Frontiers in bioscience (Scholar edition)最新文献

{"title":"Genotyping the <i>BCL11A</i> Single Nucleotide Polymorphism and Associated Levels of Fetal Hemoglobin in Mauritanian Sickle Cell Patients.","authors":"Aminetou Taleb Brahim, Mariem Taleb, Harouna Soumaré, Sidi Mohamed Ghaber, Aminetou Mohamed, Ali Ould Mohamed Salem Boukhary","doi":"10.31083/j.fbs1602011","DOIUrl":"10.31083/j.fbs1602011","url":null,"abstract":"<p><strong>Background: </strong>Sickle cell disease (SCD) is a major heritable genetic disease in sub-Saharan Africa, including Mauritania. Fetal hemoglobin (HbF) can affect the pathophysiology, moderate the clinical course, and offer prospects for curative treatment of SCD. This study aimed to investigate the influence of single nucleotide polymorphisms (SNPs) in the <i>BCL11A</i> gene on the levels of HbF and hematological parameters in Mauritanian sickle cell (<i>HbSS</i>) patients.</p><p><strong>Methods: </strong>Complete blood count was assessed in 565 patients suspected to have SCD. Polymerase chain reaction (PCR)-restriction fragment length polymorphism was performed to identify the <i>HbSS</i>, and sequencing was used for genotyping three SNPs: <i>rs4671393</i> (<i>A>G</i>) and <i>rs11886868</i> (<i>C>T</i>) in the intron 2 and <i>rs1052520</i> (<i>G>A</i>) in the <i>3'UTR</i> regions of the <i>BCL11A</i> gene in 50 sickle cell patients.</p><p><strong>Results: </strong>The prevalence of HbSS among the study population was 8.8% (50/565), and the mean (± standard deviation) of HbF level was 15.0% (± 6.0%). Sequencing showed the presence of three genotypes: AA (13.6%), AG (46.6%), GG (39.6%) in rs4671393; CC (17.6%), CT (48.7%), and TT (33.6%) in <i>rs11886868</i>. All samples from HbSS individuals displayed a wild-type genotype in the rs1052520 allele. The prevalence of minor alleles <i>A</i> (<i>rs4671393</i>) and <i>C</i> (<i>rs11886868</i>) were 37% and 39%, respectively. There was a statistically significant association (<i>p</i> = 0.034) between rs4671393 SNP and elevated HbF (mean 12.72 ± 6.26%).</p><p><strong>Conclusions: </strong>The study of three SNPs in the <i>BCL11A</i> locus in Mauritanian patients with SCD showed a significant association of <i>rs4671393</i> allele with the HbF level. Further research is needed to explore additional SNPs in the <i>BCL11A</i> locus and investigate other genetic markers reported to modulate HbF levels, such as <i>HBS1L-MYB</i> and <i>Xmn1-HBG2</i>, to improve the management of this potentially life-threatening condition in Mauritania.</p>","PeriodicalId":73070,"journal":{"name":"Frontiers in bioscience (Scholar edition)","volume":"16 2","pages":"11"},"PeriodicalIF":0.0,"publicationDate":"2024-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141473236","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Enoxaparin Effect on Interleukin-10 Levels in Iraqi Patients with COVID-19: A Case-Control Study.","authors":"Nawal Haider Al-Hashimi, Mohammed S Al-Hindawi, Ali M Mohsen, Abdulnasser M Al-Gebori","doi":"10.31083/j.fbs1602009","DOIUrl":"10.31083/j.fbs1602009","url":null,"abstract":"<p><strong>Background: </strong>Coronavirus disease 19 (COVID-19), an infectious disease resulting from a virus known as severe acute respiratory syndrome coronavirus 2 (SARS-COV-2), was discovered in China in 2019 and causes several mild to moderate respiratory conditions. This study aimed to reveal the changes in serum interleukin-10 (IL-10) and other parameters in Iraqi COVID-19 patients compared with healthy controls by studying the effects of enoxaparin and evaluating the potential of IL-10 as a disease activity marker.</p><p><strong>Methods: </strong>This was a case-control study that included 180 samples: 90 patients hospitalized with COVID-19 from November 2022 to 20 April 2023 (40 patients had never used enoxaparin, whereas 50 patients had taken enoxaparin) and 90 healthy, age- and sex-matched control. There were 44 female patients and 46 male patients. The mean age of the patients and controls was 53.8 years <i>vs.</i> 50.8 years, respectively. The sandwich enzyme-linked immunosorbent assay (ELISA) method was used to measure IL-10 levels, while other parameters were assessed using the colorimetric method.</p><p><strong>Results: </strong>The results of the study indicated highly significant changes between the patients and healthy controls in IL-10, D-dimer, and C-reactive protein (CRP) levels, as well as liver and renal functions. These findings elucidated a significant change between enoxaparin patients and non-enoxaparin patients in IL-10, D-dimer, and CRP levels. However, the liver and renal functions were not significantly altered. The Spearman's rank correlation test investigated the relationship between serum IL-10 and CRP.