Introduction: Atorvastatin, a lipid-soluble statin, is commonly used in managing high cholesterol levels and has been demonstrated to possess pleiotropic effects, such as antidepressant and neuroprotective properties. Women are more likely to suffer from depression because hormone levels change during ovariectomy and menopause. However, the role of statins in the treatment of ovariectomy-induced depressive behavior has not been adequately studied. We explored atorvastatin's potential antidepressant effects as well as the potential function of the nitric oxide pathway in ovariectomized (OVX) mice. Methods: Female mice underwent ovary removal, followed by administration of varying doses of atorvastatin alone or in conjunction with either a non-specific NO synthase inhibitor (L-NAME) or an NO precursor (L-arginine). Behavioral alterations were assessed using the Tail Suspension Test (TST), Forced Swim Test (FST), and Open Field Test (OFT), while hippocampal nitrite levels were also measured. Results: One week post-procedure, OVX mice displayed a notably longer period of immobility in comparison to the sham group. OVX animals treated with atorvastatin (0.1 and 1 mg/kg) demonstrated antidepressant properties; additionally, OVX mice that received a sub-effective dose of atorvastatin plus a sub-effective dose of L-NAME demonstrated pronounced antidepressant-like effects (P<0.05). L-arginine counteracted the antidepressant-like effects of a high dose of atorvastatin in OVX mice but did not affect their levels of locomotor activity in the OFT. Furthermore, atorvastatin administration prevented the increased hippocampal nitrite concentrations caused by ovariectomy (P<0.05). Conclusion: The research revealed that atorvastatin exhibits significant antidepressant properties in OVX mice, potentially by suppressing the nitric oxide pathway.
Introduction: Changes in the levels of serum components can help in the early and differential diagnosis of Parkinson's disease (PD). The lesion in the dopaminergic (DAergic) system is the main pathophysiological mechanism underlying PD. This system is closely related to the hypothalamic-pituitary-thyroid axis. Here, we examined the impact of PD onset, progress, and severity in rats on the serum levels of thyroid hormones (THs). Methods: The neurotoxin 6-OHDA was injected into the medial forebrain bundle. Behavioral tests were carried out for eight weeks after the toxin to assess the severity of PD and its progress. Blood was collected before the toxin and in the third and eighth weeks afterward. THs levels were determined using specific ELISA kits. Results: Our findings show that the THs levels changed significantly after the toxin. The levels of T3 and T4 decreased slightly in the third week but remarkably increased in the eighth week. The decrease in the third week depended on the severity of the PD and was observed only in the rats with severe behavioral symptoms. On the other hand, the increase in the eighth week occurred in all 6-OHDA-received rats with severe or mild behavioral symptoms. Conclusion: Our data indicate that serum levels of THs may decrease and increase in PD. At the onset of the disease, the levels may decrease if DAergic neuronal death is severe. In the progress phase of PD, THs levels may increase independent of the severity of the disease.
Introduction: As herbal drugs have the potential to influence the therapeutic outcomes of pharmaceutical drugs, we investigated the effects of co-administration of Teucrium polium L. extract (TP) and Glibenclamide (Glib) on pancreatic islets in diabetic rats. Methods: Male Wistar rats were separated into six distinct groups (n=8). The control and sham control (normal saline), while four diabetic rats received different treatments (normal saline, Glib (5mg/kg), TP (200mg/kg), or co-administration of TP and Glib), via gavage, for 6 weeks. Induction of diabetes was performed with Streptozotocin injection, intraperitoneally at a dose of 55 mg/kg. The animals were anesthetized, and their dissected pancreases were fixed in 10% Formalin. Stereological assessments were done to determine pancreas volume, islet volume, volume density of islets relative to the pancreas, and the number of beta and apoptotic cells within the islets. Ultimately, the data analysis was conducted using SPSS and ANOVA. Results: Histological examinations revealed that the administration of TP, Glib, and their co-administration did not non-significantly increase the islet volume and volume density of islets relative to the pancreas in diabetic rats. However, treatment with these drugs led to an increase in the number of beta-cells and a decrease in the number of apoptotic cells within the islet. Notably, co-administration of these drugs did not yield significant differences compared to individual treatments. Conclusion: This study demonstrates that TP and Glib have similar impacts in streptozotocininduced diabetic rats. Co-administration of the two agents did not lead to a statistically significant difference compared with either treatment alone.
