Biochemical and biophysical research communications最新文献

{"title":"In silico maturation of DNA aptamer against the prostate-specific antigen (PSA) and kinetic analysis","authors":"Chi-Ping Huang ,&nbsp;Wen-Pin Hu ,&nbsp;Wei Yang ,&nbsp;Zheng-Jie Lee ,&nbsp;Wen-Yih Chen","doi":"10.1016/j.bbrc.2025.151638","DOIUrl":"10.1016/j.bbrc.2025.151638","url":null,"abstract":"<div><div>The detection of the prostate-specific antigen (PSA) serves as a critical marker for the diagnosis and follow-up of prostate cancer. DNA aptamers targeting PSA have been successfully screened using the systematic evolution of ligands by exponential enrichment (SELEX) technique, complemented by in silico maturation processes. In this study, we aim to optimize a truncated aptamer, denoted as TA87, through computational methods and to analyze potential aptamer candidates in the aptamer-PSA interactions. The PSA antibody, aptamer ΔPSap4#5, and an identified but unpublished aptamer, PSAG221, were evaluated in quartz crystal microbalance (QCM) experiments alongside aptamers derived from TA87. The Tanimoto similarity score and the ZDOCK program, coupled with the ZRANK scoring function, were adopted to assess the secondary structure of single-point mutants of TA87 and their binding interactions with PSA, respectively. Detailed analyses of the aptamer-protein complexes were conducted using molecular dynamics (MD) simulations. Mutations TA87M24 and TA87M49, along with PSAG221 and TA87, showed superior ZDOCK scores compared to ΔPSap4#5. MD simulations further suggested that PSAG221 aptamer might offer enhanced binding to PSA over ΔPSap4#5. The affinity constant (<em>K</em>_<em>D</em>) values for the antibody, ΔPSap4#5, PSAG221, TA87, TA87M24, and TA87M49 with PSA were determined through QCM measurements to be 0.35, 0.33, 0.35, 0.56, 0.45, and 0.51 μM⁻¹, respectively. The experimental results showed that the truncated aptamers, TA87, and the two mutations, TA87M24 and TA87M49, did not demonstrate superior PSA binding affinity. Aptamer PSAG221 demonstrated performance comparable to that of the antibody, although slightly inferior to ΔPSap4#5. The aptamer PSAG221 reported in this study could be an alternative probe for developing future PSA aptasensor platforms.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"759 ","pages":"Article 151638"},"PeriodicalIF":2.5,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143679414","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of bile acid-dependent Takeda G-coupled protein receptor 5 (TGR5) in regulating AMPK expression in human podocytes","authors":"Patrycja Rachubik,&nbsp;Klaudia Grochowalska,&nbsp;Irena Audzeyenka,&nbsp;Dorota Rogacka,&nbsp;Agnieszka Piwkowska","doi":"10.1016/j.bbrc.2025.151671","DOIUrl":"10.1016/j.bbrc.2025.151671","url":null,"abstract":"<div><div>Bile acids affect podocyte function by stimulating membrane-bound Takeda G protein-coupled receptor 5 (TGR5), the activity of which is linked to the regulation of glucose and lipid metabolism. In podocytes, adenosine monophosphate-dependent protein kinase (AMPK) is critical for maintaining energy balance, suggesting that the bile acid-dependent stimulation of TGR5 may impact AMPK activity to regulate metabolic processes in podocytes. Despite the beneficial effect of TGR5 activation on AMPK activity in podocytes that are exposed to hyperglycemic conditions, the effect of TGR5 signaling on AMPKα expression and phosphorylation state under control conditions have not been studied in podocytes. Our studies confirmed TGR5 expression in podocytes at both the mRNA and protein levels. Moreover, TGR5 inhibition decreased the protein expression of both AMPKα1 and AMPKα2 isoforms, which correlated with significantly lower levels of AMPKα phosphorylation at Thr172 in podocytes. Additionally, the immunofluorescent staining of podocytes with pharmacologically inhibited TGR5 activity were characterized by a lower mean intensity of the AMPKα fluorescence signal. TGR5 stimulation decreased the mRNA expression of AMPKα1 and AMPKα2 but did not change the degree of AMPKα phosphorylation at Thr172. These data suggest that TGR5 inactivation significantly downregulates AMPK activity. This may shed new light on the bile acid-dependent regulation of glucose and lipid metabolism in podocytes, especially under pathological conditions.