Background: Preeclampsia (PE) is a hypertensive disorder in pregnancy affecting multiple organ systems. This study hypothesized that oxidative stress and inflammatory responses contribute to the pathogenesis of Preeclampsia, and that selenium and N-acetylcysteine (NAC) could mitigate these effects.
Methods: The study was initiated after approval from the Institutional Animal Ethics Committee. Twenty-four female Wistar rats were divided equally into four groups. Group I served as controls, while Groups II, III, and IV received Nω-Nitro-L-arginine methyl ester hydrochloride (L-NAME) to induce hypertension from day 10 to 20 of gestation. Additionally, Group III received selenium (240 μg/kg/day) and Group IV received NAC (160 mg/kg). On day 20, Blood Pressure (BP) monitoring and urine protein estimation were carried out to assess hypertension and proteinuria, while blood samples were collected to measure malondialdehyde (MDA) and interleukin-6 (IL-6) levels, as markers of oxidative stress and inflammation, respectively. Statistical analysis was performed using GraphPad Prism 10.2.
Results: Selenium improved L-NAME-induced hypertension (Mean BP 107.63±5.22 mmHg vs 140.9±8.38 mmHg in disease control (DC) and proteinuria (65.5±4.09 vs 140.2±11.85 mg/day in DC) and significantly reduced the inflammatory response (IL-6 23.4±1.06 vs 50.63±3.35 pg/mL in DC) but had little effect on oxidative stress (MDA 0.21±0.02 vs 0.24±0.02 nmol/mL in DC). NAC did not lower BP (Mean BP 129.33±7.96 mmHg) but significantly reduced proteinuria (92.7±6.37mg/day), IL-6 levels (18.24±0.42 pg/mL), and oxidative stress (MDA 0.16±0.01 nmol/mL).
Conclusions: These findings suggest that selenium and NAC play distinct protective roles in the pathophysiology of preeclampsia, potentially offering synergistic effects for cardiovascular and kidney health in hypertensive pregnancies.
背景:子痫前期(PE)是一种影响多器官系统的妊娠期高血压疾病。本研究假设氧化应激和炎症反应参与了子痫前期的发病机制,而硒和n -乙酰半胱氨酸(NAC)可以减轻这些作用。方法:本研究经机构动物伦理委员会批准后启动。24只雌性Wistar大鼠平均分为四组。I组作为对照组,II、III、IV组在妊娠第10 ~ 20天给予n ω-硝基- l -精氨酸甲酯盐酸盐(L-NAME)诱导高血压。另外,III组给予硒(240 μg/kg/d), IV组给予NAC (160 mg/kg)。第20天,进行血压(BP)监测和尿蛋白测定,以评估高血压和蛋白尿,同时采集血样检测丙二醛(MDA)和白细胞介素-6 (IL-6)水平,分别作为氧化应激和炎症的标志物。采用GraphPad Prism 10.2进行统计学分析。结果:硒改善l -名诱导的高血压(疾病控制组平均血压107.63±5.22 mmHg vs 140.9±8.38 mmHg)和蛋白尿(DC组平均血压65.5±4.09 vs 140.2±11.85 mg/d),显著降低炎症反应(DC组平均IL-6 23.4±1.06 vs 50.63±3.35 pg/mL),但对氧化应激影响不大(DC组平均MDA 0.21±0.02 vs 0.24±0.02 nmol/mL)。NAC没有降低血压(平均血压129.33±7.96 mmHg),但显著降低蛋白尿(92.7±6.37mg/天)、IL-6水平(18.24±0.42 pg/mL)和氧化应激(MDA 0.16±0.01 nmol/mL)。结论:这些发现提示硒和NAC在子痫前期的病理生理中具有明显的保护作用,可能对高血压妊娠的心血管和肾脏健康有协同作用。
{"title":"Potential Effects of Selenium and N-Acetylcysteine Supplementation in Ameliorating Cardinal Symptoms of Nω-Nitro-L-Arginine Methyl Ester Hydrochloride (L-NAME) Induced Preeclampsia in Wistar Rats.","authors":"Geethika Yelleti, Annayya Rao Aroor, Revathi Panduranga Shenoy, Abhibroto Karmakar, Ashwini Rao, Cheryl Rhea Lewis, Arjun Asok, Nihaal Maripini, Monalisa Biswas, Veena Varier, Arpita Roy, Varashree Bolar Suryakanth","doi":"10.61186/rbmb.13.4.495","DOIUrl":"10.61186/rbmb.13.4.495","url":null,"abstract":"<p><strong>Background: </strong>Preeclampsia (PE) is a hypertensive disorder in pregnancy affecting multiple organ systems. This study hypothesized that oxidative stress and inflammatory responses contribute to the pathogenesis of Preeclampsia, and that selenium and N-acetylcysteine (NAC) could mitigate these effects.