of Cd (p<0.05). Exposure to continuous dose of Cd caused a significant decrease in Nrf2 expression by 2.46-fold (p<0.001), but enhanced expression of NLRP3 and Caspase 1 genes by 3.13-fold and 3.16-fold), respectively (p<0.001). Compared to rats that treated to continuous dose of Cd, NAC supplementation enhanced the expression of Nrf2 by 1.67-fold (p<0.001) and reduced the expression of NLRP3 and Caspase 1 genes by 1.39-fold (p<0.001) and 1.58-fold (p<0.001), respectively. Down-regulation of Nrf2 and overexpression of NLRP3 and caspase 1 seems to be one of the main mechanisms of Cd toxicity on liver tissue. NAC protects liver tissue against Cd-induced oxidative injuries via enhancement of Nrf2 expression and reduction of NLRP3 and caspase 1 genes.

Introduction: The value of thoracic injury rule out criteria (TIRC) as a tool for decreasing the number of unnecessary chest radiographs in children has not been evaluated yet. Therefore, the present study was designed as a multi-center study to assess the validity of TIRC model in detection of very low risk children for traumatic intrathoracic injuries., Methods: In this diagnostic accuracy study, clinical data and chest radiographs of 974 children less than 18 years of age (72.0% boys) who had presented to 5 hospitals, in Iran in 2018 were assessed. Data gathering and interpretation of radiographs were done by two independent researchers in each hospital. In the end, discriminatory power and calibration of the model was assessed with a 95% confidence interval (95% Cl)., Results: In the present study, age was not a predicting factor of abnormal findings in radiographs of children and adolescents (p=0.75); therefore, it was omitted from TIRC model and pediatric TIRC (pTIRC) was designed. Area under the curve of pTIRC rule was 0.97 (95% CI: 0.96-0.98) for prediction of abnormal chest X-Ray in children and adolescents. The sensitivity and specificity of pTIRC was 100% and 90.1%, respectively. The calibration of this decision rule had great concordance with the perfect line with a slope of 0.99 and intercept of 0.001. There was a 90.1% reduction in the number of unnecessary chest radiographs when using pTIRC decision rule., Conclusion: pTIRC decision rule was introduced in the present study. pTIRC has excellent performance in identification of traumatic intrathoracic injuries and decreasing the number of unnecessary chest radiographs., Competing Interests: There is no conflict of interest.

Objective: To evaluate effects of titanium dioxide /gelatin nanocomposite on wound healing in mice as a model study., Methods: Fifty male rats were randomized into five groups of ten animals each. In group I, 0.1 mL sterile saline 0.9% solution was added to the wounds with no infection. In group II, the wounds were infected with MRSA and only treated with 0.1 mL the sterile saline 0.9% solution. In group III, infected wounds were treated with gelatin. In group IV, animals with infected wounds were treated with 0.1 mL titanium dioxide nanoparticles. In group V, animals with infected wounds were treated with titanium dioxide /gelatin nanocomposite. Wound size was measured on 2, 6, 10, 14, 18 and 20 days after surgery., Results: Reduction in wound area indicated that there was significant difference between group IV and other groups ( p <0.05). Quantitative histological and morphometric studies and mean rank of the qualitative studies demonstrated that there was significant difference between group IV and other groups ( P <0.05)., Conclusion: Titatnium dioxide nanoparticles/gelatin composite offered potential advantages in wound healing acceleration and fibroblast proliferation on early days of healing phases. Acceleration in wound repair could be associated with earlier wound contraction and stability of damaged area by rearrangement of granulation tissue and collagen fibers., Competing Interests: None declared., (© 2019 Trauma Research Center, Shiraz University of Medical Sciences.)

