Background:This study examined the protective effects of zinc oxide nanoparticles (ZnO-NPs) on hepatic ischemia-reperfusion injury (HIRI) and their possible underlying mechanisms. Methods:48 male rats were randomly divided into six groups (n=8): the sham group that received intraperitoneal normal saline solution (Sham), the HIRI group, the control groups pre-treated with 5 and 10 mg/kg ZnO-NPs for 3 consecutive days without surgery (ZnO5) and (ZnO10), the HIRI group pre-treated with 5 mg/kg ZnO-NPs for 3 consecutive days before surgery (HIRI+ZnO5), and the HIRI group pre-treated with 10 mg/kg ZnO-NPs for 3 consecutive days before surgery (HIRI+ZnO10). One hour after reperfusion, serum and tissue samples were collected for biochemical, molecular and histopathological evaluation. Results:Administration of ZnO-NPs caused significant improvement in the elevated serum concentrations of ALT, AST, TOS and MDA, improved liver histopathology, and increased TNF-α, IL-6, and NF-κB levels in liver tissue compared to HIRI group. In addition, administration of ZnO-NPs increased the expression of miR-125 in liver tissue compared than in the HIRI group. Conclusions:The administration of ZnO-NPs improved the effect on HIRI by enhancing miR-125b expression and suppressing oxidative stress and inflammatory cytokines.
Background:Hashimoto thyroiditis is a chronic autoimmune disorder influenced by genetic and environmental factors. DNA methylation, regulated by DNA methyltransferase 1 (DNMT1), may play a critical role in its pathogenesis. This study investigated the association between DNMT1 polymorphism, particularly rs2228611, and gene expression in Hashimoto thyroiditis patients and also compared serum levels of thyroid-stimulating hormone (TSH) and anti-thyroid peroxidase (anti-TPO) antibodies in both affected individuals and controls. Methods:A case-control study of 100 participants (50 Hashimoto's thyroiditis patients and 50 controls) was conducted. TSH and anti-TPO levels were measured using the enzyme-linked immunosorbent assay (ELISA). DNMT1 expression was analyzed via quantitative real time-polymerase chain reaction (qRT-PCR), while DNMT1 (rs2228611 C/T) polymorphism was assessed by high-resolution melting-polymerase chain reaction (HRM-PCR). Results:The results revealed that Hashimoto thyroiditis patients exhibited significantly elevated serum TSH and anti-TPO levels compared to healthy controls (p < 0.0001). DNMT1 gene expression was upregulated by 1.7-fold in patients relative to controls (p = 0.04), suggesting a potential role in disease pathogenesis. Genotyping of DNMT1 rs2228611 polymorphism revealed no significant differences in allelic or genotypic frequencies between groups. However, the TT genotype showed a non-significant trend toward increased disease risk (p = 0.07). The CT genotype appeared to confer a protective effect. Conclusions:The study's findings suggest that elevated DNMT1 expression and thyroid dysfunction are characteristic of Hashimoto thyroiditis, while the DNMT1 rs2228611 polymorphism may have a limited but possible influence, warranting further study with larger cohorts.
Background:Oral and lip squamous cell carcinomas (OSCC) are malignancies among head and neck cancers. OSCC is characterized by aggressive behavior and poorer prognosis compared to other squamous cell carcinomas. Galectin-3 (Gal-3) is a multifunctional protein involved in processes such as cell proliferation, apoptosis, and metastasis. This study aims to evaluate and compare Gal-3 expression among groups to investigate its role in the biological behaviors of lip and oral SCCs. Methods:Immunohistochemical analysis of Gal-3 was performed on OSCC and lip SCC samples, with oral and lip marginal tissues obtained as the control group. The clinicopathological parameters, including the invasive front (IF), depth of invasion (DOI), and muscular, neural, and vascular invasions, were assessed. The staining percentage, intensity, and cellular location of Gal-3 were compared between the study groups. A p-value of < 0.05 was considered statistically significant. Results:Gal-3 staining percentages were significantly higher in the SCC groups compared to control groups (P< 0.001 for each). Staining intensity and nuclear staining were higher in OSCC than in lip SCC (P< 0.001, P< 0.010, respectively). Nuclear Gal-3 was notably associated with the presence of muscle invasion in OSCC (P=0.030). High IF status was correlated with Gal-3 expression in lip SCC (P=0.010). Staining intensity was significantly higher in OSCC samples with vascular invasion compared to those without (P= 0.016). Conclusions:The higher Gal-3 expression and nuclear staining in OSCC may explain its aggressive nature. Gal-3 could be a diagnostic and prognostic biomarker due to its increased expression in cancerous tissues compared to normal samples.
