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1دورية أكاديمية
المؤلفون: Safia Iqbal, Md. Rezaul Karim, Shahnawaz Mohammad, Jong Chan Ahn, Anjali Kariyarath Valappil, Ramya Mathiyalagan, Deok-Chun Yang, Dae-Hyo Jung, Hyocheol Bae, Dong Uk Yang
المصدر: Current Issues in Molecular Biology, Vol 46, Iss 4, Pp 3328-3341 (2024)
مصطلحات موضوعية: kidney cancer, kidney inflammation, isoquercitrin, MD simulation, Go analysis, KEGG pathway analysis, Biology (General), QH301-705.5
الوصف: Kidney cancer has emerged as a major medical problem in recent times. Multiple compounds are used to treat kidney cancer by triggering cancer-causing gene targets. For instance, isoquercitrin (quercetin-3-O-β-d-glucopyranoside) is frequently present in fruits, vegetables, medicinal herbs, and foods and drinks made from plants. Our previous study predicted using protein-protein interaction (PPI) and molecular docking analysis that the isoquercitrin compound can control kidney cancer and inflammation by triggering potential gene targets of IGF1R, PIK3CA, IL6, and PTGS2. So, the present study is about further in silico and in vitro validation. We performed molecular dynamic (MD) simulation, gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, cytotoxicity assay, and RT-PCR and qRT-PCR validation. According to the MD simulation (250 ns), we found that IGF1R, PIK3CA, and PTGS2, except for IL6 gene targets, show stable binding energy with a stable complex with isoquercitrin. We also performed gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses of the final targets to determine their regulatory functions and signaling pathways. Furthermore, we checked the cytotoxicity effect of isoquercitrin (IQ) and found that 5 μg/mL and 10 μg/mL doses showed higher cell viability in a normal kidney cell line (HEK 293) and also inversely showed an inhibition of cell growth at 35% and 45%, respectively, in the kidney cancer cell line (A498). Lastly, the RT-PCR and qRT-PCR findings showed a significant decrease in PTGS2, PIK3CA, and IGF1R gene expression, except for IL6 expression, following dose-dependent treatments with IQ. Thus, we can conclude that isoquercitrin inhibits the expression of PTGS2, PIK3CA, and IGF1R gene targets, which in turn controls kidney cancer and inflammation.
وصف الملف: electronic resource
العلاقة: https://www.mdpi.com/1467-3045/46/4/208Test; https://doaj.org/toc/1467-3037Test; https://doaj.org/toc/1467-3045Test
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2دورية أكاديمية
المؤلفون: Julia Windi Gunadi, Diana Krisanti Jasaputra, Balqist Sriprobo Pangestuti, Roro Wahyudianigsih, Ronny Lesmana
المصدر: Althea Medical Journal, Vol 11, Iss 1, Pp 26-31 (2024)
مصطلحات موضوعية: hfd, kidney, inflammation, fat degeneration, autophagy, Medicine, Medicine (General), R5-920
الوصف: Background: High-fat diet (HFD) increases the risk of obesity, metabolic syndrome, coronary artery disease, and chronic kidney disease, resulting in lipotoxicity. Turmeric and mangosteen are two ingredients mostly used in Indonesian food, and are known for their antihyperlipidemic and antioxidant effects. The aim of this study was to explore the effect of turmeric and mangosteen on autophagy gene expression in HFD-induced kidneys in rats model. Methods: The study was an experimental study, including 25 male Wistar rats aged 8 weeks, divided into 5 groups with a completely randomized design; group with a standard diet as negative control group, the group with a high-fat diet as a positive control group, and the HFD groups with turmeric or mangosteen or fenofibrate. The study was conducted in Maranatha Biomedical Research Laboratory from January to November 2022. Autophagy gene expression (LC3, p62) was measured along with the histopathological scoring to observe necrosis, inflammation, and fat degeneration state. Data was analyzed using One Way ANOVA or Kruskal Wallis and post hoc Least Significant Difference or Mann Whitney. Results: There were significant differences in inflammation in groups treated with mangosteen (p=0.007); in fat degeneration in groups treated with mangosteen and fenofibrate (p=0.007). Furthermore, the LC3 gene expression was increased in all HFD groups as well as the p62 gene expression in group treated with turmeric (p=0.020) and fenofibrate (p=0.005). Conclusions: Mangosteen decreases inflammation and fat degeneration scoring, while turmeric increases autophagy in the kidney of HFD induced Wistar rats.
