Journal of Biochemical and Molecular Toxicology最新文献_第5页

Reprogramming of Hypoxia-Induced Metabolic Disorder in Mouse Kidneys by Mesenchymal Stem Cells Through Improving Mitochondrial Dynamics and Function

IF 3.2 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2025-05-13 DOI: 10.1002/jbt.70291

Yanjun Wang, Yanling Ding, Tana Wuren, Pengli Luo

{"title":"Reprogramming of Hypoxia-Induced Metabolic Disorder in Mouse Kidneys by Mesenchymal Stem Cells Through Improving Mitochondrial Dynamics and Function","authors":"Yanjun Wang, Yanling Ding, Tana Wuren, Pengli Luo","doi":"10.1002/jbt.70291","DOIUrl":"https://doi.org/10.1002/jbt.70291","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>To assess the effects of human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) on mitochondrial damage and metabolic disorders induced by acute and chronic hypoxia in mouse kidneys.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Method</h3>\u0000 \u0000 <p>Comprehensive analyses were conducted, including histopathology, mitochondrial morphology analysis, biochemical assessments, transcriptomics and metabolomics.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The results revealed that hUC-MSCs significantly improved renal mitochondrial integrity and maintained mitochondrial dynamic balance under both acute and chronic hypoxia. This improvement was achieved by upregulating the expression of peroxisome proliferator-activated receptor gamma coactivator-1 alpha, which ultimately enhanced mitochondrial function. Furthermore, hUC-MSCs reprogrammed renal metabolic disorders, particularly improvements in urea and purine metabolic dysfunction, increased fatty acid oxidation and amelioration of lipid metabolic disorders.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>These findings suggest that hUC-MSCs could be part of a promising strategy for enhancing renal health and metabolic stability in individuals exposed to high altitudes or other hypoxic environments, highlighting their potential therapeutic value in addressing hypoxia-induced mitochondrial damage and renal metabolic disorders.</p>\u0000 </section>\u0000 </div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 5","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143944455","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Daidzein Attenuates Cadmium-Induced Neurotoxicity via Inhibiting Apoptosis and Mitophagy in the Cerebral Cortex of Sprague–Dawley Rats

IF 3.2 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2025-05-13 DOI: 10.1002/jbt.70299

Shuangquan Wen, Yu Zhao, Liang Wang, Yan Yuan

{"title":"Daidzein Attenuates Cadmium-Induced Neurotoxicity via Inhibiting Apoptosis and Mitophagy in the Cerebral Cortex of Sprague–Dawley Rats","authors":"Shuangquan Wen, Yu Zhao, Liang Wang, Yan Yuan","doi":"10.1002/jbt.70299","DOIUrl":"https://doi.org/10.1002/jbt.70299","url":null,"abstract":"<div>\u0000 \u0000 <p>Cadmium (Cd), a prevalent environmental pollutant, is of significant concern owing to its neurotoxicity; thus, the identification of effective interventions for nerve injury caused by Cd is crucial. Mitochondrial signaling pathway-mediated apoptosis and PTEN-induced putative kinase protein 1 (PINK1)/E3 ubiquitin ligase (Parkin)-mediated mitophagy are the primary mechanisms responsible for the neurotoxic effects of Cd. Daidzein (Dz), a naturally occurring isoflavone found in leguminous plants, exhibits a wide range of pharmacological effects in the brain. To investigate the short-term protective effects of Dz against Cd-induced neurotoxicity in the rat cerebral cortex, 24 male Sprague–Dawley rats were treated with Dz (100 mg/kg) and/or CdCl<sub>2</sub> (2 mg/kg) for 12 days. Histological changes in the cerebral cortex were assessed by Nissl staining. Apoptosis- and mitophagy-related indices were detected using TUNEL staining, western blotting, and immunofluorescence assays. The administration of Dz attenuated Cd-induced nerve injury. Additionally, Dz reduced cell apoptosis by 66%, and the expression of apoptosis-related proteins Bax/Bcl-2 ratio by 27%, cleaved caspase-9 by 42%, and cleaved caspase-3 by 42%. Dz also decreased the expression of the mitophagy-related proteins LC3 by 35%, PINK1 by 37%, and Parkin by 29%, and increased that of COX IV by 36%. Furthermore, Dz abolished the Cd-induced colocalization of PINK1 and Parkin in the cerebral cortex of rats. In summary, our results indicate that Dz exerts neuroprotective effects in the cerebral cortex of rats by inhibiting mitochondrial signaling pathway-mediated apoptosis and PINK1/Parkin-mediated mitophagy. Therefore, Dz is a promising novel neuroprotective agent. However, some challenges remain, such as efficacy, bioavailability, and potential side effects. Further studies are needed to assess its potential as a therapeutic agent for Cd-induced neurotoxicity in humans.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 5","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143944495","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