Background:Chronic kidney disease (CKD) is a major cause of morbidity and mortality worldwide, often progressing silently until advanced stages. This study aimed to evaluate the diagnostic potential of serum visfatin levels and Nicotinamide Phosphoribosyl transferase (NAMPT) gene expression in peripheral blood mononuclear cells (PBMCs) among CKD patients, along with their correlation with disease severity and lipid profile. Methods:A case-control study included 30 CKD patients, divided into two subgroups: 15 end-stage renal disease (ESRD) patients undergoing hemodialysis (HD) and 15 non-dialysis patients. These patients were matched by age and body mass index (BMI) with 30 healthy subjects (HS). Serum visfatin, lipid profile, electrolytes, NAMPT gene expression, and other biochemical markers were measured. Results:This study showed significantly higher visfatin levels in CKD patients compared to HS, with the highest levels observed in the ESRD group undergoing HD (5.6±1.63 ng/mL compared with 3.5±1.4 ng/mL in CKD without HD, and 2.7±1.1 ng/mL in HS; p≤0.001). Similarly, NAMPT gene expression was significantly upregulated in CKD patients, with the highest expression in the HD group, correlating strongly with serum visfatin levels (r = 0.76, p≤0.001) and lipid profile markers, including triglycerides (r = 0.67, p=0.002) and low-density lipoprotein (LDL; r = 0.61, p=0.004). In CKD patients undergoing HD, visfatin levels showed a positive correlation with triglycerides and LDL levels, suggesting a link with dyslipidemia. No significant correlation was found between visfatin and highly sensitive C-reactive protein (hsCRP), urea, creatinine, or very-low-density lipoprotein (VLDL). Conclusions:These findings indicate that serum visfatin and NAMPT gene expression could serve as novel biomarkers for assessing CKD severity, particularly in patients undergoing hemodialysis, with potential implications for managing inflammation and cardiovascular risk in CKD.
Background:Esophageal cancer (EC) is an aggressive gastrointestinal tumor necessitating novel prognostic, diagnostic, and therapeutic strategies. It is essential to identify important markers for diagnosing malignancy and predicting outcomes. Understanding gene functions in signaling pathways and early cancer detection are vital for reducing EC mortality. CD44 upregulation is linked to cancer stem cells (CSC), metastasis, poor prognosis, and treatment response. CD44v6, a variant of CD44, plays a pivotal role in tumor invasion and metastasis by influencing the extracellular matrix, promoting cell motility, and suppressing cancer cell apoptosis. Methods:This study investigated CD44v6 expression in tumor and tumor-free tissues of the esophagus in 50 esophageal squamous cells carcinomas (ESCC) patients using real-time PCR. The aim was to assess its prognostic value and its correlation with tumor invasion. Results:Significant overexpression of CD44v6 mRNA was detected in 9 out of 50 tumor specimens (18%, p = 0.0001). CD44v6 expression showed an inverse correlation with tumor cell metastasis to lymph nodes (p = 0.047). Among the 21 patients with lymph node metastasis, 5 (23%) exhibited CD44v6 overexpression. Additionally, CD44v6 expression was linked to the tumor stage (p = 0.008). Specifically, 2 out of 9 patients with stage I tumors (22.2%), 4 out of 9 with stage II tumors (44.4%), and 3 out of 9 with stage III tumors (33.3%) showed CD44v6 overexpression. Conclusions:Our findings suggest that lower CD44v6 expression at the RNA level correlates with increased tumor invasion and more advanced stages in ESCC.
