Biochemical and biophysical research communications最新文献

{"title":"Rutin isolated from Acalypha indica L.: A comprehensive analysis of its antibacterial and anticancer activities","authors":"Sudhakar Chekuri ,&nbsp;Sanjeeva Reddy Sirigiripeta ,&nbsp;Sreenu Thupakula ,&nbsp;Satyanarayana Swamy Vyshnava ,&nbsp;Sultana Ayesha ,&nbsp;Sai Bindu Karamthote Cheniya ,&nbsp;Raghu Kuruva ,&nbsp;Roja Rani Anupalli","doi":"10.1016/j.bbrc.2025.151833","DOIUrl":"10.1016/j.bbrc.2025.151833","url":null,"abstract":"<div><h3>Background</h3><div>Antibiotic resistance and cancer demand alternative therapeutic strategies. Rutin, a polyphenol from <em>Acalypha indica</em> L., exhibits notable antioxidant, antibacterial, and anticancer properties. This study isolates and evaluates rutin for its bioactivity.</div></div><div><h3>Methods</h3><div>Rutin was extracted using Soxhlet extraction, purified via column chromatography and HPLC, and characterized by HR-MS and NMR. Antibacterial activity was assessed by disc diffusion against <em>Staphylococcus aureus</em>, <em>Escherichia coli</em>, <em>Klebsiella pneumoniae</em>, and <em>Pseudomonas aeruginosa</em>. Cytotoxicity was tested on MCF-7 and MDA-MB-231 breast cancer cells. Molecular docking evaluated binding to human protein disulfide isomerase (PDI).</div></div><div><h3>Results</h3><div>Rutin showed antibacterial activity with inhibition zones of 5.0–9.2 mm, strongest against <em>S. aureus</em>. It exhibited dose- and time-dependent cytotoxicity with IC₅₀ values of 22.31 ± 1.28 μg/mL (MCF-7) and 20.43 ± 0.81 μg/mL (MDA-MB-231) at 24 h. Docking analysis revealed strong affinity to human PDI (−5.84 kcal/mol, Ki = 52.19 μM).</div></div><div><h3>Conclusions</h3><div>Rutin from <em>Acalypha indica</em> L. demonstrates significant antibacterial and anticancer activity, with strong PDI interaction, supporting its potential as a natural therapeutic agent.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"765 ","pages":"Article 151833"},"PeriodicalIF":2.5,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143860047","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":"Integrated synchrotron radiation-based fourier transform infrared (SR-FTIR) microscopy and tandem-mass spectrometry (LC-MS/MS) used to elucidate the apoptotic effect of chamuangone in A549 cells","authors":"Panatda Wanaragthai ,&nbsp;Yodying Yingchutrakul ,&nbsp;Pharkphoom Panichayupakaranant ,&nbsp;Jitraporn Vongsvivut ,&nbsp;Chanat Aonbangkhen ,&nbsp;Meng Chieh Yang ,&nbsp;Arnatchai Maiuthed ,&nbsp;Pithi Chanvorachote ,&nbsp;Bayden R. Wood ,&nbsp;Kiattawee Choowongkomon ,&nbsp;Sucheewin Krobthong","doi":"10.1016/j.bbrc.2025.151826","DOIUrl":"10.1016/j.bbrc.2025.151826","url":null,"abstract":"<div><div>Chamuangone, a natural compound extracted from <em>Garcinia cowa</em> leaves, has demonstrated potential in cancer therapeutics, but its effects on lung cancer cells remain unclear. This study investigates the apoptotic effects of Chamuangone on human lung adenocarcinoma cells (A549). The A549 cells were treated with Chamuangone, and the cytotoxic effects were evaluated using an MTT assay, revealing a dose-dependent inhibition of cell proliferation with an IC₅₀ value of 19.43 μM. Annexin V assays further confirmed that Chamuangone induces apoptosis in A549 cells, showing increased levels of late apoptosis with higher concentrations. Synchrotron radiation-based Fourier transform infrared (SR-FTIR) microscopy provided insights into macromolecular changes, highlighting significant alterations in proteins, lipids, and nucleic acids. These structural changes in key cellular macromolecules were supported by proteomic analysis, which identified the upregulation of apoptosis-related proteins, including Peroxiredoxin-2 and Na⁺/H⁺ exchange regulatory cofactor NHE-RF1. Canonical pathway analysis indicated that Chamuangone affects oxidative phosphorylation and mitochondrial dysfunction, both crucial pathways for apoptosis. Additionally, upstream regulator analysis demonstrated significant inhibition of the epidermal growth factor receptor (EGFR), a key player in lung cancer progression. These findings suggest that Chamuangone triggers apoptosis through mitochondrial pathways and EGFR inhibition, positioning it as a promising therapeutic candidate for lung cancer treatment.