METTL14 Promotes Vascular Smooth Muscle Cell Proliferation and Neointima Formation via m6A Methylation TEAD1 mRNA

IF 3.2 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2025-05-13 DOI: 10.1002/jbt.70284

Liang Wang, Guojin Xia, Yan Tang, Yuemei Xu, Qing Li, Zhixing Chen, Tong Wen, Yunfeng Wei, Chunying Wei, Jiamin Zhou

{"title":"METTL14 Promotes Vascular Smooth Muscle Cell Proliferation and Neointima Formation via m6A Methylation TEAD1 mRNA","authors":"Liang Wang, Guojin Xia, Yan Tang, Yuemei Xu, Qing Li, Zhixing Chen, Tong Wen, Yunfeng Wei, Chunying Wei, Jiamin Zhou","doi":"10.1002/jbt.70284","DOIUrl":"https://doi.org/10.1002/jbt.70284","url":null,"abstract":"<div>\u0000 \u0000 <p>Vascular smooth muscle cell (VSMC) proliferation and neointimal hyperplasia critically contribute to atherosclerosis and post-angioplasty restenosis. Building on our prior discovery that TEA domain transcription factor 1 (TEAD1) regulates VSMCs differentiation, we now investigate methyltransferase-like 14 (METTL14) in vascular remodeling. METTL14 expression was significantly upregulated in human carotid atherosclerotic plaques versus control arteries, correlating with VSMCs dedifferentiation. This pattern was recapitulated in murine wire-induced carotid injury models during neointima formation. Functionally, METTL14 overexpression suppressed contractile markers while accelerating proliferation and migration in human coronary artery smooth muscle cells (HCASMCs). Conversely, METTL14 knockdown attenuated injury-induced neointimal hyperplasia In Vivo. Mechanistically, METTL14 stabilizes TEAD1 mRNA through m6A modification at nucleotide 513, enhancing YAP1/TEAD1 signaling. Both 513nt mutation and TEAD1 inhibitor VT103 abolished METTL14-driven phenotypic changes, restoring VSMCs differentiation and suppressing proliferation. Collectively, our findings establish METTL14-mediated m6A modification of TEAD1 mRNA as a novel mechanism promoting vascular pathology, highlighting its therapeutic potential for cardiovascular diseases.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 5","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143944499","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Naringin Mitigates Chondrocyte Apoptosis in Osteoarthritis by Suppressing the miR-29a-3p-Bax Pathway

IF 3.2 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2025-05-13 DOI: 10.1002/jbt.70304