Background:Primary hypothyroidism (HT) has been demonstrated to be associated with oxidative stress. This study was designed to assess the role of oxidative stress in the pathogenesis of primary hypothyroidism. Methods:The study included 97 subjects, age range (of 29-62 years); 57 of them had been diagnosed with primary hypothyroidism, and 40 healthy subjects as controls in Baghdad, during Oct 2023 to 2024. The primary HT subjects were sub-classified into the newly diagnosed primary HT group (n=24) and the established primary HT (n=33) group. Investigations encompassed serum evaluation of total antioxidant capacity (TAC), total oxidant status (TOS), 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG), NADPH oxidase-4 (NOX4), and Anti-TPO utilizing enzymatic colorimetric methods and enzyme-linked immunosorbent assay (ELISA). Results:The median and 1st -3rd quartile range values of serum 8-oxo-7,8-dihydro-2'-deoxyguanosine, NADPH oxidase-4, and total antioxidant capacity levels of newly diagnosed and established primary HT were significantly elevated when correlated with those of controls (for all, p < 0.0001), with non-significant differences between both groups of primary HT. The reservoir operating characteristic (ROC) and area under curve revealed that both total oxidant status and DNA damage 8-oxo-dG had high sensitivity and specificity in differentiation between hypothyroidism patients and controls at defined cutoff values. Conclusions:TheElevated levels of serum 8-oxodG, NOX4, and TOS reflect the underlying oxidative damage associated with reduced thyroid function and may participate to the pathogenesis of primary hypothyroidism.
Background:Type 2 diabetes is a complex disease resulting from interactions between genetic, epigenetic, and environmental factors. Histone deacetylases (HDAC) are essential epigenetic-regulatory enzymes that affect gene expression and, through metabolic homeostasis and beta-cell function regulation, play significant roles in the development and treatment of diabetes. In this study, we specifically focused on the effect of metformin, the first-line therapy for type 2 diabetes on the expression of class I HDAC genes. Methods:A total of 60 patients were equally allocated into two groups: those receiving metformin treatment and those without treatment. Also, 60 subjects with normal glucose tolerance were divided into two groups: non-obese (n=30) and obese individuals (n=30). All biochemical and clinical factors were estimated using standard methods, and RT-qPCR was used to quantify the expression levels of the candidate genes in peripheral blood mononuclear cells of different groups. Results:The metformin treatment group exhibited increased expression of HDAC1, HDAC3, and HDAC8 in comparison to the non-treatment group. Furthermore, the expression levels of HDAC 1, 2, and 3 were higher in the obese group than the non-obese. Interestingly, evaluation of biochemical and clinical factors revealed significant association between the expression of class I HDAC genes and several diabetes-related risk factors. Conclusions:The current findings suggest that HDAC1, 3, and 8 genes expression are affected by metformin, and obesity has a substantial ability to increase the risk of diabetes. However, changes in HDAC expression may represent potential biomarkers and therapeutic targets for future clinical studies in diabetes, particularly in exploring combination therapies involving histone deacetylase inhibitors and metformin.
