Journal of cellular biochemistry最新文献

{"title":"FOXO3 Activates MFN2 Expression to Maintain the Autophagy Response in Cancer Cells Under Amino Acid Deprivation","authors":"Xu Jiang,&nbsp;Jing Wang,&nbsp;Fang Ma,&nbsp;Yuyun Li","doi":"10.1002/jcb.30641","DOIUrl":"10.1002/jcb.30641","url":null,"abstract":"<div>\u0000 \u0000 <p>The lack of amino acids triggers the autophagic response. Some studies have shown such starvation conditions also induce mitochondrial fusion, revealing a close correlation between the two processes. Although Mitofusin-2 (MFN2) has been demonstrated to play a role in fusion regulation, its role in the autophagic response and the variables that activate MFN2 under stress remain unknown. In this investigation, we screened and confirmed that forkhead box protein O3 (FOXO3) participates in <i>MFN2</i>'s expression during short periods of starvation. Luciferase reporter test proved that FOXO3 facilitates <i>MFN2</i>'s transcription by binding to its promoter region, and FOXO3 downregulation directly depresses MFN2's expression. Consequently, inhibiting the FOXO3–MFN2 axis results in the loss of mitochondrial fusion, disrupting the normal morphology of mitochondria, impairing the degradation of substrates, and reducing autophagosome accumulation, ultimately leading to the blockage of the autophagy. In conclusion, our work demonstrates that the FOXO3–MFN2 pathway is essential for adaptive changes in mitochondrial morphology and cellular autophagy response under nutritional constraints.</p></div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142035954","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":"PLM-T3SE: Accurate Prediction of Type III Secretion Effectors Using Protein Language Model Embeddings","authors":"Mengru Gao,&nbsp;Chen Song,&nbsp;Taigang Liu","doi":"10.1002/jcb.30642","DOIUrl":"10.1002/jcb.30642","url":null,"abstract":"<div>\u0000 \u0000 <p>The Type III secretion effectors (T3SEs) are bacterial proteins synthesized by Gram-negative pathogens and delivered into host cells via the Type III secretion system (T3SS). These effectors usually play a pivotal role in the interactions between bacteria and hosts. Hence, the precise identification of T3SEs aids researchers in exploring the pathogenic mechanisms of bacterial infections. Since the diversity and complexity of T3SE sequences often make traditional experimental methods time-consuming, it is imperative to explore more efficient and convenient computational approaches for T3SE prediction. Inspired by the promising potential exhibited by pre-trained language models in protein recognition tasks, we proposed a method called PLM-T3SE that utilizes protein language models (PLMs) for effective recognition of T3SEs. First, we utilized PLM embeddings and evolutionary features from the position-specific scoring matrix (PSSM) profiles to transform protein sequences into fixed-length vectors for model training. Second, we employed the extreme gradient boosting (XGBoost) algorithm to rank these features based on their importance. Finally, a MLP neural network model was used to predict T3SEs based on the selected optimal feature set. Experimental results from the cross-validation and independent test demonstrated that our model exhibited superior performance compared to the existing models. Specifically, our model achieved an accuracy of 98.1%, which is 1.8%–42.4% higher than the state-of-the-art predictors based on the same independent data set test. These findings highlight the superiority of the PLM-T3SE and the remarkable characterization ability of PLM embeddings for T3SE prediction.