</p><p><strong>Methods: </strong>The study was initiated after approval from the Institutional Animal Ethics Committee. Twenty-four female Wistar rats were divided equally into four groups. Group I served as controls, while Groups II, III, and IV received Nω-Nitro-L-arginine methyl ester hydrochloride (L-NAME) to induce hypertension from day 10 to 20 of gestation. Additionally, Group III received selenium (240 μg/kg/day) and Group IV received NAC (160 mg/kg). On day 20, Blood Pressure (BP) monitoring and urine protein estimation were carried out to assess hypertension and proteinuria, while blood samples were collected to measure malondialdehyde (MDA) and interleukin-6 (IL-6) levels, as markers of oxidative stress and inflammation, respectively. Statistical analysis was performed using GraphPad Prism 10.2.</p><p><strong>Results: </strong>Selenium improved L-NAME-induced hypertension (Mean BP 107.63±5.22 mmHg vs 140.9±8.38 mmHg in disease control (DC) and proteinuria (65.5±4.09 vs 140.2±11.85 mg/day in DC) and significantly reduced the inflammatory response (IL-6 23.4±1.06 vs 50.63±3.35 pg/mL in DC) but had little effect on oxidative stress (MDA 0.21±0.02 vs 0.24±0.02 nmol/mL in DC). NAC did not lower BP (Mean BP 129.33±7.96 mmHg) but significantly reduced proteinuria (92.7±6.37mg/day), IL-6 levels (18.24±0.42 pg/mL), and oxidative stress (MDA 0.16±0.01 nmol/mL).</p><p><strong>Conclusions: </strong>These findings suggest that selenium and NAC play distinct protective roles in the pathophysiology of preeclampsia, potentially offering synergistic effects for cardiovascular and kidney health in hypertensive pregnancies.</p>","PeriodicalId":45319,"journal":{"name":"Reports of Biochemistry and Molecular Biology","volume":"13 4","pages":"495-506"},"PeriodicalIF":1.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12367218/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144973476","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: Apelin is a naturally produced ligand for G protein-linked receptors derived from a 77-amino acid pre-propeptide. The effect of apelin on the development of cardiovascular diseases and the relationship between the apelin gene and the apelin receptor.
Methods: The case-control study included 100 participants of people suffering from cardiovascular diseases. Samples were collected from patients hospitalized at the Nasiriyah Heart Center between November 10, 2023, and February 15, 2024. The study also included 50 healthy people who did not suffer from cardiovascular disease. The lipid profile was measured by spectrophotometer, and the Apelin level was measured by enzyme-linked immunosorbent assay. Four single nucleotide polymorphisms for Apelin (APLN) and Apelin receptor (APLNR) were chosen, and Sanger sequencing was used to genotype them accurately.
Results: The findings indicated that there was no statistically significant difference in age between the two groups. Upon comparing the age demographics of the two groups in the study, the results indicated a lack of statistical significance in the levels of APLN or the lipid profile, despite the case group exhibiting markedly elevated Apelin and lipid levels compared to the control group. After multiple test adjustments (P < 0.05), neither the APLN rs2235310T allele nor the APLNR rs9943582 allele demonstrated an association with an elevated risk of coronary heart disease.
Conclusions: The investigation revealed no significant age variations or genetic correlations associated with CHD risk. However, rather than age or genetic differences, elevated apelin and cholesterol levels in the case group indicate these factors as primary contributors to cardiovascular risk.