Background:Polycystic ovary syndrome (PCOS) is a common endocrine disorder and a major cause of infertility in women. Although studies have reported the effects of naringenin on PCOS; the underlying molecular mechanisms remain unclear. This study aimed to investigate the effect of naringenin on the expression of kisspeptin (Kiss1) and calcitonin gene-related peptide (Cgrp) genes in a rat model of PCOS. Methods:Twenty female rats (180-200 g) were used in this study. To PCOS induction, two mg of estradiol valerate was injected intramuscularly (IM) per rat. The control and PCOS groups received saline, while the other two groups were treated intraperitoneally with naringenin at either 20 mg/kg or 50 mg/kg, respectively. Subsequently, hypothalamic tissue was collected, and gene expression levels were analyzed using real-time PCR. Results:The expression Kiss1 and Cgrp genes increased significantly in the PCOS group contrasted to the control (p≤ 0/05). In the groups treated with naringenin, the levels of Kiss1 and Cgrp gene expression reduced significantly compared to the PCOS group (p≤ 0/05). Conclusions:Naringenin may ameliorate PCOS by downregulating hypothalamic Kiss1 and Cgrp gene expression in rats. These results suggest a novel mechanism of naringenin's action and highlight its potential for clinical application.
Background:The anti-oxidative and anti-inflammatory effect of memantine (an N-methyl-D-aspartate receptor inhibitor) has been shown. Therefore, the present study aimed to evaluate the preventive effects of memantine against lipopolysaccharide (LPS)-induced sub-acute lung injury in mice. Methods:Male C57BL/6 mice (n=30) were randomized in five groups as follows: (1) control (saline containing 10% DMSO); (2) LPS (5 mg/kg, intraperitoneally); and (3, 4, and 5) LPS 5 mg/kg + memantine 5, 10, 20 mg/kg, respectively. Memantine (dissolved in 10% DMSO) was administrated orally three days before the LPS injection and continued for three days after injury induction. Finally, the levels of markers of oxidative stress, malondialdehyde (MDA), catalase (CAT) and superoxide dismutase (SOD), interleukin (IL)-1β, tumor necrosis factor-α (TNF-α), and nitric oxide (NO), were measured and histopathological changes in the lung tissue were assessed. Results:Lipopolysaccharide (LPS) administration increased the TNF-α, IL-1β, NO, and MDA, levels, while decreasing the lung tissues activity of CAT (P< 0.05) and SOD (P< 0.001) and caused lung pathological damages. Memantine 20 mg/kg, alleviated LPS-induced injury score, reduced the lung tissue levels of TNF-α, IL-1β, MDA, and NO, and restored CAT activity (P< 0.05, P< 0.01). Conclusions:LPS-triggered elevation of lung injury markers including histopathological changes, inflammatory cytokines, and oxidative damage. All pathological changes were suppressed by memantine.
Background:Neonatal hyperbilirubinemia affects up to 80% of infants, and despite phototherapy as standard care, zinc inhibits heme oxygenase, lowers bilirubin and CO, and offers antioxidant benefits. This study evaluated the effect of zinc supplementation on the incidence and severity of neonatal hyperbilirubinemia. Methods:A double-blind, block-randomized trial was conducted from December 2024 to February 2025 at Prof. Dr. R. D. Kandou Hospital NICU. Neonates with serum bilirubin >5 mg/dL were randomized to receive zinc 5 mg, zinc 10 mg, or placebo, all with phototherapy. Bilirubin levels were measured at baseline, 72 hours, and 120 hours, and outcomes were analyzed using bivariate and multivariate methods. Results:Ninety neonates, median age 3.0 days; 67% male; 62% birth weight ≥2.5 kg, were evenly distributed among groups with no significant differences at baseline. By day 3, the 10 mg zinc group showed significantly lower median bilirubin levels (5.3 mg/dL) compared to other groups (p=0.027). By day 5, bilirubin levels further declined across all groups: 3.5 mg/dL (placebo), 2.5 mg/dL (5 mg), and 2.4 mg/dL (10 mg) (p=0.025). Hyperbilirubinemia resolution by day 5 was achieved in 67% (placebo), 90% (zinc 5 mg), and 87% (zinc 10 mg) (p=0.044). Multivariate analysis revealed that 5 mg zinc significantly increased the odds of bilirubin resolution (OR 8.0; 95% CI 1.48-44.22; p=0.016), whereas 10 mg did not. Vomiting occurred in 13.3% of neonates receiving 10 mg zinc. Conclusions:Zinc 5 mg supplementation significantly accelerates bilirubin reduction compared to 10 mg zinc or placebo in neonates with hyperbilirubinemia.