وصف الملف: electronic resource
العلاقة: https://journal.fk.unpad.ac.id/index.php/amj/article/view/3148Test; https://doaj.org/toc/2337-4330Test
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3دورية أكاديمية
المؤلفون: Eunchang Lee, Ho-Sueb Song
المصدر: Journal of Acupuncture Research, Vol 40, Iss 2, Pp 135-142 (2023)
مصطلحات موضوعية: gout, hyperuricemia, kidney inflammation, scutellaria baicalensis extract, xanthine oxidase, Miscellaneous systems and treatments, RZ409.7-999, Therapeutics. Pharmacology, RM1-950
الوصف: Background: This study aimed to investigate hyperuricemia, renal inflammation, and xanthine oxidase (XO) activity improvement in a rat model treated with Scutellaria baicalensis extract (SBE). Methods: The rats were divided into 4 groups (n = 5 each), including sham, potassium oxonate (PO) injected hyperuricemia (control group), PO + 10 mg/kg allopurinol administrated (allopurinol group), and a PO + 50 mg/kg SBE administrated (SBE group), to investigate the effectiveness and molecular mechanisms of SBE. The effects of SBE on PO-induced hyperuricemia rats, renal inflammation, and XO activity were measured. Body weight and organ index of the kidney and liver were measured in PO-induced hyperuricemia rats, and serum uric acid level was extracted from whole blood and was measured. Renal inflammation was observed under a microscope after sections. XO activity was measured by liver tissue and serum XO levels. Results: Organ indexes of the kidney and liver in rats were significantly decreased in the allopurinol group than in the control group and with no significant difference in the SBE group. A PO injection for 5 days significantly increased serum uric acid levels in the control group compared to the sham group. Meanwhile, the SBE and allopurinol groups have significantly decreased serum uric acid levels compared to the control group. The SBE group revealed effectively improved renal histopathological changes compared to the control group. The XO inhibitor, allopurinol, significantly decreased XO activity. Additionally, SBE significantly lowered XO activity in rats. Conclusion: SBE can be used as an effective treatment for gout in the future.
وصف الملف: electronic resource
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4دورية أكاديمية
المؤلفون: Md. Rezaul Karim, Md. Niaj Morshed, Safia Iqbal, Shahnawaz Mohammad, Ramya Mathiyalagan, Deok Chun Yang, Yeon Ju Kim, Joon Hyun Song, Dong Uk Yang
المصدر: Biomolecules, Vol 13, Iss 11, p 1678 (2023)
مصطلحات موضوعية: network pharmacology, gut microbial metabolites, SCFA-producing microbes, kidney cancer, kidney inflammation, molecular docking, Microbiology, QR1-502
الوصف: (1) Background: A large and diverse microbial population exists in the human intestinal tract, which supports gut homeostasis and the health of the host. Short-chain fatty acid (SCFA)-secreting microbes also generate several metabolites with favorable regulatory effects on various malignancies and immunological inflammations. The involvement of intestinal SCFAs in kidney diseases, such as various kidney malignancies and inflammations, has emerged as a fascinating area of study in recent years. However, the mechanisms of SCFAs and other metabolites produced by SCFA-producing bacteria against kidney cancer and inflammation have not yet been investigated. (2) Methods: We considered 177 different SCFA-producing microbial species and 114 metabolites from the gutMgene database. Further, we used different online-based database platforms to predict 1890 gene targets associated with metabolites. Moreover, DisGeNET, OMIM, and Genecard databases were used to consider 13,104 disease-related gene targets. We used a Venn diagram and various protein−protein interactions (PPIs), KEGG pathways, and GO analyses for the functional analysis of gene targets. Moreover, the subnetwork of protein−protein interactions (through string and cytoscape platforms) was used to select the top 20% of gene targets through degree centrality, betweenness centrality, and closeness centrality. To screen the possible candidate compounds, we performed an analysis of the ADMET (absorption, distribution, metabolism, excretion, and toxicity) properties of metabolites and then found the best binding affinity using molecular docking simulation. (3) Results: Finally, we found the key gene targets that interact with suitable compounds and function against kidney cancer and inflammation, such as MTOR (with glycocholic acid), PIK3CA (with 11-methoxycurvularin, glycocholic acid, and isoquercitrin), IL6 (with isoquercitrin), PTGS2 (with isoquercitrin), and IGF1R (with 2-amino-1-methyl-6-phenylimidazo[4,5-b] pyridine, isoquercitrin), showed a lower binding affinity. (4) Conclusions: This study provides evidence to support the positive effects of SCFA-producing microbial metabolites that function against kidney cancer and inflammation and makes integrative research proposals that may be used to guide future studies.