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"764 ","pages":"Article 151826"},"PeriodicalIF":2.5,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143842798","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":"The stress-associated small heat shock protein affects stem cell proliferation, differentiation, and tissue-specific transcriptional networks during regeneration in Dugesia japonica","authors":"Bingrui Sun,&nbsp;Ying Zhang,&nbsp;Ping Yu,&nbsp;Liping Dong,&nbsp;Jinlei Wang,&nbsp;Nianhong Xing,&nbsp;Jicheng Qu,&nbsp;Lili Gao,&nbsp;Dongwu Liu,&nbsp;Shujing Zhang,&nbsp;Changjian Xie,&nbsp;Weiwei Wu,&nbsp;Qiuxiang Pang,&nbsp;Ao Li","doi":"10.1016/j.bbrc.2025.151824","DOIUrl":"10.1016/j.bbrc.2025.151824","url":null,"abstract":"<div><div>Small heat shock proteins (sHSPs) represent a highly conserved family of molecular chaperones primarily known for their roles in protein homeostasis and stress responses. However, their involvement in regulating stem cell dynamics and tissue regeneration remains insufficiently characterized, particularly in planarians, a model organism renowned for its extraordinary regenerative capacity. In planarians, regeneration is driven by pluripotent stem cells, referred to as neoblasts, which are the only proliferative cells responsible for tissue repair and homeostasis. In this study, we identified a novel sHSP, DjsHSP, in <em>Dugesia japonica</em> and investigated its functional role in regeneration. Using RNA interference (RNAi), we demonstrated that <em>DjsHSP</em> knockdown significantly delayed regeneration of the blastema, intestine, eyes, and neural tissue. Mechanistically, <em>DjsHSP</em> knockdown disrupted neoblasts dynamics, leading to abnormal proliferation and impaired differentiation. This was associated with altered expression of lineage-specific transcription factors critical for triploblastic tissue differentiation. Furthermore, the knockdown of <em>DjsHSP</em> downregulated key transcription factors regulating organ-specific regeneration, contributing to defective tissue regeneration. These findings suggest that DjsHSP affects stem cell fate and organ regeneration by maintaining the balance between stem cell proliferation and differentiation and modulating tissue-specific transcriptional networks. Our study provides new insights into the molecular mechanisms underlying planarian regeneration, with potential implications for advancing regenerative medicine.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"764 ","pages":"Article 151824"},"PeriodicalIF":2.5,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143847611","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":"TRIB3 recruits and stabilizes CARM1 to confer chemoresistance by activating Akt signalling in clear cell renal cancer cells","authors":"Danfei Hu ,&nbsp;Xiaodong Fan ,&nbsp;Xiaodong Chen ,&nbsp;Mingyao Li ,&nbsp;Huacai Xiong ,&nbsp;Xiaoxiao Fan ,&nbsp;Feng Chen","doi":"10.1016/j.bbrc.2025.151827","DOIUrl":"10.1016/j.bbrc.2025.151827","url":null,"abstract":"<div><div>Sunitinib resistance remains a major obstacle in the treatment of clear cell renal cell carcinoma (ccRCC), yet the underlying mechanisms are poorly defined. Here, we identify a previously unrecognized axis involving Tribbles homolog 3 (TRIB3) and coactivator-associated arginine methyltransferase 1 (CARM1) that drives chemoresistance through modulation of Akt signaling. Mechanistically, TRIB3 directly interacts with CARM1, a pro-survival epigenetic regulator, and inhibits its ubiquitination to stabilize CARM1 protein levels. Elevated CARM1 further exacerbates therapeutic resistance, establishing a feedforward loop that sustains Akt activation. Our findings uncovering a novel TRIB3-CARM1-Akt axis as a central driver of sunitinib resistance. This study provides mechanistic insights into ccRCC chemoresistance and highlights therapeutic targeting of the TRIB3-CARM1 axis as a promising strategy to overcome treatment failure.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"766 ","pages":"Article 151827"},"PeriodicalIF":2.5,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143868608","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":"SARS-CoV-2 NSP2 specifically interacts with cellular protein SmgGDS","authors":"Xiaoyu Chu ,&nbsp;Yixuan Yang ,&nbsp;Hangtian Guo ,&nbsp;Xiaoyun Ji","doi":"10.1016/j.bbrc.2025.151828","DOIUrl":"10.1016/j.bbrc.2025.151828","url":null,"abstract":"<div><div>The novel coronavirus, SARS-CoV-2, is responsible for the ongoing global pandemic of Coronavirus disease 2019 (COVID-19). SARS-CoV-2 belongs to the <em>Coronaviridae</em> family, which also includes the Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV) and the Middle East Respiratory