Background:Human second-degree burns can form blisters that allow burn wound microenvironment (WME) fluid to accumulate, which leads to inflammation. Different types of cells are present in burn WME, including macrophages; these innate immune cells are present in tumor microenvironments (TMEs) and burn WMEs. They adapt their phenotypes according to environmental stimuli, which vary from pro-inflammatory (M1) to anti-inflammatory (M2). It is evident that these microenvironments share some similarities in terms of macrophage plasticity; therefore, this study examines whether burn blister exudate (BBE) can enhance macrophage activity against CT-26 cancer cells by macrophage polarization. Methods:Real-time PCR and ELISA were used to examine the effects of human BBE on untreated and M2 macrophages. As part of the immune response assessment, yeast phagocytosis was conducted. The impact of BBE-induced macrophages on CT-26 cancer cell survival and migration was assessed using MTT proliferation assay and scratch wound healing assay, respectively. Results:According to the results, tumor necrosis factor-alpha, interferon regulatory factor 5, induced nitric oxide synthase, and CD86 were upregulated as M1-related markers and cytokines, and M2-associated cytokines and markers, transforming growth factor beta, IL-10, Fizz1, Arginase-1, and CD206, were downregulated in untreated and M2 macrophages treated with BBE. BBE also enhanced the phagocytic capacity of untreated and M2 macrophages. Furthermore, the incubated CT-26 cell line with conditioned medium of BBE treatment groups suppresses proliferation and impedes migration of cancer cells. Conclusions:we found that BBE-treated macrophages possess an M1-like phenotype and inhibit the proliferation and motility of CT-26 cancer cells.
Background:Lung cancer is the leading cause of cancer-related deaths worldwide, yet there has been little attention given to the correlation between the cancer transcriptome and the incidence and mortality of lung cancer across different geographic regions. Methods:To analyze this correlation, we screened the transcriptome datasets of stage I lung adenocarcinoma (LAC) patients from the Lung Cancer Explorer and examined their correlation with the age-standardized incidence rate (ASIR), age-standardized mortality rate (ASMR), and mortality-to-incidence ratio (MIR). Results:The expression difference rates (DRs) of certain genes (SPARCL1, SRPX, PMP22, MSR1, BST1, AKAP12, MAOB, vimentin, serglycin, ILK, ESD, transgelin, NCOA1, and PLPP1) were significantly negatively correlated with the ASIR of female LAC. Additionally, the DR of KRT19 was significantly positively correlated with the ASIR of female LAC. Furthermore, the DRs of COL10A1, SMAD7, COL3A1, and AQP1 were significantly positively correlated with the ASMR and MIR of female LAC, while the DR of KRT15 was significantly negatively correlated with the ASMR and MIR of female LAC. In male LAC patients, the DR of RGS2 was significantly negatively correlated with the ASIR, while the DRs of SPARCL1, COX7A1, IL3RA, and ADH1B were significantly positively correlated with the ASMR and MIR. Additionally, the DR of AIMP2 was significantly negatively correlated with the ASMR and MIR. Conclusions:Our findings suggest that the expression levels of serglycin, ILK, ESD, and PLPD1 may play a significant role in the development of LAC. This information can be valuable for identifying potential treatment targets for lung cancer.
