{"title":"Trandolapril improves renal ischemia-reperfusion injury in adult male rats via activation of the autophagy pathway and inhibition of inflammation, oxidative stress, and apoptosis","authors":"Hanan Q. Jallawee, Ali M. Janabi","doi":"10.21608/jbaar.2024.315239.1077","DOIUrl":"https://doi.org/10.21608/jbaar.2024.315239.1077","url":null,"abstract":"Acute kidney injury (AKI) frequently occurs due to renal ischemia/reperfusion injury (IRI), which is marked by damaged tissue and a decrease in blood flow to the kidneys. IRI causes Oxidative damage, inflammation, and cell death. Autophagy, which recycles cytoplasmic components and breaks them down into smaller pieces, may have a role in cell death or survival in certain pathological states.Objective: Through antioxidant, anti-inflammatory, and anti-apoptotic actions, as well as activation of the autophagy system, this study explores the potential nephroprotective benefits of trandolapril against renal ischemia-reperfusion damage. Material and method: There were four groups of rats used in this study: sham, RIRI, Dimethyl sulfoxide, and Trandolapril pretreated groups. The sham group underwent the same anesthesia and surgical procedures except for ischemia. Other groups undergo bilateral renal ischemia for 30 minutes and then reperfusion for 24 hours. DMSO group vehicle for trandolapril and trandolapril group 0.3mg/kg given 2 hours before ischemia induction. Results: The study found that blood urea and serum creatinine levels increased in the RIRI and DMSO groups when compared with the sham group. Renal tissue levels of IL-6, Kim-1, caspase-3, LC-3, and Akt were also elevated in RIRI while GSH levels decreased in the RIRI. The Trandolapril group showed significant increases in GSH, LC-3, and Akt levels when compared to the sham group. Trandolapril reduced serum urea and creatinine levels, and renal tissue levels of IL-6, Kim-1, and caspase-3 also reduced.Conclusion: Male rat models of ischemia-reperfusion injury showed that trandolapril significantly decreased kidney damage.","PeriodicalId":50430,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":"10 6","pages":"114-127"},"PeriodicalIF":0.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://jbaar.journals.ekb.eg/article_397827_78d7ea1175fcabdf5da245036f1c2ee3.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147906655","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Bulimia Nervosa and Depression, from the Brain to the Gut Microbiota and Back","authors":"Marcello Romeo, Gina Cavaliere, Giovanna Traina","doi":"10.31083/j.fbl2908277","DOIUrl":"https://doi.org/10.31083/j.fbl2908277","url":null,"abstract":"","PeriodicalId":50430,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":"6 10","pages":""},"PeriodicalIF":3.1,"publicationDate":"2024-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141921529","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Exploring the Link between Metabolic Remodelling and Reactive Oxygen Species in the Aged and Diseased Heart","authors":"Lijo N. Varghese, Rajesh Katare","doi":"10.31083/j.fbl2907249","DOIUrl":"https://doi.org/10.31083/j.fbl2907249","url":null,"abstract":"","PeriodicalId":50430,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":"139 23","pages":""},"PeriodicalIF":3.1,"publicationDate":"2024-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141655990","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Role of Podocyte in Kidney Disease","authors":"Sufia Husain","doi":"10.31083/j.fbl2907250","DOIUrl":"https://doi.org/10.31083/j.fbl2907250","url":null,"abstract":"Podocytes are epithelial cells lining the outer surface of the renal glomerular capillaries and they play a pivotal role in maintaining the structural and functional integrity of the glomerular filtration barrier. Podocytes react to injury in various ways and any injury to these highly specialized cells can progress to podocyte dysfunction, resulting in a group of proteinuric renal diseases called podocytopathies. Podocytopathies include a wide spectrum of primary and secondary kidney diseases, including minimal change disease, diffuse mesangial sclerosis, focal segmental glomerulosclerosis, collapsing glomerulopathy, diabetic, membranous and lupus nephropathies. Etiologically, they can be idiopathic, genetic or secondary to infections and drugs, metabolic diseases, hemodynamic factors or associated with various immune and non-immune systemic diseases. This manuscript provides a basic understanding of podocyte structure, causes of podocyte injury, response to the injury and the subsequent progression to podocytopathies. The pathogenesis of these diseases is set around podocytes. The clinical and morphological manifestations, the commonality and heterogeneity of these podocytopathies are also discussed. As our knowledge of podocyte biology improves, so will our treatment avenues with a more podocyte-centric personalized approach.","PeriodicalId":50430,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":"73 11","pages":""},"PeriodicalIF":3.1,"publicationDate":"2024-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141655471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Harry C Blair, Jonathan Soboloff, I. Tourkova, Jamie L. McCall, Suravi Ray, Margalit E Rosenkranz, Cristina Sobacchi, Lisa J Robinson, John B Barnett