{"title":"Investigation of Genetic Variations in APLN and APLNR Genes and Their Potential Role in Cardiovascular Diseases.","authors":"Nabaa Azhar Abdulmuttaleb, Abdelhameed Abdelkhaliq Oliwi Nasir, Sami Awad Alkubaisy, Osama Akram Mohsein","doi":"10.61186/rbmb.13.4.525","DOIUrl":"10.61186/rbmb.13.4.525","url":null,"abstract":"<p><strong>Background: </strong>Apelin is a naturally produced ligand for G protein-linked receptors derived from a 77-amino acid pre-propeptide. The effect of apelin on the development of cardiovascular diseases and the relationship between the apelin gene and the apelin receptor.</p><p><strong>Methods: </strong>The case-control study included 100 participants of people suffering from cardiovascular diseases. Samples were collected from patients hospitalized at the Nasiriyah Heart Center between November 10, 2023, and February 15, 2024. The study also included 50 healthy people who did not suffer from cardiovascular disease. The lipid profile was measured by spectrophotometer, and the Apelin level was measured by enzyme-linked immunosorbent assay. Four single nucleotide polymorphisms for Apelin (APLN) and Apelin receptor (APLNR) were chosen, and Sanger sequencing was used to genotype them accurately.</p><p><strong>Results: </strong>The findings indicated that there was no statistically significant difference in age between the two groups. Upon comparing the age demographics of the two groups in the study, the results indicated a lack of statistical significance in the levels of APLN or the lipid profile, despite the case group exhibiting markedly elevated Apelin and lipid levels compared to the control group. After multiple test adjustments (P < 0.05), neither the APLN rs2235310T allele nor the APLNR rs9943582 allele demonstrated an association with an elevated risk of coronary heart disease.</p><p><strong>Conclusions: </strong>The investigation revealed no significant age variations or genetic correlations associated with CHD risk. However, rather than age or genetic differences, elevated apelin and cholesterol levels in the case group indicate these factors as primary contributors to cardiovascular risk.</p>","PeriodicalId":45319,"journal":{"name":"Reports of Biochemistry and Molecular Biology","volume":"13 4","pages":"525-539"},"PeriodicalIF":1.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12367213/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144973519","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: Arsenic (As), a toxic metalloid present in drinking water, is one of the environmental pollutants associated with diabetes in humans. Vanillic acid (VA), a bioactive compound derived from plants has various medicinal activities.
Methods: This study was conducted on NMRI male mice for 8 weeks. forty mice were randomly divided into control group, As group (50 ppm), VA (100 mg/kg) group, and two groups receiving As (50 ppm) and VA with doses of 50 mg/kg and 100 mg/kg. After 56 days of the study, the mice were fasted overnight and on day 57, fasting blood glucose was measured, and glucose tolerance test was performed. On day 59, mice were euthanized and serum factors, markers of oxidative stress, tumor necrosis factor-α (TNF-α), and expression nuclear factor kappa B (NF-κB) and Peroxisome Proliferator-Activated Receptor Gamma (PPARγ) proteins were measured.
Results: The As significantly increased fasting blood sugar, the activity level of liver function enzymes, thiobarbituric acid reactive substances (TBARS), nitric oxide (NO), TNF-α, and NF-κB expression. Furthermore, As decreased hepatic total thiol (TT) and activity levels of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) and expression of PPARγ. VA decreased the altered liver enzymes, hyperglycemia, NO, TBARS, TNF-α and the expression of NF-κB. Furthermore, increased the hepatic activity of the CAT, SOD, and GPx, TT and the expression of PPARγ.
Conclusions: The administration of VA at doses of 50 and 100 mg/kg demonstrated significant mitigation of the toxic effects induced by As on the liver.