Introduction: Alkylating agents, commonly used in chemotherapy, can cause significant liver damage by inducing cell death pathways. Human menstrual blood-derived mesenchymal stem cells (HuMenSCs), with their remarkable proliferative capacity and easy accessibility, offer a potential treatment for this injury. Methods: We investigated the impact of transplanting HuMenSCs in rats using a liver damage model caused by Busulfan injection (36 mg/kg, i.p.). Engraftment was confirmed using fluorescence microscopy and flow cytometry. Hepatic morphology was assessed via histopathological examination. Apoptosis was quantified by TUNEL assay and real-time PCR analysis of apoptotic (Bax) and anti-apoptotic (Bcl2) gene expression. Results: HuMenSCs effectively engrafted into injured liver tissue. Histopathological examination revealed hepatic morphology significantly improved in the group treated with HuMenSCs, with reduced inflammation, congestion, and sinusoidal dilation. Additionally, both the TUNEL assay and real-time PCR analysis demonstrated a significant decrease in apoptosis and a shift toward the downregulation of pro-apoptotic gene expression (Bax) in the group that received HuMenSCs treatment when compared with the sham (p < 0.0001) and negative control groups (p < 0.001). Conclusion: The results of our research suggest that HuMenSCs transplantation effectively mitigates Busulfan-induced liver injury by inhibiting apoptosis and promoting liver regeneration. These findings demonstrate the promise of HuMenSCs as a novel therapeutic approach for treating liver damage caused by chemotherapy.
Introduction: Multiple sclerosis (MS) is an autoimmune and inflammatory disease of the central nervous system characterized by demyelination, astrogliosis, blood-brainbarrier (BBB) disruption, and axonal damage. Currently available clinical and experimental approaches for MS are not completely effective because of the inability to pass the BBB, off-target distribution, and the need to increase the dosage. It has been shown that BBB disruption and fibrin deposition occur in the region of lesions in MS. Coagulation factor XIII binds to fibrin through the heptapeptide NQEQVSP in its structure. Here, NQEQVSP was used to target the lesions in animal models of MS. Methods: Microglia, astrocytes, and oligodendrocytes were immuno-stained using antibodies against Iba1, GFAP, and MBP, respectively. Results: We showed that peptide NQEQVSP binding was specific to the lesion sites induced by lysophosphatidylcholine (LPC) injection into the corpora callosa of mice. The peptide was FAM labeled, and its co-localization with different glial cells was evaluated. Co-localization was mainly detected with the microglia in the damaged area. A lower level of co-localization was also observed for oligodendrocytes. Conclusion: Our results promise the possibility of using NQEQVSP peptide to target the lesions for specific drug delivery in patients suffering from multiple sclerosis.
Introduction:Mercury chloride is commonly used in our daily lives due to its diverse applications and can induce hepatorenal toxicity even at low doses. The present investigation studies the preventive effects of lipoic acid and Cleome droserifolia extract against mercury-induced hepatorenal toxicity. Methods: Thirty male albino rats were randomly assigned to six experimental groups. The first group served as the normal control. The second group was treated with alpha-lipoic acid (ALA) at a dose of 10 mg/kg. The third group received Cleome droserifolia extract (CD) at the same dose. The fourth group was exposed to mercuric chloride (HgCl2) at 35 mg/kg (equivalent to 21% of the LD50). The fifth group was co-treated with alpha-lipoic acid (10 mg/kg) and mercuric chloride (35 mg/kg), while the sixth group received Cleome droserifolia extract (10 mg/kg) together with mercuric chloride (35 mg/kg). All treatments were administered orally once daily for a period of eight weeks. Results: Mercury induced a slight decline in body weights and relative organ weights for the liver and kidney compared to the normal control group. It caused significant elevations (p<0.05) in hamoglobin concentration and white blood cell (WBC) count; however, bone marrow cell count was not affected. Mercury triggered considerable disruption in liver and kidney functions. It also promoted a significant decline in catalase (CAT) activity and a significant elevation in malondialdehyde (MDA) levels. Mercury-induced degeneration, fibrosis, and necrosis in the liver and kidney tissues. Administration of alpha lipoic acid and Cleome droserifolia extract showed marked improvement in the different parameters under investigation. Conclusion: Lipoic acid was found to be more effective against mercury chloride-induced hepatorenal toxicity than Cleome droserifolia extract.