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"759 ","pages":"Article 151671"},"PeriodicalIF":2.5,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143704397","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The dilemma of nuclear mechanical forces in DNA damage and repair","authors":"Iqra Ali ,&nbsp;Fangning Xu ,&nbsp;Qin Peng ,&nbsp;Juhui Qiu","doi":"10.1016/j.bbrc.2025.151639","DOIUrl":"10.1016/j.bbrc.2025.151639","url":null,"abstract":"<div><div>Genomic stability, encompassing DNA damage and repair mechanisms, plays a pivotal role in the onset of diseases and the aging process. The stability of DNA is intricately linked to the chemical and mechanical forces exerted on chromatin, particularly within lamina-associated domains (LADs). Mechanical stress can induce DNA damage through the deformation and rupture of the nuclear envelope, leading to DNA bending and cleavage. However, DNA can evade such mechanical stress-induced damage by relocating away from the nuclear membrane, a process facilitated by the depletion of H3K9me3-marked heterochromatin and its cleavage from the lamina. When DNA double-stranded breaks occur, they prompt the rapid recruitment of Lamin B1 and the deposition of H3K9me3. Despite these insights, the precise mechanisms underlying DNA damage and repair under mechanical stress remain unclear. In this review, we explore the interplay between mechanical forces and the nuclear envelope in the context of DNA damage, elucidate the molecular pathways through which DNA escapes force-induced damage, and discuss the corresponding repair strategies involving the nuclear cytoskeleton. By summarizing the mechanisms of force-induced DNA damage and repair, we aim to underscore the potential for developing targeted therapeutic strategies to bolster genomic stability and alleviate the impacts of aging and disease.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"758 ","pages":"Article 151639"},"PeriodicalIF":2.5,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143683850","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Long-term aerobic exercise enhances liver health: miRNA regulation and oxidative stress alleviation","authors":"Chen-Kai Zhang ,&nbsp;Zhuang-Zhi Wang ,&nbsp;Fang-Hui Li","doi":"10.1016/j.bbrc.2025.151677","DOIUrl":"10.1016/j.bbrc.2025.151677","url":null,"abstract":"<div><div>This study aims to investigate the effects of long-term aerobic exercise on liver health in aging rats. As age increases, the continuous accumulation of endogenous reactive oxygen species (ROS) damages hepatocytes, leading to liver function decline and the development of diseases such as cirrhosis and liver cancer. Using an 18-month-old rat model, we implemented an eight-month aerobic exercise regimen to systematically evaluate its hepatoprotective effects. The results showed that aerobic exercise effectively reduced oxidative stress and inflammation levels in liver tissue, decreased the expression of cell cycle regulator P53 and inflammatory regulator NF-κB protein, upregulated NRF2 protein expression, improved mitochondrial function, and inhibited the progression of ferroptosis. These beneficial effects were achieved through the upregulation of miR-21 and miR-224 expression induced by exercise. These microRNAs inhibit the translation of MAP2K3 and MAPK14, thereby suppressing the activation of the P38 MAPK pathway. We further found that inhibiting P38 MAPK can enhance cellular antioxidant and anti-inflammatory capabilities, reversing hepatocyte damage caused by hydrogen peroxide. These results demonstrate that long-term aerobic exercise can reprogram aging-related oxidative stress and metabolic pathology by regulating miRNAs and the P38 MAPK pathway, thereby helping to prevent age-related liver diseases.