Syndrome Coronavirus (MERS-CoV). Recent studies using affinity purification mass spectrometry analysis have revealed that SARS-CoV-2 NSP2 may interact with cellular protein Small G-protein dissociation stimulator (SmgGDS), a guanine nucleotide exchange factor (GEF) that specifically regulates RhoA and RhoC proteins, which are involved in a range of cellular activities, including actin reorganization, cell motility and adhesion. Biochemical experiments have confirmed that NSP2 binds directly to SmgGDS and that this interaction requires the full-length NSP2. Given the low sequence conservation compared to other coronaviruses, this interaction with SmgGDS appears specific to SARS-CoV-2, with similar proteins in other coronaviruses unable to bind SmgGDS. Further studies have revealed that the binding of SARS-CoV-2 NSP2 to SmgGDS has a significant inhibitory effect on the GEF activity of SmgGDS. This inhibition disrupts the nucleotide exchange process on RhoA, impairing its function and potentially contributing to the pathogenic mechanisms of SARS-CoV-2. These findings highlight a novel pathway through which SARS-CoV-2 may influence host cellular processes, providing insights into the unique impact of coronaviruses on cellular regulation.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"764 ","pages":"Article 151828"},"PeriodicalIF":2.5,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143847608","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":"Crystal structure and biochemical characterization of aldehyde dehydrogenase isolated from Rhodococcus sp. PAMC28705","authors":"Gobinda Thapa ,&nbsp;Subin Kim ,&nbsp;Hyun Ho Park ,&nbsp;Tae-Jin Oh","doi":"10.1016/j.bbrc.2025.151832","DOIUrl":"10.1016/j.bbrc.2025.151832","url":null,"abstract":"<div><div>Aldehyde dehydrogenase (ALDH) is a widely recognized oxidoreductase that converts toxic aldehydes into harmless carboxylic acids, making it highly valuable for industrial applications. However, the effectiveness of ALDHs derived from <em>Rhodococcus</em> species in processing a range of aliphatic and aromatic aldehydes is still largely unexamined. Therefore, we cloned the ALDH gene from the cold-adapted strain <em>Rhodococcus</em> sp. PAMC28705 to address this gap and subsequently identified the crystal structure of rhALDH. By analyzing the unique structural features of the rhALDH active site, we evaluated its ability to process a wide range of aldehydes, with a focus on substrate specificity. Biochemical characterization revealed that at an optimal temperature of 30 °C and a pH of 8.0, it exhibited the highest catalytic efficiency, with a <em>k</em>_cat/<em>K</em>_m value of 1.12 μM⁻¹ s⁻¹ for propionaldehyde, which was higher than that of its homologous ALDHs. This indicates a strong affinity for this substrate, as demonstrated by a low <em>K</em>_m of 321.9 μM and a rapid turnover rate <em>k</em>_cat of 359.2 s⁻¹. Adding disulfide reductants, such as dithiothreitol, 2-mercaptoethanol, and the metal ion Mg²⁺, further enhanced its activity. Working at mesophilic temperatures with good stability and substrate-specific catalytic efficiency, this novel rhALDH, which favors the conversion of propionaldehyde and benzaldehyde, provides a promising catalyst for biotechnological and sustainable bio-aldehyde elimination technologies. Thus, this study lays a foundation for future structure-function analyses of rhALDH, facilitating molecular modifications, the generation of mutants for improved stability, and the development of ALDH-targeted antibiotics.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"764 ","pages":"Article 151832"},"PeriodicalIF":2.5,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143838695","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":"Exploring the impact of Gastrodin on brain aging in mice: Unraveling mechanisms through network pharmacology","authors":"Jiecai Li ,&nbsp;Rui Yuan ,&nbsp;Sheng'an Zheng,&nbsp;Ying Wang,&nbsp;Julian Miao","doi":"10.1016/j.bbrc.2025.151814","DOIUrl":"10.1016/j.bbrc.2025.151814","url":null,"abstract":"<div><h3>Background</h3><div>With the intensification of global aging, slowing down the aging process has become a topic of significant interest. Brain aging, as one of the prominent changes in the aging process, urgently requires the exploration of new therapeutic methods to delay its progression. Gastrodia, a traditional Chinese medicine, has been widely recognized for its medicinal value, particularly in its pronounced neuroprotective effects. Although previous studies have demonstrated the protective effects of Gastrodin (GAS), an active compound in Gastrodia, on the mouse nervous system, its underlying mechanisms remain unclear.