{"title":"Protective Effects of Vanillic Acid on Arsenic-Induced Hepatotoxicity and Diabetes in Mice; the Role of PPARγ and NF-κB Signaling.","authors":"Saeedeh Shariati, Mohammad Javad Khodayar, Reza Azadnasab, Narjes Moghtadaei, Layasadat Khorsandi, Maryam Shirani","doi":"10.61186/rbmb.13.4.549","DOIUrl":"10.61186/rbmb.13.4.549","url":null,"abstract":"<p><strong>Background: </strong>Arsenic (As), a toxic metalloid present in drinking water, is one of the environmental pollutants associated with diabetes in humans. Vanillic acid (VA), a bioactive compound derived from plants has various medicinal activities.</p><p><strong>Methods: </strong>This study was conducted on NMRI male mice for 8 weeks. forty mice were randomly divided into control group, As group (50 ppm), VA (100 mg/kg) group, and two groups receiving As (50 ppm) and VA with doses of 50 mg/kg and 100 mg/kg. After 56 days of the study, the mice were fasted overnight and on day 57, fasting blood glucose was measured, and glucose tolerance test was performed. On day 59, mice were euthanized and serum factors, markers of oxidative stress, tumor necrosis factor-α (TNF-α), and expression nuclear factor kappa B (NF-κB) and Peroxisome Proliferator-Activated Receptor Gamma (PPARγ) proteins were measured.</p><p><strong>Results: </strong>The As significantly increased fasting blood sugar, the activity level of liver function enzymes, thiobarbituric acid reactive substances (TBARS), nitric oxide (NO), TNF-α, and NF-κB expression. Furthermore, As decreased hepatic total thiol (TT) and activity levels of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) and expression of PPARγ. VA decreased the altered liver enzymes, hyperglycemia, NO, TBARS, TNF-α and the expression of NF-κB. Furthermore, increased the hepatic activity of the CAT, SOD, and GPx, TT and the expression of PPARγ.</p><p><strong>Conclusions: </strong>The administration of VA at doses of 50 and 100 mg/kg demonstrated significant mitigation of the toxic effects induced by As on the liver.</p>","PeriodicalId":45319,"journal":{"name":"Reports of Biochemistry and Molecular Biology","volume":"13 4","pages":"549-560"},"PeriodicalIF":1.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12367214/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144973540","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: Hospitalized Coronavirus Disease 2019 (COVID-19) patients are at a higher risk of bacterial and fungal infections. Procalcitonin is an inflammatory marker that has been suggested for distinguishing between bacterial and viral infections that predicting bacterial co-infection in COVID-19 and serving as a helpful indicator for determining the severity of the illness. This study aimed to evaluate procalcitonin levels and antimicrobial resistance (AMR) among microbial co-infections in hospitalized COVID-19 patients.
Methods: Clinical and microbiological data were obtained from the medical records of 100 COVID-19 patients.
Results: COVID-19 patients with bacterial infections had a 55% mortality rate. The majority of microbial cultures were detected in blood (49%), sputum (44%), and urine (7%). Among the isolates, 57.7% were Gram-negative bacteria, 31.7% were Gram-positive bacteria, 6.7% were mixed isolates, and 3.8% were fungal isolates. The predominant Gram-negative isolates were Klebsiella pneumoniae (37.2%), Acinetobacter baumannii (20.2%), and Streptococcus pneumoniae (14.4%). Candida albicans (2.9%) was the most commonly isolated fungal pathogen, followed by Aspergillus spp. (1%). Most of the isolates showed high resistance to broad-spectrum antibiotics. Gram-negative bacteria were detected in 29% of COVID-19 patients who died, Gram-positive bacteria in 20%, and mixed bacteria in 6%. The majority of surviving patients had procalcitonin levels below 0.25 ng/mL, whereas non- survivors had higher levels.
Conclusions: Secondary microbial infections in COVID-19 patients remain a critical concern during the pandemic. Additionally, multidrug-resistant organisms are an increasing challenge. In hospitalized COVID-19 patients, baseline procalcitonin levels were associated with patient outcomes and bacterial coinfection.