{"title":"Molecular Regulation of Bone Turnover in Juvenile Idiopathic Arthritis: Animal Models, Cellular Features and TNFα","authors":"Harry C Blair, Jonathan Soboloff, I. Tourkova, Jamie L. McCall, Suravi Ray, Margalit E Rosenkranz, Cristina Sobacchi, Lisa J Robinson, John B Barnett","doi":"10.31083/j.fbl2907248","DOIUrl":"https://doi.org/10.31083/j.fbl2907248","url":null,"abstract":"We review the abnormal bone turnover that is the basis of idiopathic inflammatory or rheumatoid arthritis and bone loss, with emphasis on Tumor Necrosis Factor-alpha (TNF α )-related mechanisms. We review selected data on idiopathic arthritis in juvenile human disease, and discuss mouse models focusing on induction of bone resorbing cells by TNF α and Receptor Activator of Nuclear Factor kappa B Ligand (RANKL). In both humans and animal models, macrophage-derived cells in the joint, particularly in the synovium and periosteum, degrade bone and cartilage. Mouse models of rheumatoid arthritis share with human disease bone resorbing cells and strong relation to TNF α expression. In humans, differences in therapy and prognosis of arthritis vary with age, and results from early intervention for inflammatory cytokines in juvenile patients are particularly interesting. Mechanisms that contribute to inflammatory arthritis reflect, in large part, inflammatory cytokines that play minor roles in normal bone turnover. Changes in inflammatory cytokines, particularly TNF α , are many times larger, and presented in different locations, than cytokines that regulate normal bone turnover. Recent data from in vitro and mouse models include novel mechanisms described in differentiation of bone resorbing cells in inflammatory arthritis dependent on the Transient Receptor Potential Channel (TRPC) family of calcium channels. Low-molecular weight (MW) inhibitors of TRPC channels add to their potential importance. Associations with inflammatory arthritis unrelated to TNF α are briefly summarized as pointing to alternative mechanisms. We suggest that early detection and monoclonal antibodies targeting cytokines mediating disease progression deserves emphasis.","PeriodicalId":50430,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":"2 3","pages":""},"PeriodicalIF":3.1,"publicationDate":"2024-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141658760","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Kaempferol Alleviates Injury in Human Retinal Pigment Epithelial Cells via STAT1 Ubiquitination-Mediated Degradation of IRF7","authors":"Hongjun Zhang, Can Liu, Cao Gu, Jun Jiang, Yu Gao","doi":"10.31083/j.fbl2907247","DOIUrl":"https://doi.org/10.31083/j.fbl2907247","url":null,"abstract":"Background : Retinal pigment epithelial (RPE) cells have a pivotal function in preserving the equilibrium of the retina and moderating the immunological interaction between the choroid and the retina. This study primarily focuses on delineating the protective effect offered by Kaempferol (Kae) against RPE cell damage. Methods : Bioinformatics analysis was performed on the GSE30719 dataset to identify hub genes associated with RPE. Subsequently, we analyzed the impact of Kae on RPE apoptosis, cell viability, and inflammatory response through cell experiments, and explored the interaction between hub genes and Kae. Results : Based on the GSE30719 dataset, nine hub genes ( ISG15 , IFIT1 , IFIT3 , STAT1 , OASL , RSAD2 , IRF7 , MX2 , and MX1 ) were identified, all of which were highly expressed in the GSE30719 case group. Kae could boost the proliferative activity of RPE cells caused by lipopolysaccharide (LPS), as well as reduce apoptosis and the generation of inflammatory factors (tumor necrosis factor receptor (TNFR), interleukin-1beta (IL-1 β )) and cytokines (IL-1, IL-6, IL-12). STAT1 was shown to inhibit cell proliferation, promote apoptosis, and secrete IL-1/IL-6/IL-12 in LPS-induced RPE cells. Moreover, IRF7 was found to interact with STAT1 in LPS-induced RPE cells, and STAT1 could maintain IRF7 levels through deubiquitination. In addition, we also found that the protective effect of Kae on LPS-induced RPE cell injury was mediated through STAT1/IRF7 axis. Conclusion : This study provided evidence that Kae protects RPE cells via regulating the STAT1/IRF7 signaling pathways, indicating its potential therapeutic relevance in the diagnosis and management of retinal disorders linked with RPE cell damage.","PeriodicalId":50430,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":" 13","pages":""},"PeriodicalIF":3.1,"publicationDate":"2024-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141678377","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M. Naveed, Khizra Jabeen, Tariq Aziz, Muhammad Saad Mughal, Hammad Arif, M. Alharbi, T. H. Albakeiri, A. Alasmari