Tianliang Chen, Guilan Li, Yongtao Xu, Bolai Chen

{"title":"Naringin Mitigates Chondrocyte Apoptosis in Osteoarthritis by Suppressing the miR-29a-3p-Bax Pathway","authors":"Tianliang Chen, Guilan Li, Yongtao Xu, Bolai Chen","doi":"10.1002/jbt.70304","DOIUrl":"https://doi.org/10.1002/jbt.70304","url":null,"abstract":"<div>\u0000 \u0000 <p>The present study aims to explore potential therapeutic effects of Naringin on osteoarthritis (OA) and investigate the underlying mechanism. The chondrocytes in the joint usually undergo detrimental changes during OA progression, including increased apoptosis. miRNAs emerge as crucial regulators in this processes. The study delves into the intricate interplay between miR-29a-3p, BAX-mediated apoptosis, and Naringin intervention. Pro-inflammatory cytokines induce chondrocyte apoptosis in OA, impacting cell viability. Naringin treatment effectively restores cell survivability (1.8-fold change), inhibiting caspase activity (0.54-fold change) and lowering matrix metalloproteinases-9 (MMP-9) (0.50-fold change) and MMP-13 expression (0.50-fold change). Furthermore, COL2A1, Sox9, Runx2, TGF-β1, and BMP-4 levels in cytokines-stimulated chondrocytes were enhanced by Naringin, accompanied by decreased productions of MMP3 and MMP13. In cartilage tissues of OA rats, Osteoarthritis Research Society International (OARSI) scores in Safranin O staining were elevated, Pro-inflammatory cytokine productions and MMP3 and MMP13 expressions were enhanced, and COL2A1, Sox9, Runx2, TGF-β1, and BMP-4 levels were reduced, which were remarkably rescued by Naringin. We further revealed the intricate connection between miR-29a-3p and the chondrocyte fate. Elevated miR-29a-3p expression corresponds to increased apoptotic chondrocytes. Naringin suppresses miR-29a-3p, curbing apoptosis and suggesting a potential therapeutic avenue. Notably, BAX emerges as a key player, with miR-29a-3p influencing its expression. Naringin's mitigation of BAX upregulation underscores its protective role. Overall, we found the potential role of Naringin in addressing chondrocyte apoptosis in OA through miR-29a-3p-BAX modulation, offering insights into innovative OA management strategies.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 5","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143944498","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Dihydroartemisinin Targets the NFIC/FBN1 Cascade to Enhance Wound Healing in Chronic Skin Ulcer by Inhibiting Fibroblast Ferroptosis

IF 3.2 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2025-05-13 DOI: 10.1002/jbt.70297

Zhiyi Wei, Biao Wang, Xiangjian Fang, Juntao Cheng

{"title":"Dihydroartemisinin Targets the NFIC/FBN1 Cascade to Enhance Wound Healing in Chronic Skin Ulcer by Inhibiting Fibroblast Ferroptosis","authors":"Zhiyi Wei, Biao Wang, Xiangjian Fang, Juntao Cheng","doi":"10.1002/jbt.70297","DOIUrl":"https://doi.org/10.1002/jbt.70297","url":null,"abstract":"<div>\u0000 \u0000 <p>Dysfunction of fibroblasts contributes to a pathological state to delay wound repair in chronic skin ulcer (CSU). Dihydroartemisinin (DHA), a derivative of artemisinin, has a therapeutic potential in diverse diseases owing to multiple pharmacological effects. However, no attempt was made to evaluate the function of DHA in CSU. Human dermal fibroblasts were isolated from the peripheral ulcerative tissues in CSU patients (uHFBs) and normal skins (nHFBs). Cell migration, proliferation, apoptosis, and ability were detected. Ferroptosis was evaluated by detecting Fe<sup>2+</sup>, iron and ROS contents. Immunoblot and quantitative PCR analyses were performed to quantify expression. The NFIC/FBN1 binding relationship was verified by luciferase reporter assay. The CSU mouse model was established, and histology and Masson's staining was used to analyze DHA efficacy. DHA increased NFIC expression in uHFBs. DHA accelerated cell proliferation and migration and impeded ferroptosis in uHFBs, which could be partially counteracted by NFIC reduction. Mechanistically, NFIC transcriptionally elevated FBN1 expression, and DHA increased FBN1 expression by NFIC. NFIC increase enhanced uHFB proliferation and migration and suppressed ferroptosis, which could be abrogated by FBN1 downregulation. Moreover, DHA improved wound repair in CSU mice by upregulating NFIC and FBN1. Additionally, NFIC and FBN1 were underexpressed in uHFBs versus nHFBs. Our findings indicate that DHA has the efficacy to improve wound repair in CSU mice and upgrades skin fibroblast function via the NFIC/FBN1 cascade. DHA may be a novel drug for CSU treatment.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 5","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143944494","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Pasireotide Exerts Anti-Inflammatory Effects in the Endothelium

IF 3.2 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2025-05-13 DOI: 10.1002/jbt.70306