Introduction:The crucial role of adipose tissue (AT) in energy balance has sparked significant interest in researching this tissue as a potential target for obesity treatment. Exercise and dietary interventions are promising strategies for addressing obesity. This study aimed to examine the impact of aerobic training and royal jelly on the expression of thermogenesis-related genes in the visceral adipose tissue (VAT) of obese rats. Methods: Rats (n=45) were divided into five groups: normal diet (ND), high-fat diet (HFD), high-fat diet-training (HFDT), high-fat diet-royal jelly (HFDRJ), and high-fat diet-training-royal jelly (HFDTRJ). Royal jelly treatment was administered at a dosage of 100 mg/kg body weight. The training was conducted at an intensity of 50-60% VO2max, five days a week for eight weeks. Thermogenesis gene expression was evaluated by the real-time PCR method. Results: Induction of an HFD significantly reduced the expression of UCP-1, PRDM16, and CREB-1 compared to the normal diet (ND) group (p=0.001). Aerobic training and RJ significantly increased the levels of UCP-1, PRDM16 and CREB-1 in the VAT of HFD rats (p=0.0001). The combined intervention of aerobic training with RJ had no significant effect on the levels of UCP-1, PRDM16 and CREB-1 in the VAT of HFD rats. Conclusion: It appears that aerobic training and RJ are effective methods for positively regulating the gene expression related to thermogenesis in AT, which may mitigate obesity induced by a high-fat diet.
Introduction: According to earlier research, fitness training can reduce the cardiovascular risks of waterpipe tobacco use. This study aimed to investigate how electrocardiogram (ECG) parameters and heart rate variability (HRV) changes occur in Wistar rats exposed to continuous hookah smoke and moderate endurance exercise training. Methods: 28 adult male Wistar rats, weighing 180-220 g, were divided into 4 groups as control group (CTL), exercise training group (Ex), waterpipe tobacco smoke exposure group (WPS), andexercise training and waterpipe tobacco smoke group (WPS+Ex). After completing the 8-week smoke exposure and exercise protocol, ECG recording, HRV characteristics, including frequency domains, temporal domains, and non-linear analysis, were computed. Results: The findings showed that, compared to the control group, hookah smoking significantly increased the RR interval (P < 0.05) and decreased heart rate (HR) and standard deviation of the second heart rate variation (SD2), an indicator of long-term HRV variability. Compared to the CTL group, exercise training decreased the low frequency/high frequency (LF/HF) band non-significantly and increased the HF band while decreasing the LF band (P<0.05). Following exposure to hookah smoking and exercise training, the WPS+Ex group's SD2 rose (P<0.05), whereas the WPS group's HF and corrected QT (QTc) interval decreased. Conclusion: Overall, our results demonstrated that 8 weeks of moderate-intensity endurance training had a slight favorable impact on the rats' HRV frequency domains. At the same time, hookah smoking inhibited this beneficial effect and lowered HR.
Introduction: Mother-infant interaction is critical for neural development and maturation, with long-term molecular and behavioral impacts on offspring. Rats' neonatal maternal separation (MS) has been introduced as a model of early life stress, which may be the basis of mental health condition in adulthood. In the present study, the gene expression of Mef2a, Tcf3, and Bdnf was studied in various brain regions of rat offspring that experienced MS to provide further insight into the molecular mechanism of MS. Methods: In this experimental study, MS was applied in rat litters separated from their mothers for four hours/day from PND 2 to PND 14. Mef2a, Tcf3, and Bdnf gene expression in various brain areas of adult offspring was measured by qPCR, and results were compared with the control group by t-test statistics. Results: Quantitative analyses indicated that Mef2a has been downregulated in the amygdala of offspring that experienced MS. Tcf3 gene expression was increased in the insula and striatum, while its level was decreased in the PFC of MS offspring. Bdnf was also upregulated in the insula but downregulated in the MS group's PFC. Conclusion: Neonatal MS-induced gene expression changes the molecular drivers of neural plasticity in the offspring's central nervous system, which may be the basis of behavioral changes in adulthood. Further investigation of signaling pathways and behavioral modifications of rats that experienced MS may uncover the underlying mechanism of MS.