</p>\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142008836","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":"Conditioned Medium From Reactive Astrocytes Inhibits Proliferation, Resistance, and Migration of p53-Mutant Glioblastoma Spheroid Through GLI-1 Downregulation","authors":"Jessica Honorato Ribeiro,&nbsp;Nícolas Jones Villarinho,&nbsp;Priscila Valverde Fernandes,&nbsp;Tania Cristina Leite de Sampaio e Spohr,&nbsp;Giselle Pinto de Faria Lopes","doi":"10.1002/jcb.30637","DOIUrl":"10.1002/jcb.30637","url":null,"abstract":"<div>\u0000 \u0000 <p>Glioblastoma (GBM) aggressiveness is partly driven by the reactivation of signaling pathways such as Sonic hedgehog (SHH) and the interaction with its microenvironment. SHH pathway activation is one of the phenomena behind the glial transformation in response to tumor growth. The reactivation of the SHH signaling cascade during GBM–astrocyte interaction is highly relevant to understanding the mechanisms used by the tumor to modulate the adjacent stroma. The role of reactive astrocytes considering SHH signaling during GBM progression is investigated using a 3D in vitro model. T98G GBM spheroids displayed significant downregulation of SHH (61.4 ± 9.3%), GLI-1 (6.5 ± 3.7%), Ki-67 (33.7 ± 8.1%), and mutant MTp53 (21.3 ± 10.6%) compared to the CONTROL group when incubated with conditioned medium of reactive astrocytes (CM-AST). The SHH pathway inhibitor, GANT-61, significantly reduced previous markers (SHH = 43.0 ± 12.1%; GLI-1 = 9.5 ± 3.4%; Ki-67 = 31.9 ± 4.6%; MTp53 = 6.5 ± 7.5%) compared to the CONTROL, and a synergistic effect could be observed between GANT-61 and CM-AST. The volume (2.0 ± 0.2 × 10⁷ µm³), cell viability (80.4 ± 3.2%), and migration (41 ± 10%) of GBM spheroids were significantly reduced in the presence of GANT-61 and CM-AST when compared to CM-AST after 72 h (volume = 2.3 ± 0.4 × 10⁷ µm³; viability = 92.2 ± 6.5%; migration = 102.5 ± 14.6%). Results demonstrated that factors released by reactive astrocytes promoted a neuroprotective effect preventing GBM progression using a 3D in vitro model potentiated by SHH pathway inhibition.</p>\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 9","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141988077","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":"Dehydrocostus Lactone Ameliorates LPS-Induced Acute Lung Injury by Inhibiting PFKFB3-Mediated Glycolysis","authors":"Yue Li,&nbsp;Xinrui Wang,&nbsp;Lirong Zhao,&nbsp;Boyu Pan,&nbsp;Xiao Xu,&nbsp;Dongrong Zhu","doi":"10.1002/jcb.30639","DOIUrl":"10.1002/jcb.30639","url":null,"abstract":"<div>\u0000 \u0000 <p>Acute lung injury (ALI) is a destructive respiratory disease characterized by alveolar structural destruction and excessive inflammation responses. Aerobic glycolysis of macrophages plays a crucial role in the pathophysiology of ALI. Previous studies have shown that the expression of the key rate-limiting enzyme 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (PFKFB3) in inflammatory cells is significantly increased, which promotes an increase in the rate of glycolysis in inflammatory cells. However, little is known about the biological functions of PFKFB3 in macrophage inflammation and ALI. In this study, we identified that PFKFB3 is markedly increased in lipopolysaccharide (LPS)-induced ALI mice and macrophages. Knockdown of <i>pfkfb3</i> attenuated LPS-induced glycolytic flux, decreased the release of pro-inflammatory cytokines, and inactivated NF-κB signaling pathway in macrophages. Subsequently, we found that dehydrocostus lactone (DL), a natural sesquiterpene lactone, significantly decreased both the mRNA and protein levels of PFKFB3. Furthermore, it reduced the release of inflammatory cytokines and inactivated NF-κB pathways in vitro. Accordingly, DL alleviated LPS-induced pulmonary edema and reduced the infiltration of inflammatory cells in mouse lung tissue. In summary, our study reveals the vital role of PFKFB3 in LPS-induced inflammation and discovers a novel molecular mechanism underlying DL's protective effects on ALI.