{"title":"Designing an mRNA Vaccine against P. jirovecii Involved in Fatal Pneumonia Infections via Comparative Proteomics and Reverse Vaccinology Approaches","authors":"M. Naveed, Khizra Jabeen, Tariq Aziz, Muhammad Saad Mughal, Hammad Arif, M. Alharbi, T. H. Albakeiri, A. Alasmari","doi":"10.31083/j.fbl2907246","DOIUrl":"https://doi.org/10.31083/j.fbl2907246","url":null,"abstract":"Background : Pneumocystis jirovecii is the most emerging life-threating health problem that causes acute and fatal pneumonia infection. It is rare and more contagious for patients with leukemia and immune-deficiency disorders. Until now there is no treatment available for this infection therefore, it is needed to develop any treatment against this pathogen. Methods : In this work, we used comparative proteomics, robust immune-informatics, and reverse vaccinology to create an mRNA vaccine against Pneumocystis jirovecii by targeting outer and transmembrane proteins. Using a comparative subtractive proteomic analysis of two Pneumocystis jirovecii proteomes, a distinct non-redundant Pneumocystis jirovecii (strain SE8) proteome was chosen. Seven Pneumocystis jirovecii transmembrane proteins were chosen from this proteome based on hydrophilicity, essentiality, virulence, antigenicity, pathway interaction, protein-protein network analysis, and allergenicity. Objective : The reverse vaccinology approach was used to predict the immunogenic and antigenic epitopes of major histocompatibility complex (MHC) I, II and B-cells from the selected proteins on the basis of their antigenicity, toxicity and allergenicity. These immunogenic epitopes were linked together to construct the mRNA-based vaccine. To enhance the immunogenicity, suitable adjuvant, linkers (GPGPG, KK, and CYY), and PRDRE sequences were used. Results : Through predictive modeling and confirmation via the Ramachandran plot, we assessed secondary and 3D structures. The adjuvant RpfE was incorporated to enhance the vaccine construct’s immunogenicity (GRAVY index: –0.271, instability index: 39.53, antigenicity: 1.0428). The physiochemical profiling of vaccine construct was predicted it an antigenic, efficient, and potential vaccine. Notably, strong interactions were observed between the vaccine construct and TLR-3/TLR-4 (–1301.7 kcal/mol − 1 and –1374.7 kcal/mol − 1 ). Conclusions : The results predicted that mRNA-based vaccines trigger a cellular and humoral immune response, making the vaccine potential candidate against Pneumocystis jirovecii and it is more suitable for in-vitro analysis and validation to prove its effectiveness.","PeriodicalId":50430,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":"33 2‐3","pages":""},"PeriodicalIF":3.1,"publicationDate":"2024-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141682147","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Wenxing Li, Lan Luo, Yue Fan, Xiangling Lv, Qianfeng Jiang, Yang Jiao
{"title":"Combining Bibliometric Analysis to Uncover the Detrimental and Protective Roles of Various Dendritic Cell Types in Cardiovascular Arterial Diseases","authors":"Wenxing Li, Lan Luo, Yue Fan, Xiangling Lv, Qianfeng Jiang, Yang Jiao","doi":"10.31083/j.fbl2907244","DOIUrl":"https://doi.org/10.31083/j.fbl2907244","url":null,"abstract":"Immune cell dysregulation is increasingly recognized as a pivotal pathological factor in cardiovascular disease. Over the past decade, a surge of research has focused on the role of immune cells such as dendritic cells (DCs), T cells, macrophages, and neutrophils in cardio-vascular diseases, findings that are frequently featured in leading cardiology journals. This review provides a comprehensive synthesis of the roles that DCs play in common and potentially fatal arterial diseases, including hypertension, coronary artery atherosclerosis, acute coronary syndrome, pulmonary arterial hypertension, aortic aneurysm, aortic dissection, and vasculitis. Combining with bibliometric analysis, this review delves into the critical mechanisms by which DCs contribute to these diseases and reveals the shared mechanisms across diverse diseases. This review also offers new advances in clinical treatment strategies involving DCs","PeriodicalId":50430,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":"5 4","pages":""},"PeriodicalIF":3.1,"publicationDate":"2024-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141687674","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}