Biochemical and biophysical research communications最新文献

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Exploring the antibiotic potential of copper carbonate nanoparticles, wound healing, and glucose-lowering effects in diabetic albino mice

IF 2.5 3区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochemical and biophysical research communications

Pub Date : 2025-02-22 DOI: 10.1016/j.bbrc.2025.151527

Muhammad Waseem Aslam , Sabeen Sabri , Ali Umar , Muhammad Saleem Khan , Muhammad Yasir Abbas , Misbah Ullah Khan , Muhammad Wajid

Bio-Nanoscience is an emerging field that integrates nanotechnology with biological systems to revolutionize medicine, agriculture, and environmental sustainability through innovative and targeted solutions. The aim of this study was to synthesize copper carbonate nanoparticles and to investigate their antibacterial, wound healing, and glucose-lowering properties. Nanoparticles (NPs) were Synthesized through chemical reduction method and confirmed by using SEM, XRD, and FTIR. Characterization revealed that the nanoparticles had an average size of 55 ± 16 nm, exhibited a crystalline structure, and were free of impurities. Antibacterial tests demonstrated enhanced inhibition zones for Pseudomonas spp., S. aureus, and other bacterial strains, with the largest zone of inhibition observed at 12 mg/ml, measuring 18.5 ± 1.05 mm for Pseudomonas spp. In wound healing activity in diabetic mice observations revealed a complete wound closure in NPs treated mice by day 14 as compared to the control group (96.10 % wound closure). Nanoparticle administration (oral) also significantly reduced glucose levels in diabetic mice after 15 days in the experimental period, whereas fasting glucose levels reduced from 398.00 ± 6.16 to 116.67 ± 12.47 mg/dl. The docking studies of copper carbonate nanoparticles (NPs) with proteins involved in wound healing, including Antileukoproteinase (−2.7 kcal/mol), Casein (−2.5 kcal/mol), Collagen (−2.9 kcal/mol), Lysozyme (−2.8 kcal/mol), and Phospholipase (−3.9 kcal/mol), revealed significant binding affinities, suggesting potential applications in enhancing wound healing processes. Therefore, the copper carbonate nanoparticles demonstrate strong antibacterial properties and show promising effects on wound healing, along with blood glucose-lowering activity. These findings suggest their potential in biomedical applications, particularly for treating diabetes and bacterial infections.

{"title":"Exploring the antibiotic potential of copper carbonate nanoparticles, wound healing, and glucose-lowering effects in diabetic albino mice","authors":"Muhammad Waseem Aslam , Sabeen Sabri , Ali Umar , Muhammad Saleem Khan , Muhammad Yasir Abbas , Misbah Ullah Khan , Muhammad Wajid","doi":"10.1016/j.bbrc.2025.151527","DOIUrl":"10.1016/j.bbrc.2025.151527","url":null,"abstract":"<div><div>Bio-Nanoscience is an emerging field that integrates nanotechnology with biological systems to revolutionize medicine, agriculture, and environmental sustainability through innovative and targeted solutions. The aim of this study was to synthesize copper carbonate nanoparticles and to investigate their antibacterial, wound healing, and glucose-lowering properties. Nanoparticles (NPs) were Synthesized through chemical reduction method and confirmed by using SEM, XRD, and FTIR. Characterization revealed that the nanoparticles had an average size of 55 ± 16 nm, exhibited a crystalline structure, and were free of impurities. Antibacterial tests demonstrated enhanced inhibition zones for <em>Pseudomonas</em> spp., <em>S. aureus</em>, and other bacterial strains, with the largest zone of inhibition observed at 12 mg/ml, measuring 18.5 ± 1.05 mm for <em>Pseudomonas</em> spp. In wound healing activity in diabetic mice observations revealed a complete wound closure in NPs treated mice by day 14 as compared to the control group (96.10 % wound closure). Nanoparticle administration (oral) also significantly reduced glucose levels in diabetic mice after 15 days in the experimental period, whereas fasting glucose levels reduced from 398.00 ± 6.16 to 116.67 ± 12.47 mg/dl. The docking studies of copper carbonate nanoparticles (NPs) with proteins involved in wound healing, including Antileukoproteinase (−2.7 kcal/mol), Casein (−2.5 kcal/mol), Collagen (−2.9 kcal/mol), Lysozyme (−2.8 kcal/mol), and Phospholipase (−3.9 kcal/mol), revealed significant binding affinities, suggesting potential applications in enhancing wound healing processes. Therefore, the copper carbonate nanoparticles demonstrate strong antibacterial properties and show promising effects on wound healing, along with blood glucose-lowering activity. These findings suggest their potential in biomedical applications, particularly for treating diabetes and bacterial infections.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"754 ","pages":"Article 151527"},"PeriodicalIF":2.5,"publicationDate":"2025-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143487609","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}