Introduction: The burn wound healing process is multi-variable, and various factors are involved. Chitosan-based dressings are acceptable materials for wound healing. PProbiotics and postbiotics can in-crease the effectiveness of these dressings. This study aimed to investigate the effect of a biodegradable dressing prepared from chitosan and external microvesicles of Bifidobacterium bifidum on burn wound healing in male Wistar rats. Methods: Bifidobacterium bifidum was cultured, the activated crude supernatant (ACS) was separated, and the microvesicles were isolated with the help of Ultra-centrifugation at 150,000xg at 4 degrees C for 30 minutes. Chitosan films containing and without microvesicles were prepared using a heater stirrer at 29 degrees C. The effectiveness of the membranes was evaluated. For this purpose, 60 male rats with second-degree burns were randomly divided into 5 groups (n=12) and were treated for 21 days. The process of wound healing was examined macroscopically and microscopically (wound histology and evaluation of gene expression of cytokines interleukin-8, interleukin-10, and VEGF) on the days 3, 7, 14 and 21. The obtained data were analyzed by IBM SPSS.21 software and using Kolmogorov-Smirnov, Kruskal-Wallis, and Mann-Whitney tests with p <= 0.05. Results: The average diameter of microvesicles was 174 +/- 52nm. The thickness of the layers was 2mm. The wounds of the group post-biotic and positive control were closed on the 14th day. Collagen production and epithelialization, as well as inflammation control in the treatment groups, were higher than negative control. Conclusion: The use of chitosan membranes, particularly those enhanced with ACS and microvesicles, represents a significant advancement in wound care by inflammation control, offering a promising strategy for improving the healing of burn wounds.
Introduction:Azoospermia is a common cause of male infertility. The latest hope for more affordable and safer therapies comes from stem cell research. In this study, the effect of mesenchymal stem cells derived from Wharton's jelly on spermatogenesis in azoospermic mice with scrotal hyperthermia was investigated. Methods: For the experimental study, 24 adult male mice were divided into four groups: 1. control (Cont), 2. scrotal hyperthermia (Hyp), 3. scrotal hyperthermia + DMEM (10 mu l) (Hyp/ DMEM), 4. scrotal hyperthermia + conditioned medium (10 mu l) (Hyp/CM). A temperature of 43 degrees C was applied for 20 minutes every other day for two weeks to induce hyperthermia. The mice in the experimental group received 10 mu l of human Jelly Wharton's Stem Cell-Conditioned Medium (hJWSC-CM) intraperitoneally every other day for 35 days after hyperthermia. Animals were sacrificed after the experiments to perform additional molecular, biochemical, and stereological analyses. Results: The results showed that CM significantly increased both the total amount of sperm and the number of testicular cells, including spermatids, primary spermatocytes, spermatogonia, Leydig cells, and Sertoli cells, compared with Hyp and Hyp/DMEM; in addition, the biochemical characteristics of testicular tissue were significantly higher in the Hyp/CM group compared with the hyperthermia-induced groups. Further analysis revealed that when the Hyp/ CM group was compared with the Hyp and Hyp/DMEM groups, Sox9 protein expression and proliferative gene expression increased significantly and the percentage of apoptotic testicular cells and pro-inflammatory gene expression decreased significantly. Conclusion: These results suggest that realistic therapeutic approaches for reproductive and regenerative medicine could benefit from hWJSC-CM.