The aim of the present study was to evaluate the acute toxicity as lethal dose 50% (LD 50 ) and sub-acute toxicity of the black caraway Bunium persicum ( Bioss) seed essential oil in male Wistar rats. The compounds of B. persicum were identified by GC/MS and amount of each compound was evaluated. 21 different compounds were determined in the essential oil and the main components were: carvone, p-cymene, gamma-terpinene, p-cymene-8-ol, limonene, isoterpinolene, and 2-beta pinene. For acute toxicity evaluation, the animals were randomly divided into nine group (n = 6) and received 500, 1000, 1500, 2000, 2500, 3000, 3500 and 4000 mg/kg seed essential oil, respectively and the LD 50 value for black caraway seed essential oil was obtained above 4000 mg/kg body weight. According to data, treatment with the black caraway seed essential oil sub-acute toxicity study attenuated histopathological changes in lung, liver, kidney, testes and spleen tissues and the results of this study show that the black caraway essential oil can not affect the immune and blood system, important enzymes and vital organs of the body.., Competing Interests: Animals received animal care, and all the experiments were performed in accordance with the Guidelines of the Institutional Animal Care and Use Committee and were approved by the Animal Ethics Committee of the Faculty of Veterinary Medicine, University of Tehran, Iran (approval No of 7506023.6.17).

Background: Ischaemic heart disease is the main cause of mortality in the world. After myocardial infarction (MI) cardiomyocytes apoptosis and ventricular remodelling have occurred. Apelin is a peptide that has been shown to exert cardioprotective effects., Aim: The aim of this study was to investigate the anti-apoptotic and anti-remodelling effects of [Pyr¹]apelin-13 in the rat model of post-MI., Methods: Thirty-six male Wistar rats were randomly divided into three groups: (1) sham, (2) MI, and (3) MI treated with [Pyr¹] apelin-13 (MI+Apel). MI animals were subjected to 30-min ligation of the left anterior descending coronary artery (LAD) and 14 days of reperfusion. Twenty-four hours after LAD ligation, [Pyr¹]apelin-13 (10 nmol/kg/day, i.p.) was administered for five consecutive days. Hypertrophic parameters, left ventricular (LV) remodelling, and gene expression of Apel, apelin receptor (Apelr), Bax, caspase-3 (Casp-3), and Bcl-2 by real-time polymerase chain reaction and cardiomyocytes apoptosis by TUNEL immunostaining were assessed on day 14 post-MI., Results: Post-infarct treatment with [Pyr¹]apelin-13 improved myocardial hypertrophic and LV remodelling parameters and led to a significant increase in the expression of Apel, Apelr, and Bcl-2, and a decrease in the expression of Bax and Casp-3. Furthermore, treatment with [Pyr¹]apelin-13 decreased cardiomyocyte apoptosis., Conclusions: [Pyr¹]apelin-13 has anti-hypertrophic, anti-remodelling, and anti-apoptotic effects via overexpression of Apel, Apelr, and Bcl-2 and reduces gene expression of Bax and Casp-3 in the infarcted myocardium, which can in turn lead to repair myocardium.

Background: Diabetic nephropathy is a serious complication of T1D (type one diabetes mellitus). Persistent hyperglycemia and subsequent hypomagnesemia is believed to develop kidney damage by activation of oxidative stress. We conducted this study to investigate the renoprotective effect of magnesium sulfate (MgSO4) on renal histopathology and oxidative stress in diabetic rats., Methods: The study included 70 male rats. The animals were divided into seven groups: control (CRL), control receiving MgSO4 (CRL + Mg1 & CRL + Mg8), diabetic (DM1 & DM8) and diabetic receiving MgSO4 (DM + Mg1 & DM + Mg8). Rats were given 20 mg/kg (i.p) Streptozocin (STZ) for 5 consecutive days in (MLD) multiple low doses to induce T1D. At day 10 treatment groups were received MgSO4 (10 g/l) in drinking water, for 1 or 8 weeks. The blood glucose, BUN and creatinine levels were measured. Renal tissue levels of malondialdehyde (MDA) were measured by thiobarbituric acid (TBA) method to evaluate the oxidative stress. Renal histopathology was done using H & E staining method., Results: Treatment with MgSO4 significantly decreased the blood glucose in DM + Mg1 and DM + Mg8 groups as compared with DM1 and DM8. Magnesium treatment also decreased serum BUN and tissue level of MDA significantly in both short and long term treatment. The body weight loss and kidney weight to body weight ratio was improved by MgSO4. Histological results showed there were no differences between DM and DM + Mg groups., Conclusion: Our findings showed that diabetic nephropathy is associated with high blood glucose level and oxidative stress (significant increase in MDA level). The renal dysfunction and oxidative stress can be improved by magnesium sulfate administration. It is suggested that protection against development of diabetic nephropathy by MgSO4 treatment involves changes in the blood glucose and oxidative stress.