Background:Chronic kidney disease (CKD) is a deadly progressive disorder, particularly when it progresses to end-stage renal disease (ESRD). Conventional diagnostic tools such as serum creatinine and estimated glomerular filtration rate (eGFR) often lack sensitivity for early detection of tubular injury. This study aimed to evaluate the diagnostic potential of Galectin-3 (Gal-3) and Kidney Injury Molecule-1 (KIM-1) in Iraqi patients with CKD. Methods:This case-control study included 150 participants from Baghdad, Iraq, between August 2022 and May 2023. Participants were categorized into three groups: healthy controls (n=50), mild CKD (n=50), and severe CKD (n=50). Serum levels of Gal-3 and KIM-1 were measured using ELISA kits. Demographic, clinical, and biochemical data were collected, including age, sex, BMI, diabetes status, hypertension, and eGFR. Statistical analyses included ANOVA, Kruskal-Wallis test, and correlation analysis. Results:Gal-3 levels were significantly higher in CKD patients compared to healthy controls, showing a progressive increase from mild to severe CKD stages (P < 0.001). It was also associated with systemic factors such as diabetes mellitus, hypertension, and obesity. In contrast, KIM-1 levels were elevated primarily in patients with advanced CKD or ESRD (P = 0.036), but no significant difference was observed between control and mild CKD groups (P = 0.149). KIM-1 did not show consistent correlations with traditional markers of renal function, suggesting its specificity for structural tubular damage rather than functional decline. Conclusions:Our findings suggest that Gal-3 may serve as a broader biomarker reflecting both systemic inflammation and fibrosis, while KIM-1 appears to be more specific to advanced renal injury.
Background:Alzheimer's Disease (AD) incidence and prevalence increase every year, commonly related to neuron inflammation and degeneration conditions. Tempeh, a traditional fermented product from Indonesia, was reported to have anti-inflammatory, antioxidant, and anti-Alzheimer properties. However, anti-Alzheimer properties of tempeh peptide extracts have not been extensively examined. This research studied the effect of the extracted peptide from tempeh in preventing and delaying Alzheimer's disease. Methods:Tempeh peptide was extracted using water maceration and quantified using HPLC and spectrophotometry. Anti-Alzheimer properties of tempeh were analyzed with Ellman's assay of anticholinesterase and in vitro gene expression analysis using LPS-induced neural Schwann cells. Results:As a result, tempeh contained 19.27% of GABA, which is reported to have anti-Alzheimer properties, and other amino acids. Tempeh peptide extract at 12.5 µg/mL had strong inhibition activity toward acetylcholinesterase at 12.61%, and 100 µg/mL of tempeh peptide extract had 8.97% butyrylcholinesterase inhibition activity. Tempeh peptides extract also altered the expression of various genes related to Alzheimer's disease, such as TNF-α, BACE 1, Ntrk 1, BDNF 2, and APP. Conclusions:This research proved that various peptides from tempeh have anti-Alzheimer properties.
Background:Paraquat (PQ) is a commonly used herbicide known for its high toxicity. Despite its hazardous nature, there are currently no effective treatments for PQ poisoning. This study aimed to evaluate the effects of Rosmarinic acid (RA), a phenolic compound, on PQ-induced lung injury in mice. Methods:Mice were divided into ten groups for two experimental periods, 6- and 24-day periods (five groups each). The first group received normal saline daily, as the control group. Animals in the second group received a single intraperitoneal (i.p.) dose of PQ (25 mg/kg) on day 3. Groups three and four received RA (50 and 100 mg/kg, respectively) orally for 6 or 24 days. Group five received 100 mg/kg of RA daily. Animals were sacrificed 24 h after the last treatment, and lung samples were collected to determine histopathological changes and expression of TLR9, IL-1β, and TNF-α genes using RT-PCR. Results:Hematoxylin and eosin staining revealed a significant reduction in lung injury following RA treatment. RA notably reduced inflammatory cell infiltration and lung tissue congestion. Furthermore, inflammatory responses triggered by PQ were suppressed after RA treatment, as demonstrated by the downregulation of IL-1β, TNF-α, and TLR9 levels. Conclusions:These findings suggest the therapeutic potential of RA for mitigating PQ-induced lung damage and inflammation.