Saikat Fakir, Madan Sigdel, Md Matiur Rahman Sarker, Nektarios Barabutis

引用次数: 0

Correction to Synthesis, Cytotoxic Activity, Antiquorum Sensing Effect, Docking and Md Simulation of Novel 1,3-Disubstituted 2-Mercapto-1H-Benzo[D]Imidazolium Chlorides

IF 3.2 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2025-05-13 DOI: 10.1002/jbt.70293

引用次数: 0

ANKRD22 Induced by Transcription Factor MAZ Promotes Proliferation and Invasion of Nasopharyngeal Carcinoma 转录因子MAZ诱导的ANKRD22促进鼻咽癌的增殖和侵袭

IF 3.2 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2025-05-10 DOI: 10.1002/jbt.70222

Guoqing Gong, Jie Yuan, Guang Yang, Liu Sun, Peng Huang, Changliang Yang

{"title":"ANKRD22 Induced by Transcription Factor MAZ Promotes Proliferation and Invasion of Nasopharyngeal Carcinoma","authors":"Guoqing Gong, Jie Yuan, Guang Yang, Liu Sun, Peng Huang, Changliang Yang","doi":"10.1002/jbt.70222","DOIUrl":"https://doi.org/10.1002/jbt.70222","url":null,"abstract":"<div>\u0000 \u0000 <p>Nasopharyngeal carcinoma (NPC) is very common in Southeast China, with the characteristics of high aggression and metastasis. Ankyrin repeat domain-containing protein 22 (ANKRD22) contributes to tumor growth in different tumors, but its role in NPC is still unknown. This study set out to address the action of ANKRD22 in the progression of NPC. The ANKRD22 expression was examined by reverse transcription quantitative polymerase chain reaction and western blot. The function of ANKRD22 in the progression of NPC was addressed through Cell Counting Kit-8, flow cytometry, transwell, luciferase, chromatin immunoprecipitation, and western blot assays. Besides, the in vivo role of ANKRD22 in NPC was assessed using immunohistochemistry and terminal deoxynucleotidyl transferase deoxyuridine triphosphate (dUTP) nick end labeling (TUNEL) assays after nude mice were administrated with HK-1 cells transfected with sh-ANKRD22. The ANKRD22 expression was upregulated in NPC, which predicted a poor prognosis in NPC patients. Knockdown of ANKRD22 suppressed growth and invasion, but enhanced apoptosis in NPC cells. Mechanically, MYC-associated zinc finger protein (MAZ) was a transcription factor of ANKRD22 that positively modulated the ANKRD22 expression in NPC cells. MAZ/ANKRD22 axis accelerated proliferation and invasion, but repressed apoptosis in NPC cells. In vivo, silencing of ANKRD22 diminished the tumor size and weight, the expression of Ki-67 and ANKRD22, but increased apoptosis of NPC. ANKRD22 was transcriptionally modulated by MAZ, which promoted proliferation and invasion, but suppressed apoptosis of NPC.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 5","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143930220","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Circ_0001715 Mediated Progression and Inflammation in Fibroblast-Like Synoviocytes of Rheumatoid Arthritis by Targeting miR-326/TLR-4-NF-κB Pathway Circ_0001715靶向miR-326/TLR-4-NF-κB通路介导类风湿关节炎成纤维细胞样滑膜细胞的进展和炎症

IF 3.2 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2025-05-09 DOI: 10.1002/jbt.70283

Min Niu, Ying Li, Hao Xu, Jingman Yuan, Meixi Yan, Ge Yang, Ziyi Yan, Xichao Yang