Background: Oxidative stress in teratozoospermic semen samples caused poor assisted reproductive techniques (ART) outcomes. Among antioxidants, ascorbic acid is a naturally occurring free radical scavenger and as such its presence assists various other mechanisms in decreasing numerous disruptive free radical processes., Objective: The main goal of this study was to evaluate potential protective effects of ascorbic acid supplementation during in vitro culture of teratozoospermic specimens., Materials and Methods: Teratozoospermic semen samples that collected from 15 volunteers were processed, centrifuged and incubated at 37(o)C until sperm swimmed-up. Supernatant was divided into four groups and incubated at 37(o)C for one hour under different experimental conditions: Control, 10 µm A23187, 600µm ascorbic acid and 10 µm A23187+600 µm ascorbic acid. After incubation sperm motility, viability, acrosome reaction, DNA damage and malondialdehyde levels were evaluated., Results: Our results indicated that after one hour incubation, ascorbic acid significantly reduced malondialdehyde level in ascorbic acid group (1.4±0.11 nmol/ml) compared to control group (1.58±0.13 nmol/ml) (p<0.001). At the end of incubation, progressive motility and viability in ascorbic acid group (64.5±8.8% and 80.3±6.4%, respectively) were significantly (p<0.05 and p<0.001, respectively) higher than the control group (54.5±6.8% and 70.9±7.3%, respectively). A23187 significantly (p<0.0001) increased acrosome reaction in A23187 group (37.3±5.6%) compared to control group (8.5±3.2%) and this effect of A23187 attenuated by ascorbic acid in ascorbic acid+A23187 group (17.2±4.4%). DNA fragmentation in ascorbic acid group (20±4.1%) was significantly (p<0.001) lower than controls (28.9±4.6%)., Conclusion: In vitro ascorbic acid supplementation during teratozoospermic semen processing for ART could protect teratozoospermic specimens against oxidative stress, and it could improve ART outcome.

Since there is evidence that lobeline-induced sensations, associated with discomfort in the mouth, throat and chest arise by stimulating juxtapulmonary or J receptors, we were interested in investigating if similar sensations are felt by patients with left ventricular dysfunction (LVD) in whom a natural stimulation of these receptors would occur by transient interstitial oedema or during augmentation of the stimulus, by increased pulmonary blood flow during exercise. Threshold doses of lobeline produced three or more respiratory sensations simultaneously in 9 out of 10 patients, which was greater than the response of the controls (P < 0.01). With mild exercise, a greater number of patients (7) than controls (1) reported feeling two or more sensations (P < 0.01); in fact half the controls did not express a respiratory sensation with equivalent exercise (P < 0.05). The predominant lobeline-like sensations reported by patients with exercise were a feeling of heat or burning and pressure in the throat or chest (P < 0.05). The presence of cough in three patients and in none of the controls was noteworthy. The mean latency with which sensations appeared during exercise in patients (4.4 +/- 0.3 min) was almost half that in controls (7.4 +/- 0.2 min) (P < 0.005). Since, respiratory sensations in response to lobeline and exercise were intensified in patients compared to controls and since both lobeline and exercise-induced sensations were similar (P < 0.05), we speculate that a common origin exists. Despite important caveats, that we discuss, in our view these respiratory sensations and cough arise from stimulation of J receptors.