</p><p><strong>Conclusions: </strong>The results displayed a strong positive relationship between IL-10 and CRP. There were no significant differences between the other analyzed parameters; consequently, the patients had higher concentrations of IL-10, D-dimer, and some other parameters than the healthy controls. Additionally, IL-10 may be used as a marker of disease activity. Enoxaparin will likely help control IL-10 and D-dimer concentrations in patients since IL-10 levels decreased in patients treated with enoxaparin.</p>","PeriodicalId":73070,"journal":{"name":"Frontiers in bioscience (Scholar edition)","volume":"16 2","pages":"9"},"PeriodicalIF":0.0,"publicationDate":"2024-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141473234","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial Dysfunction as a Factor of Energy Metabolism Disorders in Type 2 Diabetes Mellitus.","authors":"Alexander Blagov, Ludmila Nedosugova, Tatiana Kirichenko, Vasily Sukhorukov, Alexandra Melnichenko, Alexander Orekhov","doi":"10.31083/j.fbs1601005","DOIUrl":"10.31083/j.fbs1601005","url":null,"abstract":"<p><p>The pathogenesis of type 2 diabetes mellitus (T2DM) is based on the development of insulin resistance, which is a disruption to the ability of the tissues to bind to insulin, leading to a general metabolic disorder. Mitochondria are the main participants in cellular energy metabolism, meaning their dysfunction is associated with the development of insulin resistance in T2DM. Mitochondrial function is affected by insulin resistance in various tissues, including skeletal muscle and the liver, which greatly influence glucose homeostasis throughout the body. This review studies mitochondrial dysfunction in T2DM and its impact on disease progression. In addition, it considers the causes underlying the development of mitochondrial dysfunction in T2DM, including mutations in the mitochondrial genome, mitochondrial DNA methylation, and other epigenetic influences, as well as the impact of impaired mitochondrial membrane potential. New therapeutic strategies for diabetes that have been developed to target the mitochondria will also be presented.</p>","PeriodicalId":73070,"journal":{"name":"Frontiers in bioscience (Scholar edition)","volume":"16 1","pages":"5"},"PeriodicalIF":0.0,"publicationDate":"2024-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140308192","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetics and Age-Related Macular Degeneration: A Practical Review for Clinicians.","authors":"Julia Nguyen, Milam A Brantley, Stephen G Schwartz","doi":"10.31083/j.fbs1601003","DOIUrl":"10.31083/j.fbs1601003","url":null,"abstract":"<p><p>Age-related macular degeneration (AMD) is a multifactorial genetic disease, with at least 52 identifiable associated gene variants at 34 loci, including variants in <i>complement factor H</i> (<i>CFH</i>) and <i>age-related maculopathy susceptibility 2/high-temperature requirement A serine peptidase-1</i> (<i>ARMS2/HTRA1</i>). Genetic factors account for up to 70% of disease variability. However, population-based genetic risk scores are generally more helpful for clinical trial design and stratification of risk groups than for individual patient counseling. There is some evidence of pharmacogenetic influences on various treatment modalities used in AMD patients, including Age-Related Eye Disease Study (AREDS) supplements, photodynamic therapy (PDT), and anti-vascular endothelial growth factor (anti-VEGF) agents. However, there is currently no convincing evidence that genetic information plays a role in routine clinical care.</p>","PeriodicalId":73070,"journal":{"name":"Frontiers in bioscience (Scholar edition)","volume":"16 1","pages":"3"},"PeriodicalIF":0.0,"publicationDate":"2024-02-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140308191","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CpG Islands, Gene Expression and Pseudogenization: A Case for a Potential Trilogy.","authors":"Ammad Aslam Khan, Anees Fatima","doi":"10.31083/j.fbs1601002","DOIUrl":"10.31083/j.fbs1601002","url":null,"abstract":"<p><strong>Background: </strong>The promoters of mammalian genes contain clusters of CG dinucleotides known as CpG islands. Most mammalian housekeeping genes predominantly contain CpG islands (CGIs), facilitating gene transcription. Numerous studies have explored the physiological implications of the relationship between CGIs and gene expression. However, the evolutionary implications of this relationship remain largely unexplored. Pseudogenes, in contrast, are genomic remnants that have lost their function over evolutionary time.