{"title":"Circ_0001715 Mediated Progression and Inflammation in Fibroblast-Like Synoviocytes of Rheumatoid Arthritis by Targeting miR-326/TLR-4-NF-κB Pathway","authors":"Min Niu, Ying Li, Hao Xu, Jingman Yuan, Meixi Yan, Ge Yang, Ziyi Yan, Xichao Yang","doi":"10.1002/jbt.70283","DOIUrl":"https://doi.org/10.1002/jbt.70283","url":null,"abstract":"<div>\u0000 \u0000 <p>Rheumatoid arthritis (RA) is a systemic autoimmune disease. Circular RNA_0001715 (circ_0001715) has been demonstrated to be involved in the progression of cancers. This study aimed to discuss the function of circ_0001715 on the development of RA. Tumor necrosis factor-α (TNF-α) was used to active human RA fibroblast-like synoviocytes (FLS) (HFLS-RA) cells. The role of circ_0001715 in the progression of RA was determined by cell counting kit-8, flow cytometry, enzyme-linked immunosorbent assay. The target of circ_0001715 was predicted using the circinteractome database and validated by the luciferase reporter assay. The relative protein expression of toll-like receptor (TLR)-4/nuclear factor-kappa B (NF-κB) axis was detected by western blot. Moreover, a collagen-induced arthritis (CIA) mouse model was constructed through the secondary immunization. The role of circ_0001715 in vivo was determined by hematoxylin and eosin (H&E), Safranin O, TRAP, ELISA and western blot. Increased levels of circ_0001715 were discovered in tissues from RA patients, TNF-α-induced HFLS-RA cells, and synovial tissues of CIA-induced mice. Knockdown of circ_0001715 decreased proliferation and inflammation, but promoted apoptosis of RA both in vitro and in vivo. Additionally, miR-326 was predicted as the target of circ_0001715, which was confirmed by the luciferase reporter assay. Knockdown of miR-326 reversed the results of proliferation, apoptosis and inflammation resulted from the circ_0001715 knockdown. Mechanically, knockdown of circ_0001715 reduced the expression of TLR-4/NF-κB axis, which were rescued by the downregulation of miR-326. Circ_0001715 sequestered miR-326 to regulate the growth, apoptosis and inflammation of HFLS-RA cells via TLR-4/NF-κB axis.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 5","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143926047","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Morin Hydrate Improves Kidney Functions in DEHP-Intoxicated Mice via NF-kB/TNFα/Oxidative Stress/Apoptosis Pathway 莫宁水合物通过NF-kB/ tnf - α/氧化应激/凋亡通路改善dehp中毒小鼠肾功能

IF 3.2 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2025-05-08 DOI: 10.1002/jbt.70294

Vikash Kumar, Rahul Kumar, Guruswami Gurusubramanian, Saurabh Singh Rathore, Vikas Kumar Roy

{"title":"Morin Hydrate Improves Kidney Functions in DEHP-Intoxicated Mice via NF-kB/TNFα/Oxidative Stress/Apoptosis Pathway","authors":"Vikash Kumar, Rahul Kumar, Guruswami Gurusubramanian, Saurabh Singh Rathore, Vikas Kumar Roy","doi":"10.1002/jbt.70294","DOIUrl":"https://doi.org/10.1002/jbt.70294","url":null,"abstract":"<div>\u0000 \u0000 <p>Di (2-ethylhexyl) phthalate (DEHP) is a plasticiser used in plastic products; and it dissolves easily and leaks into the environment. Due to its lipophilic nature, DEHP accumulates in organisms and can bioaccumulate through food chains. The natural flavonoid, like morin hydrate, possesses various pharmacological properties, including anti-inflammatory, antioxidant, and free radical scavenging. The purpose of this study was to investigate the effect of morin hydrate (MH) on kidney function of DEHP-treated mice. To investigate the underlying processes of the proposed objective, DEHP (500 mg/kg) and DEHP, along with MH at doses of 10 and 100 mg/kg, were administered to Swiss albino mice for 14 days. Our results showed that MH treatment improved kidney function by decreasing creatinine and urea levels in DEHP-intoxicated mice. Furthermore, the MH also alleviates DEHP-induced kidney fibrosis and kidney histoarchitecture. DEHP-mediated oxidative stress and stimulated apoptosis in the kidney were also mitigated by MH treatment. The elevated expression of NF-kB/TNF-α by the DEHP treatment was also down-regulated by the MH treatment. In addition, the abundance of HSP70 increased in the kidneys after DEHP treatment, and MH treatment also decreased the abundance of HSP70 in the kidneys. In conclusion, DEHP treatment caused kidney toxicity in mice, and MH mitigates the kidney functions via modulating NF-kB/TNF-α/oxidative stress/apoptosis pathway. Our findings provide the new findings that MH protects the kidneys from DEHP intoxication, highlighting the potential of MH as a protective treatment for DEHP toxicity and offering hope for future research and treatments.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 5","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143919578","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0