引用次数: 0

The Class II LBD protein MdLBD37 positively regulates the adaptability of apples to drought and salt stress

IF 2.5 3区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochemical and biophysical research communications

Pub Date : 2025-02-22 DOI: 10.1016/j.bbrc.2025.151528

Dan Li, Xiuzheng Chen, Shouqian Feng

Lateral Organ Boundaries Domain (LBD) transcription factors are crucial for plant stress adaptation, yet their functional diversity in perennial crops remains unexplored. In this study, we characterized MdLBD37, a Class II LBD protein in apple (Malus domestica), and identified its key role in enhancing resilience to abiotic stresses. Phylogenetically clustered with anthocyanin repressors AtLBD37/38/39 from Arabidopsis thaliana, MdLBD37 exhibited conserved nuclear localization, supporting its transcriptional regulatory potential. The qRT-PCR analysis revealed that MdLBD37 expression was highest in the stems of ‘Royal Gala’ apple trees. MdLBD37 expression in apple seedlings was significantly induced by ABA, NaCl, and PEG treatments. Moreover, over-expression of MdLBD37 alleviated the growth inhibition of apple calli under PEG, NaCl, and ABA treatments, marked by increased biomass and reduced MDA accumulation, which suggested a reduction in oxidative damage. These findings not only broaden our understanding of Class II LBD proteins but also establish MdLBD37 as a promising target for developing climate-resilient apple cultivars through modulation of ABA-mediated stress signaling pathways.

{"title":"The Class II LBD protein MdLBD37 positively regulates the adaptability of apples to drought and salt stress","authors":"Dan Li, Xiuzheng Chen, Shouqian Feng","doi":"10.1016/j.bbrc.2025.151528","DOIUrl":"10.1016/j.bbrc.2025.151528","url":null,"abstract":"<div><div>Lateral Organ Boundaries Domain (LBD) transcription factors are crucial for plant stress adaptation, yet their functional diversity in perennial crops remains unexplored. In this study, we characterized MdLBD37, a Class II LBD protein in apple (<em>Malus domestica</em>), and identified its key role in enhancing resilience to abiotic stresses. Phylogenetically clustered with anthocyanin repressors <em>AtLBD37/38/39</em> from <em>Arabidopsis thaliana</em>, <em>MdLBD37</em> exhibited conserved nuclear localization, supporting its transcriptional regulatory potential. The qRT-PCR analysis revealed that <em>MdLBD37</em> expression was highest in the stems of ‘Royal Gala’ apple trees. <em>MdLBD37</em> expression in apple seedlings was significantly induced by ABA, NaCl, and PEG treatments. Moreover, over-expression of <em>MdLBD37</em> alleviated the growth inhibition of apple calli under PEG, NaCl, and ABA treatments, marked by increased biomass and reduced MDA accumulation, which suggested a reduction in oxidative damage. These findings not only broaden our understanding of Class II LBD proteins but also establish MdLBD37 as a promising target for developing climate-resilient apple cultivars through modulation of ABA-mediated stress signaling pathways.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"754 ","pages":"Article 151528"},"PeriodicalIF":2.5,"publicationDate":"2025-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143487607","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}

引用次数: 0

The role and mechanism study of Cxcl14 in chronic critically ill cardiac dysfunction

IF 2.5 3区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochemical and biophysical research communications

Pub Date : 2025-02-21 DOI: 10.1016/j.bbrc.2025.151525

Yongke Zheng , Nanyuan Gu , Kai Qiu , Fu Tian , Leifei Chen , Yang Chen , Longhuan Zeng

Objective

To investigate the role and mechanism of Cxcl14 in cardiac function impairment in chronic critical illness (CCI).