Background:SF3B1 is a splicing factor that plays a crucial role in cancer progression and is commonly found in various types of solid cancers. However, the reports regarding the clinical implications of SF3B1 in terms of therapy response, survival, and its relationship with patients' clinicopathological features are still limited. This study aimed to assess SF3B1 expression for neoadjuvant chemotherapy response in stage III triple-negative breast cancer. Methods:This case-control study was conducted at Prof. Dr. I.G.N.G. Ngoerah General Hospital from March to October 2021. Stage III TNBC breast cancer patients who received neoadjuvant chemotherapy were included. Variables assessed included SF3B1 expression, NAC response, and various histological and clinical parameters. Immunohistochemistry (IHC) for SF3B1 expression was performed using the avidin-biotin method. Data analysis involved univariate, bivariate (chi-square), and multivariate (logistic regression) methods using SPSS, with significance set at p ≤ 0.05. Results:Analysis showed that high Ki-67, tumor-infiltrating lymphocytes (TILs), and SF3B1 status significantly increased the risk of chemoresistance in TNBC breast cancer (OR=6.4, 95%CI=1.20-34.19, p-value=0.017; OR=4.8, 95%CI=1.05-21.75, p-value=0.031; OR=13.5, 95%CI=1.56-116.24, p-value=0.008, respectively) No significant relationships were found with age, grading, or menopausal status. Multivariate analysis confirmed these variables independently influenced chemoresistance, with aOR=14.4, 95%CI=1.80-115.73 for Ki-67 (p-value=0.012), aOR=6.7, 95%CI=1.12-40.46 for TIL (p-value=0.037), and aOR=13.714, 95%CI=1.56-116.24 for SF3B1 (p-value=0.018). Conclusions:High SF3B1 expression, alongside high Ki-67 and TIL levels, is potentially a prognostic marker for chemoresistance in stage III TNBC. These findings suggest that targeting SF3B1 could offer a novel therapeutic approach in TNBC patients.
Background:Many natural substances generated from plant crude extracts have recently been shown to protect against the harmful effects of a variety of pollutants. Ginger (Zingiber officinalis) is a widely used spice and medicinal herb. Methods:To study the effect of aqueous ginger extract in inhibiting the genotoxicity of dexamethasone, we gave the first group dexamethasone (0.4 mg/kg) only. The second group was treated with an aqueous extract of ginger (50 mg/kg) only. The third group was treated with an aqueous extract of ginger followed by dexamethasone with a two-hour interval between doses. The last group was treated with dexamethasone and an aqueous ginger extract simultaneously. To perform genetic tests, we used mitotic index, chromosomal aberrations, and micronuclei tests. Results:After the treatment with dexamethasone, chromosome aberration and micronuclei formation were induced; however, after treatment with an aqueous extract of ginger, chromosomal aberrations and micronuclei were significantly reduced in male mice. The aqueous extract of ginger did not exhibit cytotoxicity and showed high inhibitory efficiency against the toxicity and mutagenicity of dexamethasone. Conclusions:The aqueous extract of ginger plays a promising role in protecting somatic cells from the cytogenetic effects of dexamethasone, and it reduces chromosomal aberrations and micronuclei in male albino mice.