</p><p><strong>Methods: </strong>In our current research, we employed comparative genomic techniques to demonstrate a correlation between the absence of gene expression due to a lack of CGIs in the gene promoters and pseudogenization.</p><p><strong>Results: </strong>We showed that there is a significant enrichment of tissue-specific genes in the functional orthologs of pseudogenes. We also found a significant correlation between the lack of CGIs and enriched tissue specificity in these functional orthologs of pseudogenes.</p><p><strong>Conclusions: </strong>We inferred that perhaps tissue-specific genes are more prone to the process of pseudogenization. In this way, because of their impact on gene expression, CGIs may affect the fate of a gene. To our knowledge, this is the first study to propose a connection between CGIs, gene expression, and the pseudogenization process and discuss the evolutionary implications of this potential trilogy.</p>","PeriodicalId":73070,"journal":{"name":"Frontiers in bioscience (Scholar edition)","volume":"16 1","pages":"2"},"PeriodicalIF":0.0,"publicationDate":"2024-02-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140308190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A New Leu714Arg Variant in the Converter Domain of <i>MYH7</i> is Associated with a Severe Form of Familial Hypertrophic Cardiomyopathy.","authors":"Maria V Golubenko, Elena N Pavlyukova, Ramil R Salakhov, Oksana A Makeeva, Konstantin V Puzyrev, Oleg S Glotov, Valery P Puzyrev, Maria S Nazarenko","doi":"10.31083/j.fbs1601001","DOIUrl":"10.31083/j.fbs1601001","url":null,"abstract":"<p><strong>Background: </strong>Hypertrophic cardiomyopathy is the most frequent autosomal dominant disease, yet due to genetic heterogeneity, incomplete penetrance, and phenotype variability, the prognosis of the disease course in pathogenic variant carriers remains an issue. Identifying common patterns among the effects of different genetic variants is important.</p><p><strong>Methods: </strong>We investigated the cause of familial hypertrophic cardiomyopathy (HCM) in a family with two patients suffering from a particularly severe disease. Searching for the genetic variants in HCM genes was performed using different sequencing methods.</p><p><strong>Results: </strong>A new missense variant, p.Leu714Arg, was identified in exon 19 of the beta-myosin heavy chain gene (<i>MYH7</i>). The mutation was found in a region that encodes the 'converter domain' in the globular myosin head. This domain is essential for the conformational change of myosin during ATP cleavage and contraction cycle. Most reports on different mutations in this region describe severe phenotypic consequences. The two patients with the p.Leu714Arg mutation had heart failure early in life and died from HCM complications.</p><p><strong>Conclusions: </strong>This case presents a new likely pathogenic variant in <i>MYH7</i> and supports the hypothesis that myosin converter mutations constitute a subclass of HCM mutations with a poor prognosis for the patient.</p>","PeriodicalId":73070,"journal":{"name":"Frontiers in bioscience (Scholar edition)","volume":"16 1","pages":"1"},"PeriodicalIF":0.0,"publicationDate":"2024-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140308189","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of 5-aminolevulinic Acid on Mitochondrial Activity.","authors":"Yuliya V Markina, Alexander M Markin, Tatiana V Kirichenko, Taisiya V Tolstik, Vadim R Cherednichenko, Diana G Kiseleva, Alexander N Orekhov","doi":"10.31083/j.fbs1504017","DOIUrl":"10.31083/j.fbs1504017","url":null,"abstract":"<p><strong>Background: </strong>Mitochondrial dysfunction is considered an important mechanism in the pathogenesis of various diseases. Therefore, mitochondria are currently being considered as subjects for targeted therapies, particularly, phototherapy using 5-aminolevulinic acid. This study aimed to investigate the activity of mitochondria in cells with different mutation loads.</p><p><strong>Materials and methods: </strong>The study was conducted using 11 cybrid lines obtained from the THP-1 cell line (a human monocytic leukemia cell line) and platelets of patients with different mitochondrial mutations.