{"title":"Procalcitonin Level and Antimicrobial Resistance among Microbial Coinfection in Hospitalized COVID-19 Patients.","authors":"Abdulqadr Khdir Hamad, Suhayla Hamad Shareef, Chiman Hameed Saeed, Ramiar Kamal Kheder, Pshtiwan Dhahir Majeed","doi":"10.61186/rbmb.13.4.474","DOIUrl":"10.61186/rbmb.13.4.474","url":null,"abstract":"<p><strong>Background: </strong>Hospitalized Coronavirus Disease 2019 (COVID-19) patients are at a higher risk of bacterial and fungal infections. Procalcitonin is an inflammatory marker that has been suggested for distinguishing between bacterial and viral infections that predicting bacterial co-infection in COVID-19 and serving as a helpful indicator for determining the severity of the illness. This study aimed to evaluate procalcitonin levels and antimicrobial resistance (AMR) among microbial co-infections in hospitalized COVID-19 patients.</p><p><strong>Methods: </strong>Clinical and microbiological data were obtained from the medical records of 100 COVID-19 patients.</p><p><strong>Results: </strong>COVID-19 patients with bacterial infections had a 55% mortality rate. The majority of microbial cultures were detected in blood (49%), sputum (44%), and urine (7%). Among the isolates, 57.7% were Gram-negative bacteria, 31.7% were Gram-positive bacteria, 6.7% were mixed isolates, and 3.8% were fungal isolates. The predominant Gram-negative isolates were <i>Klebsiella pneumoniae</i> (37.2%), <i>Acinetobacter baumannii</i> (20.2%), and <i>Streptococcus pneumoniae</i> (14.4%). <i>Candida albicans</i> (2.9%) was the most commonly isolated fungal pathogen, followed by <i>Aspergillus spp</i>. (1%). Most of the isolates showed high resistance to broad-spectrum antibiotics. Gram-negative bacteria were detected in 29% of COVID-19 patients who died, Gram-positive bacteria in 20%, and mixed bacteria in 6%. The majority of surviving patients had procalcitonin levels below 0.25 ng/mL, whereas non- survivors had higher levels.</p><p><strong>Conclusions: </strong>Secondary microbial infections in COVID-19 patients remain a critical concern during the pandemic. Additionally, multidrug-resistant organisms are an increasing challenge. In hospitalized COVID-19 patients, baseline procalcitonin levels were associated with patient outcomes and bacterial coinfection.</p>","PeriodicalId":45319,"journal":{"name":"Reports of Biochemistry and Molecular Biology","volume":"13 4","pages":"474-483"},"PeriodicalIF":1.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12367216/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144973448","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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.
{"title":"The Inhibitory Effect of Aqueous Ginger Extract on the Genotoxicity of Dexamethasone in Male Albino Mice.","authors":"Aseel Raheem Al-Aamiri","doi":"10.61186/rbmb.13.4.466","DOIUrl":"10.61186/rbmb.13.4.466","url":null,"abstract":"<p><strong>Background: </strong>Many natural substances generated from plant crude extracts have recently been shown to protect against the harmful effects of a variety of pollutants. Ginger (<i>Zingiber officinalis</i>) is a widely used spice and medicinal herb.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusions: </strong>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.</p>","PeriodicalId":45319,"journal":{"name":"Reports of Biochemistry and Molecular Biology","volume":"13 4","pages":"466-473"},"PeriodicalIF":1.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12367212/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144973517","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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.
{"title":"Mir-let-7a Differential Expression in Oral Squamous Cell Carcinoma and Oral Lichen Planus: Insights for Early Diagnostic Biomarker Development.","authors":"Seyedmovahed Seyedhoseini, Nooshin Mohtasham, Shadi Saghafi, Negin Alahkhani, Farnaz Mohajertehran, Fahimeh Afzaljavan, Mahammad Taghi Shakeri, Amirkian Bokharaei","doi":"10.61186/rbmb.13.4.456","DOIUrl":"10.61186/rbmb.13.4.456","url":null,"abstract":"<p><strong>Background: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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).</p><p><strong>Conclusions: </strong>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.</p>","PeriodicalId":45319,"journal":{"name":"Reports of Biochemistry and Molecular Biology","volume":"13 4","pages":"456-465"},"PeriodicalIF":1.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12367217/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144972963","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mohammad Reza Karimzadeh, Atefeh Najmadini, Sara Azhdari, Negin Zatalian, Fatemeh Zandi, Neda Salmani, Kolsoum Saeidi
Background: Alzheimer's disease (AD) is a widespread neurodegenerative disorder among the elderly, characterized by dementia. The development of AD is significantly influenced by genetic risk factors.