</p>\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 10","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141988013","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":"De Novo Rational Design of Peptide-Based Protein–Protein Inhibitors (Pep-PPIs) Approach by Mapping the Interaction Motifs of the PP Interface and Physicochemical Filtration: A Case on p25-Cdk5-Mediated Neurodegenerative Diseases","authors":"Ernest Oduro-Kwateng,&nbsp;Musab Ali,&nbsp;Ibrahim Oluwatobi Kehinde,&nbsp;Zhichao Zhang,&nbsp;Mahmoud E. S. Soliman","doi":"10.1002/jcb.30633","DOIUrl":"10.1002/jcb.30633","url":null,"abstract":"&lt;p&gt;Protein–protein interactions, or PPIs, are a part of every biological activity and have been linked to a number of diseases, including cancer, infectious diseases, and neurological disorders. As such, targeting PPIs is considered a strategic and vital approach in the development of new medications. Nonetheless, the wide and flat contact interface makes it difficult to find small-molecule PP inhibitors. An alternative strategy would be to use the PPI interaction motifs as building blocks for the design of peptide-based inhibitors. Herein, we designed 12-mer peptide inhibitors to target p25-inducing-cyclin-dependent kinase (Cdk5) hyperregulation, a PPI that has been shown to perpetuate neuroinflammation, which is one of the major causal implications of neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease, and frontotemporal dementia. We generated a library of 5 062 500 peptide combination sequences (PCS) derived from the interaction motif of Cdk5/p25 PP interface. The 20 amino acids were differentiated into six groups, namely, hydrophobic (aliphatic), aromatic, basic, acidic, unique, and polar uncharged, on the basis of their physiochemical properties. To preserve the interaction motif necessary for ideal binding, de novo modeling of all possible peptide sequence substitutions was considered. A set of filters, backed by the Support Vector Machine (SVM) algorithm, was then used to create a shortlisted custom peptide library that met specific bioavailability, toxicity, and therapeutic relevance, leading to a refined library of 15 PCS. A greedy algorithm and coarse-grained force field were used to predict peptide structure and folding before subsequent modeling studies. Molecular docking was performed to estimate the relative binding affinities, and out of the top hits, Pep15 was subjected to molecular dynamics simulations and binding free-energy calculations in comparison to a known peptide inhibitor with experimental data (template peptide). Interestingly, the identified peptide through our protocol, Pep15, was found to show a significantly higher binding affinity than the reference template peptide (−48.10 ± 0.23 kcal/mol and −17.53 ± 0.27 kcal/mol, respectively). In comparison to the template peptide, Pep15 was found to possess a more compact and buried surface area, tighter binding landscape, and reduced conformational variability, leading to enhanced structural and kinetic stability of the Cdk5/p25 complex. Notably, both peptide inhibitors were found to have a minimal impact on the architectural integrity of the Cdk5/p25 secondary structure.&lt;/p&gt;&lt;p&gt;Herein, we propose Pep15 as a novel and potentially disruptive peptide drug for Cdk5/p25-mediated neurodegenerative phenotypes that require further clinical investigation. The systematic protocol and findings of this report would serve as a valuable tool in the identification of critical PPI interface reactive residues, designing of analogs, and identification of more potent ","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 9","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.30633","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141988012","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":"Neuregulin 4 Attenuates Podocyte Injury and Proteinuria in Part by Activating AMPK/mTOR-Mediated Autophagy in Mice","authors":"Juntian Deng,&nbsp;Qiansheng Yang,&nbsp;Wanyu Zhu,&nbsp;Yanhua Zhang,&nbsp;Meng Lin,&nbsp;Juyan She,&nbsp;Jing Li,&nbsp;Yuxin Xiao,&nbsp;Jun Xiao,&nbsp;Xinyue Xu,&nbsp;Hebei He,&nbsp;Biao Zhu,&nbsp;Yan Ding","doi":"10.1002/jcb.30634","DOIUrl":"10.1002/jcb.30634","url":null,"abstract":"<div>\u0000 \u0000 <p>In this study, we investigate the effect of neuregulin 4 (NRG4) on podocyte damage in a mouse model of diabetic nephropathy (DN) and we elucidate the underlying molecular mechanisms. In vivo experiments were conducted using a C57BL/6 mouse model of DN to determine the effect of NRG4 on proteinuria and podocyte injury, and in