</p><p><strong>Results: </strong>Our results illustrate that 5-aminolevulinic acid was metabolized equally in all cell lines, however, there was a significant decrease in mitochondrial potential, which differed among lines.</p><p><strong>Conclusions: </strong>The results of this study can be used to develop a personalized therapeutic approach based on different mitochondrial activities.</p>","PeriodicalId":73070,"journal":{"name":"Frontiers in bioscience (Scholar edition)","volume":"15 4","pages":"17"},"PeriodicalIF":0.0,"publicationDate":"2023-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139076083","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Systemic Sclerosis and Atherosclerosis: Potential Cellular Biomarkers and Mechanisms.","authors":"Elena V Gerasimova, Rushana U Shayakhmetova, Daria A Gerasimova, Tatiana V Popkova, Lidia P Ananyeva","doi":"10.31083/j.fbs1504016","DOIUrl":"10.31083/j.fbs1504016","url":null,"abstract":"<p><p>Systemic sclerosis (SSc) is a rare systemic autoimmune disease of unknown etiology, which is characterized by endothelial dysfunction, pathologic vasculopathy, and increased tissue fibrosis. Traditionally, SSc has been regarded as a prototypical fibrotic disease in the family of systemic autoimmune diseases. Traditionally, emphasis has been placed on the three components of the pathogenesis of SSc: vascular, immune, and mesenchymal. Microvascular lesions, including endothelial dysfunction and smooth muscle cell migration into the intima of vessels in SSc, resemble the atherosclerotic process. Although microvascular disease is a hallmark of SSc, understanding the role of atherosclerotic vascular lesions in patients with SSc remains limited. It is still unknown whether the increased cardiovascular risk in SSc is related to specific cardiac complications (such as myocardial fibrosis) or the accelerated development of atherosclerosis. Different immune cell types appear to be involved in the immunopathogenesis of SSc via the activation of other immune cells, fibrosis, or vascular damage. Macrophages, B cells, T cells, dendritic cells, neutrophils, and endothelial cells have been reported to play the most important role in the pathogenesis of SSc and atherosclerosis. In our article, we reviewed the most significant and recent studies on the pathogenetic links between the development of SSc and the atherosclerotic process.</p>","PeriodicalId":73070,"journal":{"name":"Frontiers in bioscience (Scholar edition)","volume":"15 4","pages":"16"},"PeriodicalIF":0.0,"publicationDate":"2023-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139076086","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Characterization of the <i>Cambaroides wladiwostokiensis</i> Birstein & Vinogradov, 1934 (Decapoda: Astacidea) Mitochondrial Genome Using Genome Skimming and the Phylogenetic Implications within the Astacidea Infraorder.","authors":"Sergei V Turanov, Evgeny I Barabanshchikov","doi":"10.31083/j.fbs1504015","DOIUrl":"10.31083/j.fbs1504015","url":null,"abstract":"<p><strong>Background: </strong>The mitochondrial genome is a powerful tool for exploring and confirming species identity and understanding evolutionary trajectories. The genus <i>Cambaroides</i>, which consists of freshwater crayfish, is recognized for its evolutionary and morphological complexities. However, comprehensive genetic and mitogenomic data on species within this genus, such as <i>C. wladiwostokiensis</i>, remain scarce, thereby necessitating an in-depth mitogenomic exploration to decipher its evolutionary position and validate its species identity.</p><p><strong>Methods: </strong>The mitochondrial genome of <i>C. wladiwostokiensis</i> was obtained through shallow Illumina paired-end sequencing of total DNA, followed by hybrid assembly using both <i>de novo</i> and reference-based techniques. Comparative analysis was performed using available <i>Cambaroides</i> mitochondrial genomes obtained from National Center for Biotechnology Information (NCBI). Additionally, phylogenetic analyses of 23 representatives from three families within the Astacidea infraorder were employed using the PhyloSuite platform for sequence management and phylogenetic preparation, to elucidate phylogenetic relationships via Bayesian Inference (BI), based on concatenated mitochondrial fragments.