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"759 ","pages":"Article 151677"},"PeriodicalIF":2.5,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143696120","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Net charge driven recruitment of supercharged GFP mutants into FUS droplets","authors":"Kiyoto Kamagata ,&nbsp;Yuxing Hong ,&nbsp;Trishit Banerjee ,&nbsp;Hiroto Takahashi ,&nbsp;Eriko Mano","doi":"10.1016/j.bbrc.2025.151661","DOIUrl":"10.1016/j.bbrc.2025.151661","url":null,"abstract":"<div><div>Liquid droplets recruit their relevant proteins and function together. Previous studies for a series of guest proteins clarified several rules of the recruitment and translational dynamics in the droplets; however, the other guest parameters such as structures, sizes, and amino-acid compositions might mask the single parameter effect. Here, we characterized the properties of GFP mutants with different charged compositions, but the same structure and size, in fused in sarcoma (FUS) droplets using single-molecule fluorescence microscopy. The recruitment of GFP mutants depended on their absolute net charge, whereas the diffusion did not. In the recruitment vs. diffusion plots, GFP mutants with large net charges were distinct from other proteins, demonstrating the importance of long-range electrostatic interaction on the recruitment.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"759 ","pages":"Article 151661"},"PeriodicalIF":2.5,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143679471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A liver-specific mouse model for MYO5B-associated cholestasis reveals a toxic gain-of-function as underlying disease mechanism","authors":"Hui-Yu She ,&nbsp;Yi-Ling Qiu ,&nbsp;Jia-Yan Feng ,&nbsp;Ye Cheng ,&nbsp;Hao Chi ,&nbsp;Sven C.D. van IJzendoorn ,&nbsp;Qing-He Xing ,&nbsp;Jian-She Wang","doi":"10.1016/j.bbrc.2025.151669","DOIUrl":"10.1016/j.bbrc.2025.151669","url":null,"abstract":"<div><div>Myosin Vb (MYO5B) deficiency, referring to the loss of protein expression or function, causes microvillus inclusion disease (MVID) and/or progressive familial intrahepatic cholestasis-type 10 (PFIC10) in humans. MYO5B plays a role in intracellular trafficking, but the mechanisms by which it contributes to cholestasis are not understood. The aim of this study was to generate a liver-specific mouse model and investigate the mechanism of MYO5B-associated cholestasis. In this study, we generated a liver-specific <em>Myo5b</em> cKO mice via CRISPR/Cas9 genome editing in conjunction with albumin-cre recombinase. Cholestatic stress was induced by dietary-administration of cholic acid (CA) or 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC). To investigate the frequently recurring <em>MYO5B</em> variant (c.2470C &gt; T/p.(Arg824Cys)), adenoviral vectors encoding either the missense variant or blank control sequence were delivered to wild-type and <em>Myo5b</em> cKO mice through tail-vein injection. Serum and liver tissues were harvested from all mice for biochemical and histological analysis. Our findings indicated that loss of Myo5b expression did not cause cholestatic liver disease and did not augment CA or DDC feeding-induced cholestatic stress. By contrast, expression of the <em>MYO5B</em> c.2470C &gt; T/p. (Arg824Cys) variant induced cholestasis, evidenced by elevated levels of serum alanine aminotransferase, alkaline phosphatase and bilirubin, mild hepatocellular injury, and altered bile salt export pump (Bsep) localization, resembling that observed in human PFIC10. In summary, we have developed a mouse model of MYO5B-associated cholestasis. The expression of the MYO5B-p. (Arg824Cys) variant but not the loss of Myo5b expression caused cholestasis, indicating a toxic gain-of-function as underlying disease mechanism.