Method

Clinical data from CCI patients with heart failure and uncomplicated CCI cases were collected. Serum Cxcl14 concentrations were quantified via ELISA. A CCI heart function injury mouse model (CLP model) was established, and the heart function and morphological indicators was measured. The inflammatory infiltration of myocardial tissue, the Cxcl4 expression levels and myocardial fibrosis related proteins, and the alleviating effect of anti-Cxcl14 antibody on CCI cardiac dysfunction was detected.

Result

The serum level of Cxcl14 was found to exhibit a positive correlation with N-terminal pro-brain natriuretic peptide (NT-proBNP) levels and a negative correlation with left ventricular ejection fraction (LVEF) in patients with CCI. Subsequent investigations into the role of Cxcl14 in CCI-related cardiac dysfunction revealed significant findings. In the CLP model, Cxcl14 was shown to reduce both LVEF and left ventricular intramural shortening fraction (LVFS), while simultaneously increasing the expression of α-smooth muscle actin (α-SMA) and collagen III in myocardial tissue. Additionally, Cxcl14 elevated the levels of ED-1, myeloperoxidase (MPO), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6), promoting inflammatory cell infiltration in the myocardium. Administration of an anti-Cxcl14 antibody mitigated these effects, providing a potential therapeutic intervention.

Conclusion

The expression of Cxcl14 was positively associated with the onset and severity of cardiac dysfunction in CCI patients. In the CLP mouse model, Cxcl14 aggravated myocardial injury and fibrosis, while promoting the infiltration of inflammatory cells into myocardial tissue.

{"title":"The role and mechanism study of Cxcl14 in chronic critically ill cardiac dysfunction","authors":"Yongke Zheng , Nanyuan Gu , Kai Qiu , Fu Tian , Leifei Chen , Yang Chen , Longhuan Zeng","doi":"10.1016/j.bbrc.2025.151525","DOIUrl":"10.1016/j.bbrc.2025.151525","url":null,"abstract":"<div><h3>Objective</h3><div>To investigate the role and mechanism of Cxcl14 in cardiac function impairment in chronic critical illness (CCI).</div></div><div><h3>Method</h3><div>Clinical data from CCI patients with heart failure and uncomplicated CCI cases were collected. Serum Cxcl14 concentrations were quantified via ELISA. A CCI heart function injury mouse model (CLP model) was established, and the heart function and morphological indicators was measured. The inflammatory infiltration of myocardial tissue, the Cxcl4 expression levels and myocardial fibrosis related proteins, and the alleviating effect of anti-Cxcl14 antibody on CCI cardiac dysfunction was detected.</div></div><div><h3>Result</h3><div>The serum level of Cxcl14 was found to exhibit a positive correlation with N-terminal pro-brain natriuretic peptide (NT-proBNP) levels and a negative correlation with left ventricular ejection fraction (LVEF) in patients with CCI. Subsequent investigations into the role of Cxcl14 in CCI-related cardiac dysfunction revealed significant findings. In the CLP model, Cxcl14 was shown to reduce both LVEF and left ventricular intramural shortening fraction (LVFS), while simultaneously increasing the expression of α-smooth muscle actin (α-SMA) and collagen III in myocardial tissue. Additionally, Cxcl14 elevated the levels of ED-1, myeloperoxidase (MPO), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6), promoting inflammatory cell infiltration in the myocardium. Administration of an anti-Cxcl14 antibody mitigated these effects, providing a potential therapeutic intervention.</div></div><div><h3>Conclusion</h3><div>The expression of Cxcl14 was positively associated with the onset and severity of cardiac dysfunction in CCI patients. In the CLP mouse model, Cxcl14 aggravated myocardial injury and fibrosis, while promoting the infiltration of inflammatory cells into myocardial tissue.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"754 ","pages":"Article 151525"},"PeriodicalIF":2.5,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143480454","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}

引用次数: 0

2-Methoxy-4-vinylphenol mitigates malignancy of cholangiocarcinoma cells through the blockade of sonic hedgehog signalling