وصف الملف: electronic resource
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5دورية أكاديمية
المؤلفون: Zhihuan Wang, Liqiong Song, Xianping Li, Yuchun Xiao, Yuanming Huang, Yue Zhang, Jintong Li, Mingding Li, Zhihong Ren
المصدر: Frontiers in Nutrition, Vol 10 (2023)
مصطلحات موضوعية: hyperuricemia, probiotics, Lactiplantibacillus pentosus, gut microbiota, kidney inflammation, urate reabsorption transporter, Nutrition. Foods and food supply, TX341-641
الوصف: IntroductionHyperuricemia (HUA) is a common metabolic disease, and its prevalence has been increasing worldwide. Pharmaceutical drugs have been used for controlling HUA but they all have certain side effects, which thus calls for discovering alternative options including using treatment of probiotics to prevent the development of HUA.MethodsWe established HUA mice model induced by potassium oxonate and adenine and performed in vivo experiments to verify the ability to lower serum uric acid of Lactiplantibacillus pentosus P2020 (LPP), a probiotics stain extracted from Chinese pickle. We also tried to discussed the underlying mechanisms.ResultsOral administration with LPP significantly decreased serum uric acid and reduced renal inflammatory response by downregulating multiple inflammation pathways including NK-kB, MAPK, and TNFα. We also found that LPP administration significantly promoted uric acid excretion by regulating expression of transporters in the kidney and ileum. In addition, LPP intake improved intestinal barrier function and modulated the composition of gut microbiota.DiscussionThese results suggest that probiotics LPP may have a promising potential to protect against development of HUA and HUA-related renal damage, and its working mechanisms involve regulation of inflammation pathways and expression of transporters in the kidney and ileum.
وصف الملف: electronic resource
العلاقة: https://www.frontiersin.org/articles/10.3389/fnut.2023.1094483/fullTest; https://doaj.org/toc/2296-861XTest
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6دورية أكاديمية
المؤلفون: F Gholampour, J Roozbeh, S Janfashan, L Malek Mahal, K Rahimi Jaberi, Z Karimi
المصدر: Armaghane Danesh Bimonthly Journal, Vol 25, Iss 1, Pp 12-22 (2021)
مصطلحات موضوعية: ischemia-renal reperfusion, remote ischemic per conditioning, toll like receptor-4, tnf-α, kidney inflammation, creatinine clearance, Medicine (General), R5-920
الوصف: Background & aim: Acute Kidney Injury (AKI) is an inflammatory process in which multiple inflammatory factors are involved. Recently, one of the ways to alleviate inflammation in AKI is to apply pre-conditioned ischemic remote control (RIPerC). The aim of the present study was to determine and investigate the protective role of long-term ischemic preconditioning in acute injury of all ischemia due to resection through the TLR-4 and TNF-α signaling pathways in the rat. Methods: The present experimental study was conducted in 2016 on 30 male rats of Sprag Dolly breed with a weight range of 250 to 280 grams. Ratings were divided into three equal groups of control, re-ischemic resection (I / R) and re-ischemic resection with long-term ischemic preconditioning (RIPerC) predisposition. In this study, I / R re-bleeding was observed with bilateral closure of the artery and renal vein for 45 minutes and 24 hours. The RIPerC model consisted of four five-minute cycles (two minutes for closing the left femoral artery and three minutes for re-bleeding) at the onset of ischemic-renal failure. At the end of the resuscitation period, urine, blood, and kidney tissue samples were collected for functional, structural, and molecular analysis. The collected data were analyzed using SPSS software. Results: Ischemia-reperfusion caused tissue damage and subsequently impaired renal function, which was demonstrated by a decrease in creatinine clearance and an increase in its relative sodium excretion. In addition, in the I/R group, mRNA level of TLR-4 and TNF-α in tissue increased, whereas RIPerC (in this group, during ischemia, ischemia, and reperfusion in the femoral artery was done) simultaneously with I/R improved kidney structure and function and decreased expression of TLR-4 and TNF-α. Conclusion: RIPerC protected the kidney against ischemia-reperfusion-induced kidney injury and probably this protective effect was exerted by inhibition of TLR-4 signaling pathway in the kidney.