Introduction: Histamine directly interacts with airways smooth muscles to initiate contraction. This occurs even at low concentrations among individuals predisposed to increased airway inflammation and asthma. Methods: A digital vitalograph, nebulizer, histamine, and pulse oximeter were used in this research. A total of one hundred and sixty subjects were selected and categorized into two groups; Group 1 (Test subject) and Group 2 (Control), each group contained eighty (80) subjects. Group 1 comprised occupationally exposed vulcanizers and Group 2 comprised selected students from the University of Calabar as control. Both groups comprised young male subjects of equal age (20-40 years), devoid of pre-existing respiratory disorders or on any medication(s). Demographic parameters were used to obtain sufficient information for overall analysis. Lung parameters (FVC, FEV1, PEFR, and FEV1%) were evaluated using a Vitalograph Spirometer. Results: Basal measurement showed that Group 1 had a moderate decrease in lung volumes (FVC, FEV1, PEFR, and FEV1%) of 65 subjects (representing 81.25%) and a mild decrease in 15 subjects (18.75%); all the subjects in Group 2 showed a mild decrease in lung volumes. Inhalation of histamine mist of different concentrations showed that Group 1 had a severe decrease in lung volumes of 70 subjects (87.5%) and a mild decrease in 10 subjects (12.5%). All Subjects in Group 2 showed a mild decrease in lung volumes. Conclusion: Histamine provocative test helps to evaluate asthma signs and symptoms. Airways Hyper reactiv-ity is associated with inflammation as a consequence of airway hyperreflexia. It is evidenced that associated pollutants and their chronic inhalation by the vulcanizers have a retrogressive impact on their airways which manifests with hyper response an indication for asthma signs.
Introduction: Caffeine, as a popular drink, along with exercise training, may help restore altered gene expression in high-fat diet (HFD)-induced obesity. This study examined the effects of exercise training, caffeine consumption, and their interaction on inflammation and genes involved in metabolism in rats fed an HFD. Methods: Eighty male Wistar rats were separated into two groups: HFD and normal diet (ND). Each group was subsequently divided into four groups: sedentary, caffeine-only, exercise, and caffeine-plus-exercise. For eight weeks, the animals in the training groups engaged in aerobic exercise on a motorized treadmill for 60 minutes, five times per week. Animals in the caffeine group ingested a solution containing caffeine daily (6 mg/kg/bw). The expression of Peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (PGC-1 alpha) and fibronectin type III domain-containing (FNDC5) genes in the calf muscle, uncoupling protein-1 (UCP1) in subcutaneous adipose tissue, NF-KB and TLR4 in vis-ceral adipose tissue, and fetuin-A (Fet-A) in the liver were investigated. Results: The findings demonstrated that HFD significantly elevated the NF-K beta gene and downregulated the skeletal muscle PGC-1 alpha and FNDC5 genes, as well as serum fetuin-A. UCP-1 (366% vs. 56%), FNDC5 (26% vs. 54%), and PGC-1 alpha (40% vs. 1700%) genes were all considerably elevated by exercise training and caffeine supplementation, respectively. Additionally, exercise training reduced TLR4 and NF-K beta expression in visceral adipose tissue and liver Fet-A gene expression. Furthermore, following HFD, when compared to the sedentary group, exercise training with and without caffeine consumption decreased the NF-K beta gene and liver Fet-A and increased PGC1-alpha, FNDC5, UCP1, and serum Fet-A. Conclusion: These findings support the idea that exercise and caffeine may reduce inflammation by downregulating genes involved in inflammation and adipose tissue browning.
Introduction: Endometriosis (EMS) is a highly prevalent gynecological disorder with substantial health consequences, affecting as many as 10% of women in their reproductive years. Although EMS is widespread, its intricate origin and pathophysiology are not well understood. This study investigated the molecular characteristics of EMS by examining the expression patterns of long noncoding RNAs (lncRNAs), microRNAs (miRNAs), and genes linked to the condition. Methods: The study used publicly accessible datasets, namely RNA-seq data for long non-coding RNAs (GSE105764), miRNA expression data (GSE105765), and gene expression data (GSE12768), to compare samples of ectopic and eutopic endometrial samples. The study conducted differential expression analysis, pathway enrichment analyses, protein-protein interaction network creation, and hub gene identification to uncover the molecular markers linked to EMS. Results: The investigation identified substantial dysregulation of lncRNAs, miRNAs, and genes in endometriotic tissues compared with the control eutopic endometrium. Hub genes, including CDH1, ESR1, GATA4, PGR, FOXA2, EPCAM, APOA1, BDNF, FGFR2, and PAX2, dominate the molecular landscape. miR-6500-3p has been identified as a pivotal regulator that influences the expression of seven essential genes. Pathway enrichment analysis identified biological processes, including embryonic organ morphogenesis, immunological response, and medication metabolism. Exploring lncRNA-mediated regulatory axes, particularly H19 and MIR600HG, suggests complex networks that may clarify the molecular underpinnings of EMS. Conclusion: This thorough investigation offers significant insight into the molecular pathways underlying EMS. Hub genes and regulatory miRNAs, including miR-6500-3p, have been identified as prospective targets for therapeutic interventions. Pathway enrichment studies provide a more comprehensive understanding of the biological processes implicated in EMS, indicating new possibilities for therapeutic interventions.