vitro experiments were performed with conditionally immortalized mouse podocytes treated with high glucose and NRG4 to assess the protective effects of NRG4 on podocyte injury. Autophagy-related protein levels and related signaling pathways were evaluated both in vivo and in vitro. The involvement of the adenosine monophosphate-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) pathway was detected using chloroquine or AMPK inhibitors. The results showed that the AMPK/mTOR pathway was involved in the protective roles of NRG4 against high glucose-mediated podocyte injury. Also, NRG4 significantly decreased albuminuria in DN mice. PAS staining indicated that NRG4 mitigated glomerular volume and mesangium expansion in DN mice. Consistently, western blot and RT-PCR analyses confirmed that NRG4 decreased the expression of pro-fibrotic molecules in the glomeruli of DN mice. The immunofluorescence results showed that NRG4 retained expression of podocin and nephrin, whereas transmission electron microscopy revealed that NRG4 alleviated podocyte injury. In DN mice, NRG4 decreased podocyte apoptosis and increased expression of nephrin and podocin, while decreasing the expression of desmin and HIF1α. Overall, NRG4 improved albuminuria, glomerulosclerosis, glomerulomegaly, and hypoxia in DN mice. The in vitro experiments showed that NRG4 inhibited HG-induced podocyte injury and apoptosis. Furthermore, autophagy of the glomeruli decreased in DN mice, but reactivated following NRG4 intervention. NRG4 intervention was found to partially activate autophagy via the AMPK/mTOR signaling pathway. Consequently, when the AMPK/mTOR pathway was suppressed or autophagy was inhibited, the beneficial effects of NRG4 intervention on podocyte injury were diminished. These results indicate that NRG4 intervention attenuates podocyte injury and apoptosis by promoting autophagy in the kidneys of DN mice, in part, by activating the AMPK/mTOR signaling pathway.</p></div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 10","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141874862","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":"RETRACTION: Downregulation of microRNA-23b Protects Against Ischemia-Reperfusion Injury via p53 Signaling Pathway by Upregulating MDM4 in Rats","authors":"","doi":"10.1002/jcb.30622","DOIUrl":"10.1002/jcb.30622","url":null,"abstract":"<p><b>RETRACTION:</b> Z. Zhao, J.-Z. Guan, M. Wu, G.-H. Lai, and Z.-L. Zhu. Downregulation of microRNA-23b Protects Against Ischemia-Reperfusion Injury via p53 Signaling Pathway by Upregulating MDM4 in Rats. <i>Journal of Cellular Biochemistry</i> 120, no. 3 (2019): 4599-4612, https://doi.org/10.1002/jcb.27748.</p><p>The above article, published online on 9 December 2018 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties on the data presented in the article. Several flaws and inconsistencies between results presented and experimental methods described were found. Furthermore, the same sample used to depict the immunofluorescence staining in Figure 5B was found to have been used in a different scientific context in a previous publication from a different author group. Thus, the editors consider the conclusions of this article to be invalid.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 10","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.30622","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141626837","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":"RETRACTION: Methyl Helicterate Inhibits Hepatic Stellate Cell Activation through Downregulating the ERK1/2 Signaling Pathway","authors":"","doi":"10.1002/jcb.30623","DOIUrl":"10.1002/jcb.30623","url":null,"abstract":"<p><b>RETRACTION:</b> Y. Wei, X. Zhang, S. Wen, S. Huang, Q. Huang, S. Lu, F. Bai, J. Nie, J. Wei, Z. Lu, and X. Lin. Methyl Helicterate Inhibits Hepatic Stellate Cell Activation Through Downregulating the ERK1/2 Signaling Pathway. <i>Journal of Cellular Biochemistry</i> 120, no. 9 (2019): 14936-14945, https://doi.org/10.1002/jcb.28756.