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"758 ","pages":"Article 151669"},"PeriodicalIF":2.5,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143684429","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Formononetin prevents intestinal injury caused by radiotherapy in colorectal cancer mice via the Keap1-Nrf2 signaling pathway","authors":"Rongjun Tang ,&nbsp;Lidan Zhang ,&nbsp;Jun Lou ,&nbsp;Weixing Mo ,&nbsp;Linfang Zhao ,&nbsp;Lingdi Li ,&nbsp;Ke Zhang ,&nbsp;Qingqing Yu","doi":"10.1016/j.bbrc.2025.151676","DOIUrl":"10.1016/j.bbrc.2025.151676","url":null,"abstract":"<div><div>Radiation-induced intestinal injury (RIII) is a serious complication of radiation therapy. Formononetin (FT) is a methoxy isoflavone with anti-tumor and anti-oxidant properties. This study explored whether FT reduces ROS by activating the Keap1/Nrf2 pathway and thereby protecting against RIII. 30 BABL/C mice were used to construct a colorectal cancer model with CT26 cells and validated the model on day 7. Then, the cancer model mice were divided into 3 groups on day 14 (model control, model, and model + FT) with administration of FT or saline and radiated them on day 21. All samples were collected on day 28. Mechanical intestinal barrier assessed via intestinal absorption function, HE staining, and Claudin-1, Occludin, ZO-1 expression. Apoptosis was measured by TUNEL and cleaved-caspase 3, angiogenesis by CD31, and oxidative stress by NO and ROS levels. Keap1, Nrf2 (cytoplasm) and Nrf2 (nucleus) expression were measured by Western blot. FT treatment enhanced absorption and reduced damage and apoptosis in intestinal tissue. During FT treatment, inhibition of NO and ROS leads to suppression of oxidative stress and promotion of CD31 expression promotes angiogenesis. FT upregulated the expression of nuclear Nrf2 and reduced cytoplasmic Keap1 and Nrf2. FT strengthens mechanical barrier and decreases oxidative stress in intestinal tissue, providing radiation injury protection. Its anti-radiation effect may be through Keap1/Nrf2 pathway activation.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"761 ","pages":"Article 151676"},"PeriodicalIF":2.5,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143760956","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oxidation of active site cysteine leads to inactivation of peptide deformylase from Salmonella enterica","authors":"Sanjay Kumar Rohaun ,&nbsp;Pradip K. Chakraborti","doi":"10.1016/j.bbrc.2025.151675","DOIUrl":"10.1016/j.bbrc.2025.151675","url":null,"abstract":"<div><div>Peptide deformylase (PDF) is an essential bacterial enzyme involved in first step of N-methionine excision (NME) pathway during bacterial protein synthesis. In first step of NME, N-formyl group of nascent polypeptide chains is removed by PDF. PDF is a metallo-protease where metal cofactor is co-ordinated to a Cys and two His residues. We cloned and expressed this iron containing metallo-protease from <em>Salmonella typhimurium</em> (sPDF). We characterized the sPDF which is a mononuclear iron containing enzyme that displayed optimal <em>in vitro</em> activity in the presence of oxidation preventing agent like catalase. To have an insight into the role of metal ion in catalase dependent enzyme activity, we generated surrogate sPDF-Ni²⁺ and sPDF-Co²⁺. Interestingly, these proteins also showed catalase requirement for optimum enzyme activity. Thus our results argue the presence of the target (amino acid) of oxidation in the protein itself that might be crucial for the activity of the enzyme. To ascertain this aspect, we examined the oxidation status of active site cysteine of sPDF by mass spectrometry. Our results indicated that the direct oxidation/over-oxidation of active site cysteine is responsible for inactivation of sPDF protein. Furthermore, a comparison of PDF sequences from Gram-negative bacteria revealed the presence of this cysteine throughout the lineage. Thus, our results per se are indicative of a similar behaviour of all these Gram-negative peptide deformylase proteins.