IF 2.5 3区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochemical and biophysical research communications

Pub Date : 2025-02-21 DOI: 10.1016/j.bbrc.2025.151515

Jungwhoi Lee , Nur Azizah Arryanie Binti Morshidi , Jungsul Lee , Woogwang Sim , Jae-Hoon Kim

Background

Cholangiocarcinoma (CCA) is one of the most refractory malignancies with a grave prognosis. 2-Methoxy-4-vinylpenol (2M4VP) is a well-known flavonoid having beneficial functions in human health including an anti-cancer effect in various malignant tumours. However, the anti-cancer effect of 2M4VP against CCA remains ambiguous.

Purpose

The present study aimed to investigate the bio-activity of 2M4VP in human CCA.

Methods

Biological activities of 2M4VP were examined using in vitro assays. Prognostic values were assessed using Kaplan-Meier and Liptak's z score analyses.

Results

2M4VP significantly attenuated the anti-migratory features of CCA cells when compared to human intrahepatic bile duct epithelial cells (HIBEpiC), but not in viability. The anti-cancer effect of 2M4VP was induced by down-regulating the expression of cellular sonic hedgehog (Shh) signalling molecule such as GLI family zinc finger 3 (GLI3). In addition, 2M4VP treatment evoked a synergic anti-cancer effect when used in combination with gemcitabine. Furthermore, high GLI3 expression was significantly associated with a poor prognosis in patients with CCA.

Conclusions

These results collectively indicate that 2M4VP might be a natural reagent against CCA metastasis, functioning through the ablating Shh signalling associated GLI3 expression, which provides the rationale for further investigation and a potential clinical trial using 2M4VP against CCA.

{"title":"2-Methoxy-4-vinylphenol mitigates malignancy of cholangiocarcinoma cells through the blockade of sonic hedgehog signalling","authors":"Jungwhoi Lee , Nur Azizah Arryanie Binti Morshidi , Jungsul Lee , Woogwang Sim , Jae-Hoon Kim","doi":"10.1016/j.bbrc.2025.151515","DOIUrl":"10.1016/j.bbrc.2025.151515","url":null,"abstract":"<div><h3>Background</h3><div>Cholangiocarcinoma (CCA) is one of the most refractory malignancies with a grave prognosis. 2-Methoxy-4-vinylpenol (2M4VP) is a well-known flavonoid having beneficial functions in human health including an anti-cancer effect in various malignant tumours. However, the anti-cancer effect of 2M4VP against CCA remains ambiguous.</div></div><div><h3>Purpose</h3><div>The present study aimed to investigate the bio-activity of 2M4VP in human CCA.</div></div><div><h3>Methods</h3><div>Biological activities of 2M4VP were examined using in vitro assays. Prognostic values were assessed using Kaplan-Meier and Liptak's z score analyses.</div></div><div><h3>Results</h3><div>2M4VP significantly attenuated the anti-migratory features of CCA cells when compared to human intrahepatic bile duct epithelial cells (HIBEpiC), but not in viability. The anti-cancer effect of 2M4VP was induced by down-regulating the expression of cellular sonic hedgehog (Shh) signalling molecule such as GLI family zinc finger 3 (GLI3). In addition, 2M4VP treatment evoked a synergic anti-cancer effect when used in combination with gemcitabine. Furthermore, high GLI3 expression was significantly associated with a poor prognosis in patients with CCA.</div></div><div><h3>Conclusions</h3><div>These results collectively indicate that 2M4VP might be a natural reagent against CCA metastasis, functioning through the ablating Shh signalling associated GLI3 expression, which provides the rationale for further investigation and a potential clinical trial using 2M4VP against CCA.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"754 ","pages":"Article 151515"},"PeriodicalIF":2.5,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143512709","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}

引用次数: 0

Muscle cells affect the promoting effect of FGF21 on lipid accumulation in porcine adipocytes through AhR/FGFR1 signaling pathway

IF 2.5 3区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochemical and biophysical research communications