</div></div><div><h3>Objective</h3><div>This study aims to investigate comprehensively the impact and mechanisms of GAS in delaying brain aging through the combined approach of network pharmacology and animal experiments, providing a theoretical basis for the clinical application of GAS in treating age-related decline.</div></div><div><h3>Methods</h3><div>A D-galactose (D-gal)-induced aging mouse model was employed, and the anti-aging effects of GAS were evaluated through behavioral experiments and morphological observations. A “compound-target-pathway” network was constructed using network pharmacology. Gene and protein expression related to potential targets and pathways were verified and analyzed using RT-qPCR and immunohistochemistry (IHC) methods.</div></div><div><h3>Results</h3><div>GAS exposure significantly alleviated signs of brain aging in mice, including reduced body weight index, improved behavioral memory, mitigation of hippocampal morphological damage due to aging, and relief of oxidative stress levels in the mouse brain. Target screening through network pharmacology identified four key targets related to the AMPK/mTOR pathway and autophagy: AMPK, ULK1, ATG5, and Beclin1. Validation of the network pharmacology results using RT-qPCR and IHC confirmed that GAS upregulates cellular autophagy levels through the AMPK/mTOR/ULK1 signaling pathway.</div></div><div><h3>Conclusion</h3><div>GAS demonstrates a pronounced alleviating effect on age-related symptoms in D-galactose-induced brain aging mice by suppressing oxidative stress in the mouse brain. The mechanism involves the upregulation of cellular autophagy through the AMPK/mTOR/ULK1 signaling pathway.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"764 ","pages":"Article 151814"},"PeriodicalIF":2.5,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143838696","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":"Integrated transcriptomic and proteomic profiling reveals the anti-inflammatory mechanism of dihydroartemisinin in the treatment of acute liver injury by targeting CYBA and CYBB","authors":"Honglian Li ,&nbsp;Jiayun Chen ,&nbsp;Huiyi Guo ,&nbsp;Hao Yang ,&nbsp;Jing Liu ,&nbsp;Haoxing Yuan ,&nbsp;Junzhe Zhang ,&nbsp;Jigang Wang ,&nbsp;Shuwen Liu","doi":"10.1016/j.bbrc.2025.151821","DOIUrl":"10.1016/j.bbrc.2025.151821","url":null,"abstract":"<div><div>Acute liver injury (ALI) is a prevalent inflammatory disease with no currently available effective targeted therapies that characterized by high mortality and morbidity. Dihydroartemisinin (DHA), a derivative of the renowned antimalarial compound artemisinin, has garnered attention for its anti-inflammatory property. However, the precise anti-inflammatory mechanisms underlying its efficacy in treating ALI remain unclear. Notably, the excessive inflammatory cytokines secreted by macrophages represents a critical factor of liver damage. In our comprehensive study, transcriptome and proteomic analysis of M1 macrophages after DHA treatment was performed to unearth the potential anti-inflammatory targets for ALI treatment. Transcriptomics analysis indicated that DHA significantly mitigated inflammation, primarily by downregulating the expressions of CCL1, CCL2, CCL7, CCL13, and CXCL13. Concurrently, proteomics analysis identified six proteins, such as CYBA and CYBB, that were consistently downregulated in the DHA intervention groups compared to the M1 group. Intriguingly, a protein-protein interaction network analysis highlighted the close association of CYBA and CYBB with the aforementioned chemokine genes. Through meticulous screening, DHA curtailed the production of reactive oxygen species (ROS) by targeting CYBA and CYBB, subsequently suppressing the secretion of several chemokines and dampening the inflammatory response in M1 macrophages. More importantly, DHA not only reduced ROS and chemokine levels but also restored liver function by downregulating CYBA and CYBB to inhibit NF-κB pathway in ALI mice, demonstrating strong anti-inflammatory effects. In conclusion, our findings throw novel light into the underlying anti-inflammatory mechanism of DHA in ALI management, offering valuable insights for future clinical research and therapeutic strategies for inflammatory diseases.