وصف الملف: electronic resource
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7دورية أكاديمية
المؤلفون: Tiankui Ma, Xin Li, Yonghong Zhu, Shufan Yu, Tianyan Liu, Xiaodan Zhang, Dong Chen, Shuyan Du, Tong Chen, Shuo Chen, Yanyan Xu, Qiuling Fan
المصدر: Frontiers in Immunology, Vol 13 (2022)
مصطلحات موضوعية: diabetic kidney disease, macrophages, kidney inflammation, renal fibrosis, necroptosis, diabetic nephropathy, Immunologic diseases. Allergy, RC581-607
الوصف: Diabetic nephropathy (DN) is one of the main causes of end-stage renal disease (ESRD). Existing treatments cannot control the progression of diabetic nephropathy very well. In diabetic nephropathy, Many monocytes and macrophages infiltrate kidney tissue. However, the role of these cells in the pathogenesis of diabetic nephropathy has not been fully elucidated. In this study, we analyzed patient kidney biopsy specimens, diabetic nephropathy model animals. Meanwhile, we cocultured cells and found that in diabetic nephropathy, damaged intrinsic renal cells (glomerular mesangial cells and renal tubular epithelial cells) recruited monocytes/macrophages to the area of tissue damage to defend against and clear cell damage. This process often involved the activation of different types of macrophages. Interestingly, the infiltrating macrophages were mainly M1 (CD68+iNOS+) macrophages. In diabetic nephropathy, crosstalk between the Notch pathway and NF-κB signaling in macrophages contributed to the polarization of macrophages. Hyperpolarized macrophages secreted large amounts of inflammatory cytokines and exacerbated the inflammatory response, extracellular matrix secretion, fibrosis, and necroptosis of intrinsic kidney cells. Additionally, macrophage depletion therapy with clodronate liposomes and inhibition of the Notch pathway in macrophages alleviated the pathological changes in kidney cells. This study provides new information regarding diabetic nephropathy-related renal inflammation, the causes of macrophage polarization, and therapeutic targets for diabetic nephropathy.
وصف الملف: electronic resource
العلاقة: https://www.frontiersin.org/articles/10.3389/fimmu.2022.835879/fullTest; https://doaj.org/toc/1664-3224Test
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8دورية أكاديمية
المؤلفون: Can Lu, Huihui Chen, Chang Wang, Fei Yang, Jun Li, Hong Liu, Guochun Chen
المصدر: Frontiers in Immunology, Vol 12 (2022)
مصطلحات موضوعية: TIM3, T cell, macrophage, infection, chronic kidney inflammation, Immunologic diseases. Allergy, RC581-607
الوصف: T cell immunoglobulin domain and mucin domain 3 (TIM3) was initially identified as an inhibitory molecule on IFNγ-producing T cells. Further research discovered the broad expression of TIM3 on different immune cells binding to multiple ligands. Apart from its suppressive effects on the Th1 cells, recent compelling experiments highlighted the indispensable role of TIM3 in the myeloid cell-mediated inflammatory response, supporting that TIM3 exerts pleiotropic effects on both adaptive and innate immune cells in a context-dependent manner. A large number of studies have been conducted on TIM3 biology in the disease settings of infection, cancer, and autoimmunity. However, there is a lack of clinical evidence to closely evaluate the role of T cell-expressing TIM3 in the pathogenesis of chronic kidney disease (CKD). Here, we reported an intriguing case of Mycobacterium tuberculosis (Mtb) infection that was characterized by persistent overexpression of TIM3 on circulating T cells and ongoing kidney tubulointerstitial inflammation for a period of 12 months. In this case, multiple histopathological biopsies revealed a massive accumulation of recruited T cells and macrophages in the enlarged kidney and liver. After standard anti-Mtb treatment, repeated renal biopsy identified a dramatic remission of the infiltrated immune cells in the tubulointerstitial compartment. This is the first clinical report to reveal a time-course expression of TIM3 on the T cells, which is pathologically associated with the progression of severe kidney inflammation in a non-autoimmunity setting. Based on this case, we summarize the recent findings on TIM3 biology and propose a novel model of CKD progression due to the aberrant crosstalk among immune cells.