Methods: in this study, we have investigated the impact of rs2234759 and rs12507396 polymorphisms in the neuropeptide Y receptor Y2 (NPY2R) gene on AD. Nineteen AD patients and nineteen healthy controls were enlisted in our research. and the DNA samples of all participants were genotyped using amplification refractory mutation system-polymerase chain reaction (ARMS-PCR).
Results: The results revealed a noteworthy association between rs2234759 and AD, with a noticeable difference observed in the frequency of genotypes and alleles of this polymorphism between patients and healthy controls (P< 0.001 for both). However, no significant difference was detected in the genotype distribution concerning the rs12507396 polymorphism between the two groups.
Conclusions: Our findings provide compelling evidence of an association between the rs2234759 polymorphism in NPY2R and Alzheimer's disease. Given the significant role of NPY2R in brain tissue, this particular polymorphism may result in strengthened presynaptic inhibition of glutamate release.
{"title":"Association of Alzheimer's Disease with Promoter Variations in NPY2R Gene.","authors":"Mohammad Reza Karimzadeh, Atefeh Najmadini, Sara Azhdari, Negin Zatalian, Fatemeh Zandi, Neda Salmani, Kolsoum Saeidi","doi":"10.61186/rbmb.13.4.507","DOIUrl":"10.61186/rbmb.13.4.507","url":null,"abstract":"<p><strong>Background: </strong>Alzheimer's disease (AD) is a widespread neurodegenerative disorder among the elderly, characterized by dementia. The development of AD is significantly influenced by genetic risk factors.</p><p><strong>Methods: </strong>in this study, we have investigated the impact of rs2234759 and rs12507396 polymorphisms in the neuropeptide Y receptor Y2 (NPY2R) gene on AD. Nineteen AD patients and nineteen healthy controls were enlisted in our research. and the DNA samples of all participants were genotyped using amplification refractory mutation system-polymerase chain reaction (ARMS-PCR).</p><p><strong>Results: </strong>The results revealed a noteworthy association between rs2234759 and AD, with a noticeable difference observed in the frequency of genotypes and alleles of this polymorphism between patients and healthy controls (P< 0.001 for both). However, no significant difference was detected in the genotype distribution concerning the rs12507396 polymorphism between the two groups.</p><p><strong>Conclusions: </strong>Our findings provide compelling evidence of an association between the rs2234759 polymorphism in NPY2R and Alzheimer's disease. Given the significant role of NPY2R in brain tissue, this particular polymorphism may result in strengthened presynaptic inhibition of glutamate release.</p>","PeriodicalId":45319,"journal":{"name":"Reports of Biochemistry and Molecular Biology","volume":"13 4","pages":"507-515"},"PeriodicalIF":1.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12367215/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144973462","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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.
{"title":"Protective Effects of Liposomal Vitamin C on SARS-CoV-2 Target Viral Entry Genes in Renal Cells.","authors":"Abtin Behmardi, Leila Zolghadr, Farzad Rajaei, Saeideh Gholamzadeh Khoei, Nematollah Gheibi","doi":"10.61186/rbmb.13.4.484","DOIUrl":"10.61186/rbmb.13.4.484","url":null,"abstract":"<p><strong>Background: </strong>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.</p><p><strong>Methods: </strong>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, <i>angiotensin-converting enzyme 2</i> (ACE2) and <i>transmembrane protease serine 2</i> (TMPRSS2), key mediators of SARS-CoV-2 entry into kidney cells, was investigated using RTq-PCR.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusions: </strong>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.</p>","PeriodicalId":45319,"journal":{"name":"Reports of Biochemistry and Molecular Biology","volume":"13 4","pages":"484-494"},"PeriodicalIF":1.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12367220/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144973483","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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.