Background:Early detection of oral squamous cell carcinoma (OSCC) is essential for improving treatment outcomes. Oral lichen planus (OLP) is recognized as a premalignant condition that may progress to OSCC. Recently, microRNAs, particularly miR-let-7a, have emerged as promising biomarkers for gene regulation and early disease diagnosis. This study aimed to evaluate the expression level of miR-let-7a in OSCC and OLP patients, and to compare it with healthy controls, to determine its potential as an early diagnostic marker. Methods:In this cross-sectional study, serum samples were collected from 36 OSCC patients, 38 OLP patients, and 38 healthy controls. Diagnosis of OSCC and OLP was confirmed via biopsy. Serum RNA was isolated, and after quality verification, cDNA was synthesized. Quantitative real-time PCR (qRT-PCR) was performed to assess miR-let-7a expression across the three groups. Statistical analysis was conducted using SPSS version 16.0. Results:Significant differences in miR-let-7a expression were observed among the groups. Mean expression levels of miR-let-7a were 1.55 ± 1.19 in OSCC, 2.97 ± 2.00 in OLP, and 7.02 ± 4.10 in the control group (p< 0.001). Lower miR-let-7a expression in OSCC was notably correlated with adverse clinicopathological features, including higher tumor grade (p < 0.001), advanced clinical stage (p= 0.011), larger tumor size (T2) (p< 0.0001), and lymph node involvement (p< 0.0001). Conclusions:The findings demonstrate that miR-let-7a expression is significantly reduced in OSCC and OLP patients compared to healthy controls, highlighting its potential as an early biomarker for detecting malignant transformation in oral lesions and understanding disease progression in OSCC and OLP.
Background:The kidneys are a potential target for SARS-CoV-2 infection. Ascorbic acid (vitamin C) has been shown to play an important role in reducing the symptoms of SARS-CoV-2. Recently liposomal drug delivery platforms have demonstrated promising results in enhancing the effectiveness of various therapeutics including infectious diseases. In this study, we designed a liposomal delivery system containing vitamin C to evaluate its antiviral efficacy in COVID-19, focusing on its effects on viral entry gene expression in Vero cells. Methods:Vitamin C was loaded into a liposome made up of hydrogenated soybean phosphatidylcholine, cholesterol, and 1,2-distearoyl-sn-glycero-3 phosphoethanolamine-N-[methoxy (polyethylene glycol)-2000], and their physicochemical properties were assessed. Next, the cytotoxicity of free and liposomal vitamin C on the survival of the Vero cell line was evaluated using the MTT assay. In addition, the expression of viral entry genes, angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2), key mediators of SARS-CoV-2 entry into kidney cells, was investigated using RTq-PCR. Results:Liposomes were successfully loaded with vitamin C, achieving an encapsulation efficiency of 88.03%. The liposomal vitamin C formulation exhibited a brilliant surface morphology as observed by SEM. Both free and liposomal forms of vitamin C showed cytotoxic effects at higher concentrations. Moreover, both forms downregulated the expression of viral entry genes, although the liposomal form showed superior inhibitory performance compared to the free form. Conclusions:The study suggests liposomal vitamin C as a safe, effective treatment for COVID-19 by targeting viral entry genes in kidney cells, protecting them from viral damage and inflammation.
Background:Unilateral nephrectomy and renal ischemia-reperfusion injury (I/R) are causes of acute kidney injury that can cause renal dysfunction, decreased glomerular filtration rate, impaired homeostasis, and increased mortality. This study aimed to evaluate the combined effects of curcumin (Cur) and metformin (Met), both protective antioxidants, on renal tissue structure and Neutrophil gelatinase-associated lipocalin (Ngal) and Kidney injury molecule 1 (Kim-1) genes expression levels in rats undergoing unilateral nephrectomy and ischemia/reperfusion. Methods:In this experimental study, 40 male rats were randomly divided into five groups. The animals underwent unilateral nephrectomy and ischemia/reperfusion and were then treated with curcumin and metformin or both for 14 days. Subsequently, histopathological and morphometric analyses were performed, and Ngal and Kim-1 gene expression levels were evaluated using real-time PCR. Results:Histopathological damage, expression levels of blood urea nitrogen (BUN), creatinine (Cr), blood biochemical parameters and oxidative stress and expression levels of Ngal and Kim-1 genes were significantly reduced in the patient group that received metformin and curcumin simultaneously. However, total antioxidant capacity (TAC) was increased in the patient group that received curcumin + metformin. Morphometric parameters also improved in this group. Conclusions:The results showed that the combination therapy with curcumin and metformin effectively protected the kidneys against unilateral nephrectomy and I/R injury.