Pub Date : 2025-02-21 DOI: 10.1016/j.bbrc.2025.151520

Shengda Qiu, Xiaolei Ding, Xiangfei Ma, Lifan Zhang, Jie Chen, Wei Wei

The intramuscular fat (IMF) content, as an important meat quality trait, can directly affect the tenderness, juiciness, and flavor of pork. Reasonably increasing the IMF content can improve the palatability of pork. Therefore, identification of important factors for the lipid accumulation among muscles is the breakthrough point for improving meat quality. FGF21, identified as a novel metabolic regulator, has been found to regulate glucose and lipid metabolism in 3T3-L1 adipocytes, but its function in porcine adipocytes remains unclear. In this study, we discovered that the administration of recombinant FGF21 protein promotes adipogenic differentiation and increases triglyceride accumulation in porcine adipocytes. While the expression of FGFR1 in adipocytes under muscle conditions is inhibited, affecting the signal transduction of FGF21. This inhibitory effect is accompanied by activation of the AhR signaling pathway. When treated with the AhR antagonist CH223191, there was a partial restoration of FGFR1 expression levels. This indicates that muscle cells suppress the expression of FGFR1 in adipocytes by activating the AhR signaling pathway, thereby affecting the signal transduction of FGF21. Our results reveal the regulatory role of FGF21 in pig adipocyte differentiation and the regulatory mechanism of muscle environment on FGFR1 expression, providing new theoretical basis for IMF content improvement from the perspective of FGF21-FGFR1 signaling transduction.

{"title":"Muscle cells affect the promoting effect of FGF21 on lipid accumulation in porcine adipocytes through AhR/FGFR1 signaling pathway","authors":"Shengda Qiu, Xiaolei Ding, Xiangfei Ma, Lifan Zhang, Jie Chen, Wei Wei","doi":"10.1016/j.bbrc.2025.151520","DOIUrl":"10.1016/j.bbrc.2025.151520","url":null,"abstract":"<div><div>The intramuscular fat (IMF) content, as an important meat quality trait, can directly affect the tenderness, juiciness, and flavor of pork. Reasonably increasing the IMF content can improve the palatability of pork. Therefore, identification of important factors for the lipid accumulation among muscles is the breakthrough point for improving meat quality. FGF21, identified as a novel metabolic regulator, has been found to regulate glucose and lipid metabolism in 3T3-L1 adipocytes, but its function in porcine adipocytes remains unclear. In this study, we discovered that the administration of recombinant FGF21 protein promotes adipogenic differentiation and increases triglyceride accumulation in porcine adipocytes. While the expression of FGFR1 in adipocytes under muscle conditions is inhibited, affecting the signal transduction of FGF21. This inhibitory effect is accompanied by activation of the AhR signaling pathway. When treated with the AhR antagonist CH223191, there was a partial restoration of FGFR1 expression levels. This indicates that muscle cells suppress the expression of FGFR1 in adipocytes by activating the AhR signaling pathway, thereby affecting the signal transduction of FGF21. Our results reveal the regulatory role of FGF21 in pig adipocyte differentiation and the regulatory mechanism of muscle environment on FGFR1 expression, providing new theoretical basis for IMF content improvement from the perspective of FGF21-FGFR1 signaling transduction.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"754 ","pages":"Article 151520"},"PeriodicalIF":2.5,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143487606","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}

引用次数: 0

The role of exosomes in diagnosis, pathophysiology, and management of Alzheimer's Disease

IF 2.5 3区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochemical and biophysical research communications

Pub Date : 2025-02-21 DOI: 10.1016/j.bbrc.2025.151526

Rajni Daksh , Meby Susan Mathew , Aan Mery Bosco , Christy Sojan , Antriya Annie Tom , Sree Lalitha Bojja , Madhavan Nampoothiri

Alzheimer's disease (AD) is a neurodegenerative disorder associated with impaired cognitive function and memory loss. Currently, available therapeutics can effectively alleviate the symptoms of AD, but there is a lack of treatment to halt the progression of the disease. In recent years, exosomes have gained much attention due to their involvement in various neurological disorders. Exosomes are small extracellular vesicles comprising lipids, proteins, DNA, non-coding RNA, and mRNAs, can carry various therapeutic molecules, and are potential drug delivery vehicles. Exosomes are known as a double-edged sword due to their involvement in both the pathogenesis and management of AD. This review explores the function of exosomes in the pathophysiology, treatment, and diagnosis of AD, also emphasizing their potential as a targeted drug delivery carrier to the brain. This review seeks to provide novel perspectives to understand better the onset, targeted treatment, and diagnosis of AD using exosomes.