Introduction: As a chronic neurological disorder, epilepsy is affected by social stress, which is one of the numerous complications in societies. In addition to medication, enriched environment (EE) and exercise are among the complementary strategies in the treatment of epilepsy. Oxidative stress, which potentially can activate the inflammatory pathways, is one of the causes of this disorder. So, we tried to examine thoroughly the beneficial impacts of EE and exercise on neuroinflammation in epileptic rats. Methods: Male Wistar rats were divided into five groups of twelve rats each, including: a control group, a group induced with pilocarpine to simulate epilepsy, an epileptic group subjected to social stress, an epileptic group placed in an enriched environment, and an epileptic group subjected to an exercise regimen. The impact of social stress, enriched environment, and exercise on oxidative stress biomarkers was investigated through TBARS spectrophotometric test and the gene expression of NLRP3, Caspase-1, IL18, and IL1 beta were evaluated through real-time PCR method Results: Epilepsy and social stress caused a reduction in superoxide dismutase (SOD) and glutathione peroxidase (GPx) (p<0.05). Moreover, they resulted in an enhancement of plasma (p<0.05). Exercise increased the GPx and diminished the expression of Caspase-1 and IL 18 inflammatory genes (p<0.05). Accordingly, EE enhanced the SOD and GPx antioxidant indicators and reduced proinflammatory gene expression Conclusion: In this research, social stress resulted in elevated levels of oxidative markers and upregulation of inflammatory gene expression. EE and regular exercise improved the situation.
Introduction: This study aimed to evaluate the efficacy and safety concerns of remdesivir and type 1 interferons on the clinical outcomes of hospitalized multiple sclerosis patients with COVID-19. Methods: Using electronic health records systems; this is a cross-sectional study of two years of hospital admissions in terms of COVID-19 in Iran from March 2019 to August 2021. The severities of COVID-19 outcomes were ICU admission, hospitalization days, and 30-day survival rates. Results: A total of 993 hospitalized multiple sclerosis patients with a confirmed diagnosis of COVID-19 based on PCR testing were recorded in the electronic health systems. Nearly half of these patients (50.3%) had received treatment with an anti-CD20 agent (rituximab or ocrelizumab) at the hospital admission. This group exhibited higher mortality rates, increased need for ICU admission, and longer hospitalization (p<0.05). There was a significant association between taking interferon-beta 1 alone (adjusted IRR=1.21, 95% CI 1.32 to 1.42) or in combination with remdesivir (adjusted IRR=1.30, 95% CI 1.18 to 1.5042) and longer hospitalization. There were no significant associations between antiviral treatment (remdesivir alone, interferon-beta 1- beta 1 alone, and interferon-beta 1plus remdesivir) and ICU admission (p>0.2), the in-hospital mortality rate (p>0.2), or 30-day survival rate (p>0.2). The results were similar in patients who did or did not receive anti-CD20 agents. These results were consistent among patients regardless of whether they received anti-CD20 agents. Conclusion: Our data suggest that remdesivir, interferon-beta 1, or a combination of both does not benefit hospitalized MS patients with COVID-19.
Introduction: Genotoxicity is one of the safety concerns that can lead to damage at the genetic level. The observation of DLBS1033 using AMES and micronucleus tests was conducted to ensure the safety precautions. Methods: Ames test was done using 3 strains of Salmonella typhimurium (TA98, TA100, and TA1535) with or without metabolic activation (S9 enzyme). In vitro micronucleus test was performed with prolonged exposure without S9. The variation of DLBS1033 concentrations were 100, 600, and 1200 mu g/ml. Results: The results of the Ames test (with/without S9) and in vitro micronucleus (prolonged exposure without S9) showed that DLBS1033 did not have a mutagenic effect. Conclusion: DLBS1033 was safe and did not show any genotoxic activity.