وصف الملف: electronic resource
العلاقة: https://www.frontiersin.org/articles/10.3389/fimmu.2021.798683/fullTest; https://doaj.org/toc/1664-3224Test
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9دورية أكاديمية
المؤلفون: Changyu Wu (1485628), Qing Hu (152962), Xichun Peng (530604), Jianming Luo (430422), Guangwen Zhang (7120487)
مصطلحات موضوعية: Genetics, Physiology, Pharmacology, Ecology, Immunology, Marine Biology, Inorganic Chemistry, Biological Sciences not elsewhere classified, Chemical Sciences not elsewhere classified, serum uric acid, metabolic disease hyperuricemia, restore kidney function, uric acid metabolism, model group rats, induced kidney inflammation, induced intestinal dysfunction, mfpp attenuated hua, kidney histopathology, purine metabolism, intestinal barrier, hua rats, therapeutic strategy, results showed, relieve hua, related genes, potassium oxonate, nr4a3 <, mfpp restored, mfpp ), marine fish
الوصف: The metabolic disease hyperuricemia (HUA) is characterized by a disturbance in purine metabolism. Peptides, such as marine fish-derived peptides, have previously been shown to be effective in alleviating HUA. In this study, HUA rats were induced by potassium oxonate with 100 mg/kg (L), 200 mg/kg (M), and 400 mg/kg (H) of marine fish protein peptide (MFPP). The results showed that MFPP could effectively reduce the serum uric acid (SUA) levels compared with the model group rats; kidney histopathology and the levels of inflammatory factors (TNF-α, IL-6, and IL-10) indicated that MFPP attenuated HUA-induced kidney inflammation. Meanwhile, MFPP restored the abundance of beneficial bacteria, including Lactobacillus, Blautia, Colidextribacter, and Intestinimonas. MFPP further repaired the intestinal barrier by recovering the expression of gene Ildr2 encoding the tricellular tight junction protein ILDR2 and the immune-related genes Ccr7 and Nr4a3 and also regulated the expression of Entpd8 and Cyp27b1 to restore kidney function and uric acid metabolism. MFPP was proved to have potential as a therapeutic strategy to be included in dietary intervention to relieve HUA.
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10دورية أكاديمية
المؤلفون: Alexandra Linke, Gisa Tiegs, Katrin Neumann
المصدر: Cells; Volume 11; Issue 10; Pages: 1625
مصطلحات موضوعية: immune-mediated GN, kidney inflammation, crescent formation, renal Th1 and Th17 responses, cytotoxic CD8 + T cells, tissue-resident memory T cells
الوصف: Glomerulonephritis (GN) comprises a group of immune-mediated kidney diseases affecting glomeruli and the tubulointerstitium. Glomerular crescent formation is a histopathological characteristic of severe forms of GN, also referred to as crescentic GN (cGN). Based on histological findings, cGN includes anti-neutrophil cytoplasmic antibody (ANCA)-associated GN, a severe form of ANCA-associated vasculitis, lupus nephritis associated with systemic lupus erythematosus, Goodpasture’s disease, and IgA nephropathy. The immunopathogenesis of cGN is associated with activation of CD4+ and CD8+ T cells, which particularly accumulate in the periglomerular and tubulointerstitial space but also infiltrate glomeruli. Clinical observations and functional studies in pre-clinical animal models provide evidence for a pathogenic role of Th1 and Th17 cell-mediated immune responses in cGN. Emerging evidence further argues that CD8+ T cells have a role in disease pathology and the mechanisms of activation and function of recently identified tissue-resident CD4+ and CD8+ T cells in cGN are currently under investigation. This review summarizes the mechanisms of pathogenic T-cell responses leading to glomerular damage and renal inflammation in cGN. Advanced knowledge of the underlying immune mechanisms involved with cGN will enable the identification of novel therapeutic targets for the replacement or reduction in standard immunosuppressive therapy or the treatment of refractory disease.
وصف الملف: application/pdf
العلاقة: Cellular Immunology; https://dx.doi.org/10.3390/cells11101625Test
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