{"title":"The role of exosomes in diagnosis, pathophysiology, and management of Alzheimer's Disease","authors":"Rajni Daksh , Meby Susan Mathew , Aan Mery Bosco , Christy Sojan , Antriya Annie Tom , Sree Lalitha Bojja , Madhavan Nampoothiri","doi":"10.1016/j.bbrc.2025.151526","DOIUrl":"10.1016/j.bbrc.2025.151526","url":null,"abstract":"<div><div>Alzheimer's disease (AD) is a neurodegenerative disorder associated with impaired cognitive function and memory loss. Currently, available therapeutics can effectively alleviate the symptoms of AD, but there is a lack of treatment to halt the progression of the disease. In recent years, exosomes have gained much attention due to their involvement in various neurological disorders. Exosomes are small extracellular vesicles comprising lipids, proteins, DNA, non-coding RNA, and mRNAs, can carry various therapeutic molecules, and are potential drug delivery vehicles. Exosomes are known as a double-edged sword due to their involvement in both the pathogenesis and management of AD. This review explores the function of exosomes in the pathophysiology, treatment, and diagnosis of AD, also emphasizing their potential as a targeted drug delivery carrier to the brain. This review seeks to provide novel perspectives to understand better the onset, targeted treatment, and diagnosis of AD using exosomes.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"754 ","pages":"Article 151526"},"PeriodicalIF":2.5,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143487610","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}

引用次数: 0

Lectin-like oxidized low-density lipoprotein receptor-1 reduces 5-FU sensitivity in gastric cancer cells via JAK/STAT/NOX4 axis

IF 2.5 3区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochemical and biophysical research communications

Pub Date : 2025-02-20 DOI: 10.1016/j.bbrc.2025.151519

Lanxin Wang, Gaofei He, Kangwei Qi, Long Yu, Di Kong, Jianxin Gu, Lan Wang

5-Fluorouracil (5-FU) is the primary chemotherapeutic agent for the clinical management of advanced gastric cancer (GC). However, the emergence of drug resistance remains an inescapable challenge. In drug-resistant cancer cells, prior treatments contribute to elevated oxidative stress, resulting in higher level of reactive oxygen species (ROS) compared to treatment-naïve cancer cells. Activation of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) has been shown to promote ROS production and facilitate epithelial-mesenchymal transition in GC. In this study, we found that LOX-1 silencing significantly increased 5-FU sensitivity by reducing tumor cell viability and colony-forming ability. Enrichment analysis suggested that nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4) might act as a downstream effector of LOX-1, and overexpression of NOX4 was able to counteract the increased sensitivity to 5-FU induced by LOX-1 depletion. Additionally, bioinformatic predictions and in vitro experiments indicated that LOX-1 regulated NOX4 expression through JAK2/STAT3 signaling pathway. Altogether, this study provides novel evidence that LOX-1 mediated JAK2/STAT3/NOX4 axis plays a crucial role in modulating 5-FU sensitivity of GC and targeting LOX-1 may offer a promising therapeutic strategy to enhance the efficacy of 5-FU in advanced gastric cancer treatment.