{"title":"Comparative Analysis of Curcumin and Metformin Effects on the Kidney in a Model of Unilateral Nephrectomy and Ischemia-Reperfusion Injury.","authors":"Samaneh Karimi, Farhad Koohpeyma, Layasadat Khorsandi, Armin Panahi, Fatemeh Rezaei-Tazangi, Fereshtesadat Fakhredini","doi":"10.61186/rbmb.13.4.579","DOIUrl":"10.61186/rbmb.13.4.579","url":null,"abstract":"<p><strong>Background: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusions: </strong>The results showed that the combination therapy with curcumin and metformin effectively protected the kidneys against unilateral nephrectomy and I/R injury.</p>","PeriodicalId":45319,"journal":{"name":"Reports of Biochemistry and Molecular Biology","volume":"13 4","pages":"579-589"},"PeriodicalIF":1.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12367211/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144973494","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
El Hadji Malick Ndour, Rokhaya Dione, Fatou Gueye-Tall, Sokhna Mara, Gora Fall, Coumba Kamby, El Hadji Ousmane Sene, Moustapha Djite, Nene Oumou Kesso Barry, Pape Matar Kandji, Papa Madieye Gueye, Philomene Lopez-Sall, Aynina Cisse
Background: Moderately increased albuminuria is a biomarker for early onset diabetic nephropathy. The aim of this study was to evaluate the performance of use proteinuria-to-creatininuria ratio (UPCR) at different cut-off to screen for increased albuminuria using albuminuria-to-creatininuria ratio (UACR) as a gold standard.
Methods: This was a cross-sectional study. A random spot urine sample was collected from patients with type 1 diabetes to measure albuminuria and total proteinuria using respectively an immunoturbidimetric and a colorimetric assay. Albuminuria was expressed as UACR and proteinuria as UPCR. The area under the curve (AUC) method and the kappa coefficient were used to compare UPCR and UACR.
Results: In 150 diabetic patients, moderately increased albuminuria was detected in 33.3% using UACR and 35.3% using UPCR at 272 mg/g. UPCR thresholds of 130, 150, 180 and 200 mg/g yielded higher detection rates than UACR. However, all UPCR cut-offs showed low diagnostic accuracy (AUC < 70%), and agreement with UACR was mild (kappa < 0.40).
Conclusions: The level of agreement between UPCR and UACR was moderate. It is not sufficient for UPCR to replace UACR to screen for increased albuminuria in patient with type 1 diabetes.
{"title":"Usefulness of A Random Spot Urine Proteins-to-Creatinine Ratio to Screen for Increased Albuminuria in Patients with Type 1 Diabetes.","authors":"El Hadji Malick Ndour, Rokhaya Dione, Fatou Gueye-Tall, Sokhna Mara, Gora Fall, Coumba Kamby, El Hadji Ousmane Sene, Moustapha Djite, Nene Oumou Kesso Barry, Pape Matar Kandji, Papa Madieye Gueye, Philomene Lopez-Sall, Aynina Cisse","doi":"10.61186/rbmb.13.4.561","DOIUrl":"10.61186/rbmb.13.4.561","url":null,"abstract":"<p><strong>Background: </strong>Moderately increased albuminuria is a biomarker for early onset diabetic nephropathy. The aim of this study was to evaluate the performance of use proteinuria-to-creatininuria ratio (UPCR) at different cut-off to screen for increased albuminuria using albuminuria-to-creatininuria ratio (UACR) as a gold standard.</p><p><strong>Methods: </strong>This was a cross-sectional study. A random spot urine sample was collected from patients with type 1 diabetes to measure albuminuria and total proteinuria using respectively an immunoturbidimetric and a colorimetric assay. Albuminuria was expressed as UACR and proteinuria as UPCR. The area under the curve (AUC) method and the kappa coefficient were used to compare UPCR and UACR.</p><p><strong>Results: </strong>In 150 diabetic patients, moderately increased albuminuria was detected in 33.3% using UACR and 35.3% using UPCR at 272 mg/g. UPCR thresholds of 130, 150, 180 and 200 mg/g yielded higher detection rates than UACR. However, all UPCR cut-offs showed low diagnostic accuracy (AUC < 70%), and agreement with UACR was mild (kappa < 0.40).</p><p><strong>Conclusions: </strong>The level of agreement between UPCR and UACR was moderate. It is not sufficient for UPCR to replace UACR to screen for increased albuminuria in patient with type 1 diabetes.</p>","PeriodicalId":45319,"journal":{"name":"Reports of Biochemistry and Molecular Biology","volume":"13 4","pages":"561-569"},"PeriodicalIF":1.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12367222/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144973492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}