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"759 ","pages":"Article 151675"},"PeriodicalIF":2.5,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143698089","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RAB18 deficiency disrupts lipid metabolism and autophagy in mice","authors":"Li-Wei Zhang ,&nbsp;Ya-Qi Han ,&nbsp;Yan Yang ,&nbsp;Yun-Jie Li ,&nbsp;Ying-Xian Ma ,&nbsp;Sheng-Li Ming","doi":"10.1016/j.bbrc.2025.151673","DOIUrl":"10.1016/j.bbrc.2025.151673","url":null,"abstract":"<div><div>Mutation of the small G protein member RAB18 can lead to Warburg Micro Syndrome, characterized clinically by visual impairment and hind limb weakness. However, the cellular and molecular functions of RAB18 in mice are not fully understood. We obtained 3 Rab18^+/+ and 3 Rab18^−/− mice by using CRISPR/Cas9 technology. Rab18^−/− mice exhibit symptoms of ocular shrinkage and hind limb weakness, along with griping/curling when tail suspended. Through metabolomics analysis, we found that Rab18 knockout affects lipid, vitamin, and amino acid metabolism while also impacting the autophagy signaling pathway. Lipid analysis of the mouse liver revealed that Rab18 knockout led to an increase in hepatic lipid droplets, promoted elevated TC and TG levels, and impaired fatty acid release. Interestingly, Rab18 knockout promoted the expression of lipogenic genes and proteins but did not affect the expression of lipolytic genes and proteins. Since lipophagy, involved in lipid droplet breakdown, plays a key role, we found that Rab18 knockout inhibited the expression of liver autophagy-related genes and proteins. In summary, our results suggest that Rab18 plays a role in autophagy in mice, likely contributing to mechanisms of lipid accumulation.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"760 ","pages":"Article 151673"},"PeriodicalIF":2.5,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143725679","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Silymarin attenuates post-weaning bisphenol A-induced renal injury by suppressing ferroptosis and amyloidosis through Kim-1/Nrf2/HO-1 signaling modulation in male Wistar rats","authors":"Roland Eghoghosoa Akhigbe ,&nbsp;Adebayo Oluwafemi Adekunle ,&nbsp;Mutiyat Damilola Ajao ,&nbsp;Temiloluwa Angela Sunmola ,&nbsp;Deborah Oluwatimileyin Aboyeji ,&nbsp;Cecilia Adedeji Adegbola ,&nbsp;Ayoola Abimbola Oladipo ,&nbsp;Tunmise Maryanne Akhigbe","doi":"10.1016/j.bbrc.2025.151668","DOIUrl":"10.1016/j.bbrc.2025.151668","url":null,"abstract":"<div><div>Bisphenol A (BPA) is a synthetic chemical used in producing polycarbonate plastics and epoxy resins and is commonly found in everyday items like water bottles and food containers. Although its usefulness cannot be overemphasized, the major challenge is its toxicity, including renal toxicity. BPA has been reported to induce ferroptosis and amyloidosis via the modulation of Nrf2/HO-1 signaling. On the other hand, silymarin activates the Nrf2/HO-1 pathway, thus providing cellular defense. However, the effect of silymarin on BPA-induced renal toxicity is yet to be reported. This study investigated the potential impact of silymarin on renal structure and function following post-weaning BPA exposure. Twenty-four male Wistar rats were randomly assigned into four equal groups. The control was vehicle-treated, while the silymarin-treated received 100 mg/kg/day of silymarin and BPA-treated rats received 50 mg/kg/day of BPA. The BPA + silymarin-treated rats received treatments as BPA-treated and silymarin-treated. Silymarin diminished BPA-induced rise in serum urea, creatinine, BUN, and plasma kim-1 levels. Also, silymarin improved BPA-induced dyslipidemia. More so, silymarin abrogated toxic amyloid formation and improved renal histoarchitecture in BPA-exposed rats. These events were associated with the suppression of BPA-induced rise in renal iron, MDA, TNF-α, IL-1β, and cytochrome <em>c</em> levels, and myeloperoxidase and caspase 3 activities by silymarin therapy. Furthermore, silymarin attenuated BPA-induced downregulation of Nrf2 and GSH levels, and HO-1, GPX4, SOD, catalase, GST, and GR activities. In conclusion, silymarin mitigated post-weaning BPA-induced renal toxicity by suppressing ferroptosis and amyloidosis through Kim-1/Nrf2/HO-1 modulation.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"758 ","pages":"Article 151668"},"PeriodicalIF":2.5,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143684424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}