{"title":"Lectin-like oxidized low-density lipoprotein receptor-1 reduces 5-FU sensitivity in gastric cancer cells via JAK/STAT/NOX4 axis","authors":"Lanxin Wang, Gaofei He, Kangwei Qi, Long Yu, Di Kong, Jianxin Gu, Lan Wang","doi":"10.1016/j.bbrc.2025.151519","DOIUrl":"10.1016/j.bbrc.2025.151519","url":null,"abstract":"<div><div>5-Fluorouracil (5-FU) is the primary chemotherapeutic agent for the clinical management of advanced gastric cancer (GC). However, the emergence of drug resistance remains an inescapable challenge. In drug-resistant cancer cells, prior treatments contribute to elevated oxidative stress, resulting in higher level of reactive oxygen species (ROS) compared to treatment-naïve cancer cells. Activation of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) has been shown to promote ROS production and facilitate epithelial-mesenchymal transition in GC. In this study, we found that LOX-1 silencing significantly increased 5-FU sensitivity by reducing tumor cell viability and colony-forming ability. Enrichment analysis suggested that nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4) might act as a downstream effector of LOX-1, and overexpression of NOX4 was able to counteract the increased sensitivity to 5-FU induced by LOX-1 depletion. Additionally, bioinformatic predictions and <em>in vitro</em> experiments indicated that LOX-1 regulated NOX4 expression through JAK2/STAT3 signaling pathway. Altogether, this study provides novel evidence that LOX-1 mediated JAK2/STAT3/NOX4 axis plays a crucial role in modulating 5-FU sensitivity of GC and targeting LOX-1 may offer a promising therapeutic strategy to enhance the efficacy of 5-FU in advanced gastric cancer treatment.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"753 ","pages":"Article 151519"},"PeriodicalIF":2.5,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143465248","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}

引用次数: 0

Identification of age-related metabolomic signatures in vascular tissues

IF 2.5 3区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochemical and biophysical research communications

Pub Date : 2025-02-19 DOI: 10.1016/j.bbrc.2025.151513

Ya Zhao , Jingyue Zhang , Jiao Xia , Xiaoyan Han , Shuai Ben , Tianyi Liu , Wan Mu , Mudi Yao , Qin Jiang , Biao Yan

Vascular aging contributes to the morbidity and mortality in older individuals, closely linked to an imbalance between energy consumption and production. Despite its importance, our understanding of how aging affects vascular metabolism and leads to vascular diseases remains limited. In this study, we explored the metabolomic characteristics of vascular aging by analyzing aortic tissues from young and old mice through untargeted metabolomic analysis using ultra-high-performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS). We identified 85 differential metabolites, with 37 up-regulated and 48 down-regulated, primarily consisting of lipids and lipid-like molecules, based on the criteria of variable importance in projection (VIP) > 1 and P < 0.05. Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis revealed significant involvement of these metabolites in six metabolic pathways (P < 0.05), particularly in glycerophospholipid metabolism. Receiver operating characteristic (ROC) curve analysis highlighted eight altered metabolites in glycerophospholipid metabolism, such as phosphatidylcholine (PC) (17:0/22:6) and lysophosphatidylcholine (LPC) (18:2), which demonstrated strong discriminatory ability for vascular aging with an area under the curve (AUC) exceeding 0.85. This study provides novel insights into metabolomic signature of vascular aging, offering important clues for future treatments of age-related vascular disorders.

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引用次数: 0

Comparative analysis of transcriptomic profiles of mesenchymal stem cells at the onset of senescence and after exposure to acute exogenous oxidative stress

IF 2.5 3区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochemical and biophysical research communications

Pub Date : 2025-02-19 DOI: 10.1016/j.bbrc.2025.151506

Zozo Outskouni , Stavroula Prapa , Andreas Goutas , Eleftheria Klagkou , Giannis Vatsellas , Artemis Kosta , Varvara Trachana , Ioanna Papathanasiou

Cellular senescence can be triggered by a wide range of stress-inducing factors, including environmental and internal damaging events, such as oxidative stress. Moreover, stressed and senescent cells exhibit modifications in their transcriptional expression profile, but little is known regarding the common genes and pathways regulating these processes. Here, we analyzed the effects of long-term culture as well as exogenous acute oxidative stress on the transcriptional program of Wharton's jelly mesenchymal stem cells (WJ-MSCs). We demonstrate that, exposure to H₂O₂ compromised genomic stability and mitochondrial function in early passage WJ-MSCs, potentially initiating senescence to prevent cellular transformation. On the other hand, prolonged in vitro expansion of WJ-MSCs activated processes linked to integrins and extracellular matrix organization, possibly indicating the unfavorable consequences that senescence has on tissue integrity. Additionally, cells entering senescence and oxidative stressed young WJ-MSCs over-activated transcription factors related to permanent proliferative arrest and suppressed anti-senescence factors. Common differentially expressed genes in the late passage and H₂O₂-treated WJ-MSCs were implicated in DNA damage response and cell cycle arrest, which are known to trigger a senescent phenotype. Notably, the TP53INP1 gene emerged as a significantly upregulated gene in both late passage and H₂O₂-treated young WJ-MSCs, marking it as a potent senescence indicator. Silencing TP53INP1 mitigated the senescent phenotype, a role that appeared to be facilitated by autophagy regulation. Taken together, our results shed light on how transcriptomic changes govern MSCs' senescence program and identify key molecular drivers that could prove crucial for WJ-MSCs-based clinical applications.