Introduction: One of the most common cancers of the oral cavity is oral squamous cell carcinoma (OSCC). Previous studies have provided evidence that apolipoprotein C-I (Apo C-I) has an oncogenic role beyond its classical function. Although it has been investigated in prostate, breast, and lung cancer, there is no information available regarding Apo C-I expression in tumor and pri-tumor tissues of OSCC patients. Thus, the goal of the present study was to unravel the expression of Apo C-I in OSCC and investigate its correlation with the survival and grade of OSCC patients. Methods: The Apo C-I mRNA level was measured in tumor and pri-tumor tissues of 16 OSCC patients. In addition, the 34 paraffin-embedded tissues of OSCC patients and IHC technique were used to analyze the association of Apo C-I protein with the survival of OSCC patients. Results: The mRNA (P=0.0386) gene expression of Apo C-I showed a statistically significant difference between tumor and pri-tumor tissues of OSCC patients. It seems that a high protein level of Apo C-I is related with poor survival of OSCC patients (P=0.04). The Apo C-I protein was positively correlated with the tumor site (Pearson r= 0.485, P=0.0036) but not the grade (Pearson r= 0.2295, P=0.1917). Our data showed that high Apo C-I protein levels might be correlated with poor survival of OSCC patients. Conclusion: Our findings suggest that patients with high protein levels of Apo C-I may have lower survival, making it a potential prognostic factor for OSCC. However, further investigation is necessary to establish this concept.
Introduction: Ovarian torsion is an emergency condition that occurs when the adnexa undergoes complete or partial rotation. Following ovarian torsion, damage caused by ischemia/ reperfusion can impact fertility and sex hormone secretion. Our study aims to investigate the role of safranal in preventing ovarian ischemia-reperfusion injury in rats. Methods: Animal subgroups included: sham, ovarian torsion/detorsion (OT), ovarian torsion/ detorsion with the treatment of safranal (OTS 0.1, 0.5), and safranal group (OS 0.1, 0.5). Ovarian torsion was induced in the left ovary of rats for 2 hours. Intraperitoneal treatment with safranal at 0.1 and 0.5 mg/kg doses was performed 30 minutes before the detorsion operation. 48 h after detorsion, ovarian tissue was collected to evaluate the histopathological scores and apoptosis gene expression of Bcl-2, caspase 3, and Bax. Blood samples were collected to measure plasma estradiol levels and oxidative stress parameters. Results: Analyses demonstrated that ovarian follicular damage was accompanied by increased serum malondialdehyde (MDA) levels and increased expression of Bcl2 and caspase-3 genes. Additionally, serum levels of glutathione peroxidase (GPX), estrogen, and superoxide dismutase (SOD) decreased in the OT group. However, treatment with safranal 0.5 mg/kg was accompanied by an improvement in the histopathological score of the ovarian tissue and a reduction in apoptosis and oxidative stress. Conclusion: Safranal exhibits antioxidant properties in a rat model of ovarian torsion and could be considered a cost-effective therapeutic option for ovarian detorsion in gynecological clinics.
Introduction: Methamphetamine (MA) addiction is a major global public health concern, yet there is currently no approved medication that effectively treats this addiction. Kisspeptin is a neuropeptide that has a role in the reproductive system, metabolism and energy balance, and metastasis suppression in different types of cancers. The kisspeptin receptors, GPR54 are widely distributed in the brain's memory-related structures. Previous studies have revealed that the opioid system contributes to the addictive effects of MA. Additionally, preclinical studies have shown that a derivative of kisspeptin possesses anti-opioid properties. This study aimed to clarify the role of kisspeptin-13 (KP-13) on reward and reinstatement-related memory associated with MA in the conditioned place preference test. Methods: We evaluated pre-treatment with intracerebroventricular KP-13 for 3 consecutive days (2.5 mu l/nostril, once a day) in a conditioned place preference test induced by MA. MA was administered intraperitoneally at a dose ranging from 1 to 7 mg/kg, once daily, beginning at 1 mg/kg on day one and increasing by 1 mg/kg per day up to the day 7. Results: We found that KP-13 suppresses the reward behavior in MA-treated rats, while it has no significant effect on reinstatement behavior after one week of MA cessation, which could be attributed to the ineffective dose of KP-13. Conclusion: The findings indicate that KP-13 alters the rewarding and motivating effects of MA. Further research involving both multiple and single administrations of KP-13 before the reinstatement test is necessary to throw light on its impact on withdrawal-related reinstatement.