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"764 ","pages":"Article 151821"},"PeriodicalIF":2.5,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143838697","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":"Monocatechol metabolites of sesamin and episesamin promote higher autophagy flux compared to their unmetabolized forms by mTORC1-selective inhibition","authors":"Jiro Takano ,&nbsp;Daisuke Takemoto ,&nbsp;Hisashi Tatebe ,&nbsp;Shisako Shoji ,&nbsp;Kanako Fukuda ,&nbsp;Yoshinori Kitagawa ,&nbsp;Tomohiro Rogi ,&nbsp;Takayuki Izumo ,&nbsp;Yoshihiro Nakao ,&nbsp;Miwako Ishido ,&nbsp;Tamotsu Yoshimori","doi":"10.1016/j.bbrc.2025.151816","DOIUrl":"10.1016/j.bbrc.2025.151816","url":null,"abstract":"<div><div>Sesamin and episesamin, the major lignans found in refined sesame oil, reportedly exert antioxidant, anti-inflammatory, and hypocholesterolemic effects. Sesamin has also been suggested by previous studies to promote autophagy; however, concerns have been raised regarding the use of non-physiological concentrations, inaccurate methods for evaluating autophagic activity, and incomplete understanding of underlying mechanisms. Additionally, the effects of its metabolic kinetics on autophagy remain unclear. In this study, we demonstrated that sesamin, episesamin, and their metabolites induced autophagy flux at physiological concentrations in human cell cultures expressing monomeric red fluorescent protein-green fluorescent protein tandem fluorescent-tagged microtubule-associated protein 1A/1B-light-chain 3 proteins, a robust method for monitoring autophagy flux. Notably, the monocatechol metabolites of sesamin and episesamin exhibited higher autophagy flux than their unmetabolized forms. Immunoblotting analysis revealed that sesamin and its monocatechol metabolite promoted autophagy by inhibiting mammalian target of rapamycin complex 1 (mTORC1), leading to decreased phosphorylation of unc-51 like autophagy activating kinase 1 and transcription factor EB. This suppression enhanced the isolation membrane formation and transcriptionally stimulated autophagy and lysosomal biogenesis. Importantly, mTORC1 inhibition by sesamin and its metabolites did not affect mTORC2 activity, mirroring the mTORC1-selective inhibition observed with rapamycin. These results suggest that sesamin and episesamin contribute to diverse biological activities via their metabolism in the human body, regulating autophagy and mTORC1 signaling pathways.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"765 ","pages":"Article 151816"},"PeriodicalIF":2.5,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143864411","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":"Molecular mechanism of rapamycin-induced autophagy activation to attenuate smoking-induced COPD","authors":"Li Wang ,&nbsp;Jianhu Jia ,&nbsp;Xinyan Yu ,&nbsp;Mengmeng Luo ,&nbsp;Jie Li ,&nbsp;Ghulam Jilany Khan ,&nbsp;Chenghui He ,&nbsp;Hong Duan ,&nbsp;Kefeng Zhai","doi":"10.1016/j.bbrc.2025.151819","DOIUrl":"10.1016/j.bbrc.2025.151819","url":null,"abstract":"<div><div>Chronic obstructive pulmonary disease (COPD) is one of the severe lung and respiratory airway disorders, with high prevalence rate in China. In this paper, we employed network pharmacology predictions to identify autophagy as a signaling pathway associated with COPD. To explore the protective effect of autophagy against COPD and its specific mechanism, we established a mouse model of COPD and administered 3-methyladenine (3-MA) and rapamycin (RAPA) to intervene in autophagy. The lung function of the mice was assessed using an animal pulmonary function analysis system, and lung tissue structure was evaluated through hematoxylin and eosin (HE) staining. The TUNEL staining method was employed to determine the level of apoptosis in lung tissue. Western blot analysis was conducted to measure the expression of autophagy and apoptosis-related proteins, while RT-qPCR was used to assess the expression of apoptosis-related mRNA. The results showed that RAPA effectively improved lung function, attenuated pathological lung injury and increased autophagy level in COPD mice. Apoptosis analysis showed that the apoptosis rate was elevated in COPD and 3- MA mice, whereas it was significantly reduced in RAPA mice. Our findings suggest that stimulation of autophagy may be a potential therapy for the future treatment of COPD.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"764 ","pages":"Article 151819"},"PeriodicalIF":2.5,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143847609","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}