{"title":"Comparative analysis of transcriptomic profiles of mesenchymal stem cells at the onset of senescence and after exposure to acute exogenous oxidative stress","authors":"Zozo Outskouni , Stavroula Prapa , Andreas Goutas , Eleftheria Klagkou , Giannis Vatsellas , Artemis Kosta , Varvara Trachana , Ioanna Papathanasiou","doi":"10.1016/j.bbrc.2025.151506","DOIUrl":"10.1016/j.bbrc.2025.151506","url":null,"abstract":"<div><div>Cellular senescence can be triggered by a wide range of stress-inducing factors, including environmental and internal damaging events, such as oxidative stress. Moreover, stressed and senescent cells exhibit modifications in their transcriptional expression profile, but little is known regarding the common genes and pathways regulating these processes. Here, we analyzed the effects of long-term culture as well as exogenous acute oxidative stress on the transcriptional program of Wharton's jelly mesenchymal stem cells (WJ-MSCs). We demonstrate that, exposure to H<sub>2</sub>O<sub>2</sub> compromised genomic stability and mitochondrial function in early passage WJ-MSCs, potentially initiating senescence to prevent cellular transformation. On the other hand, prolonged <em>in vitro</em> expansion of WJ-MSCs activated processes linked to integrins and extracellular matrix organization, possibly indicating the unfavorable consequences that senescence has on tissue integrity. Additionally, cells entering senescence and oxidative stressed young WJ-MSCs over-activated transcription factors related to permanent proliferative arrest and suppressed anti-senescence factors. Common differentially expressed genes in the late passage and H<sub>2</sub>O<sub>2</sub>-treated WJ-MSCs were implicated in DNA damage response and cell cycle arrest, which are known to trigger a senescent phenotype. Notably, the <em>TP53INP1</em> gene emerged as a significantly upregulated gene in both late passage and H<sub>2</sub>O<sub>2</sub>-treated young WJ-MSCs, marking it as a potent senescence indicator. Silencing <em>TP53INP1</em> mitigated the senescent phenotype, a role that appeared to be facilitated by autophagy regulation. Taken together, our results shed light on how transcriptomic changes govern MSCs' senescence program and identify key molecular drivers that could prove crucial for WJ-MSCs-based clinical applications.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"754 ","pages":"Article 151506"},"PeriodicalIF":2.5,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143474280","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}

引用次数: 0

Visualizing thiazolidine ring formation in the reaction of D-cysteine and pyridoxal-5′-phosphate within L-cysteine desulfurase SufS

IF 2.5 3区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochemical and biophysical research communications

Pub Date : 2025-02-19 DOI: 10.1016/j.bbrc.2025.151497

Ryosuke Nakamura, Takashi Fujishiro

The reactivity of pyridoxal-5′-phosphate (PLP) with cysteine and its derivatives has been of increasing interest because the corresponding product, a thiazolidine PLP-cysteine adduct, can be formed via PLP-dependent enzymatic and non-enzymatic reactions. Here, we report biochemical and X-ray crystallographic snapshots of thiazolidine formation in reaction of D-cysteine with PLP in SufS, a PLP-dependent L-cysteine desulfurase. By comparing L- and D-penicillamine-bound SufS showing no thiazolidine formation in the crystals with D-cysteine SufS, we proposed a thiazolidine formation mechanism with important factors: the polar environments provided by the carbonyl groups of Ala28-Ala29 and Lys224-mediated base catalysis for the nucleophilic thiolate of D-cysteine.

引用次数: 0

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