</p><p><strong>Results: </strong>The resulting genome, which spans 16,391 base pairs was investigated, revealing 13 protein-coding genes, rRNAs (<i>12S</i> and <i>16S</i>), 19 tRNAs, and a putative control region. Comparative analysis together with five other <i>Cambaroides</i> mitogenomes retrieved from GenBank unveiled regions that remained unread due to challenges associated with the genome skimming technique. Protein-coding genes varied in size and typically exhibited common start (ATG) and stop (TAA) codons. However, exceptions were noted in ND5 (start codon: GTG) and ND1 (stop codon: TAG). Landscape analysis was used to explore sequence variation across the five available mitochondrial genomes of <i>Cambaroides</i>.</p><p><strong>Conclusions: </strong>Collectively, these findings reveal variable sites and contribute to a deeper understanding of the genetic diversity in this genus alongside the further development of species-specific primers for noninvasive monitoring techniques. The partitioned phylogenetic analysis of Astacidea revealed a paraphyletic origin of Asian cambarids, which confirms the data in recent studies based on both multilocus analyses and integrative approaches.</p>","PeriodicalId":73070,"journal":{"name":"Frontiers in bioscience (Scholar edition)","volume":"15 4","pages":"15"},"PeriodicalIF":0.0,"publicationDate":"2023-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139076070","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fisetin Treats Kidney Oxidative Stress, Inflammation, and Apoptosis in Rat Diarrhea.","authors":"Khaled M M Koriem, Yousra K O Farouk","doi":"10.31083/j.fbs1504014","DOIUrl":"10.31083/j.fbs1504014","url":null,"abstract":"<p><strong>Background: </strong>Diarrhea is the increase in the excretion of human water; meanwhile, fisetin, a bioactive flavonol molecule, is widely used in the treatment/prevention of gastrointestinal disorders. The purpose of this study is to investigate the anti-diarrheal activity of fisetin by restoring kidney function, antioxidant activity, inflammatory markers, Na+/K+-ATPase level, apoptosis, and protein content in diarrheal rats.</p><p><strong>Methods: </strong>A total of 36 male rats were distributed into two groups (18 rats/group): normal and diarrheal. The normal group was further divided into three subgroups (6 rats/subgroup): Control, fisetin, and desmopressin drug subgroups, consisting of normal rats orally treated once a day for 4 weeks with 1 mL distilled water, 50 mg/kg fisetin, and 1 mg/kg desmopressin drug, respectively. A lactose diet containing 35% lactose was fed to the normal rats for a month. The diarrheal rats were also divided into three subgroups (6 rats/subgroup): diarrheal rats, diarrheal rats + fisetin, and diarrheal rats + desmopressin drug groups, whereby the diarrheal rats were orally treated once a day for 4 weeks with 1 mL distilled water, 50 mg/kg fisetin, and 1 mg/kg desmopressin drug, respectively.</p><p><strong>Results: </strong>Fisetin significantly decreased serum urea (41.20 ± 2.6-29.74 ± 2.65), creatinine (1.43 ± 0.05-0.79 ± 0.06), and urinary volume (1.30 ± 0.41-0.98 ± 0.20), while significantly increasing kidney weight (0.48 ± 0.03-0.67 ± 0.07), sodium, potassium, and chloride balance in both serum and urine. Fisetin significantly increased the antioxidant activity (superoxide dismutase (1170 ± 40-3230 ± 50), glutathione peroxidase (365 ± 18-775 ± 16), catalase (0.09 ± 0.03-0.14 ± 0.06), and nicotinamide adenine dinucleotide phosphate hydrogen (NADPH) oxidase activity (8.6 ± 1.31-10.5 ± 1.25), while significantly decreasing malondialdehyde (19.38 ± 0.54-9.54 ± 0.83), conjugated dienes (1.86 ± 0.24-1.64 ± 0.19), and oxidative index (0.62 ± 0.04-0.54 ± 0.05)), alongside the inflammatory markers (tumor necrosis factor-α (65.2 ± 2.59-45.3 ± 2.64), interleukin-1β, interleukin-6 (107 ± 4.5-56.1 ± 7.2), and interleukin-10) in the diarrheal rats to values approaching the control values. Fisetin also restored the Na+/K+-ATPase level, apoptosis, protein content, and kidney architecture in diarrheal rats to be near the control group.</p><p><strong>Conclusions: </strong>Fisetin treated diarrhea in rats by restoring kidney function, antioxidant activity, inflammatory markers, apoptosis, proteome content, and histology.</p>","PeriodicalId":73070,"journal":{"name":"Frontiers in bioscience (Scholar edition)","volume":"15 4","pages":"14"},"PeriodicalIF":0.0,"publicationDate":"2023-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139076084","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}