</p><p>The above article, published online on 22 April 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties on the data presented in the article. Multiple image elements in Figures 2A, 3B, and 4 were found to have been previously published by the same author group in a different scientific context. Furthermore, splicing affecting Figures 5B and 5C has been detected. The authors state that, due to inadequate data management, they were unable to verify whether Figures 2A, 3B, and 4 pertain to this study or to other works, and that Figure 5B and 5C were inappropriately employed. The article is retracted as the editors have lost confidence in the accuracy of the data presented and consider the conclusions of the article to be invalid. The authors agree with the decision to retract the article and would like to extend their sincere apologies for any inconvenience caused.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 10","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.30623","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141626838","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":"Activation of α7 Nicotinic Acetylcholine Receptor Improves Muscle Endurance by Upregulating Orosomucoid Expression and Glycogen Content in Mice","authors":"Fei Chen,&nbsp;Zhen Zhang,&nbsp;Huimin Zhang,&nbsp;Pengyue Guo,&nbsp;Jiayi Feng,&nbsp;Hui Shen,&nbsp;Xia Liu","doi":"10.1002/jcb.30630","DOIUrl":"10.1002/jcb.30630","url":null,"abstract":"<div>\u0000 \u0000 <p>There are presently no acknowledged therapeutic targets or official drugs for the treatment of muscle fatigue. The alpha7 nicotinic acetylcholine receptor (α7nAChR) is expressed in skeletal muscle, with an unknown role in muscle endurance. Here, we try to explore whether α7nAChR could act as a potential therapeutic target for the treatment of muscle fatigue. Results showed that nicotine and PNU-282987 (PNU), as nonspecific and specific agonists of α7nAChR, respectively, could both significantly increase C57BL6/J mice treadmill-running time in a time- and dose-dependent manner. The improvement effect of PNU on running time and ex vivo muscle fatigue index disappeared when α7nAChR deletion. RNA sequencing revealed that the differential mRNAs affected by PNU were enriched in glycolysis/gluconeogenesis signaling pathways. Further studies found that PNU treatment significantly elevates glycogen content and ATP level in the muscle tissues of α7nAChR^+/+ mice but not α7nAChR^-/- mice. α7nAChR activation specifically increased endogenous glycogen-targeting protein orosomucoid (ORM) expression both in vivo skeletal muscle tissues and in vitro C2C12 skeletal muscle cells. In ORM1 deficient mice, the positive effects of PNU on running time, glycogen and ATP content, as well as muscle fatigue index, were abolished. Therefore, the activation of α7nAChR could enhance muscle endurance via elevating endogenous anti-fatigue protein ORM and might act as a promising therapeutic strategy for the treatment of muscle fatigue.</p></div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 9","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141626835","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":"Effect of Oridonin on Experimental Animal Model of Bronchopulmonary Dysplasia","authors":"Shanshan Zhang,&nbsp;Junfu Wang,&nbsp;Zhihong Xin,&nbsp;Chao Sun,&nbsp;Zhiye Ju,&nbsp;Xia Xue,&nbsp;Wen Jiang,&nbsp;Qian Xin,&nbsp;Jue Wang,&nbsp;Zhaohua Zhang,&nbsp;Yun Luan","doi":"10.1002/jcb.30632","DOIUrl":"10.1002/jcb.30632","url":null,"abstract":"<div>\u0000 \u0000 <p>Bronchopulmonary dysplasia (BPD) is a serious disease that occurs in premature and low-birth-weight infants. In recent years, the incidence of BPD has not decreased, and there is no effective treatment for it. Oridonin (Ori) is a traditional Chinese medicine with a wide range of biological activities, especially pharmacological and anti-inflammatory. It is well known that inflammation plays a key role in BPD. However, the therapeutic effect of Ori on BPD has not been studied. Therefore, in the present study, we will observe the anti-inflammatory activity of Ori in an experimental animal model of BPD. Here, we showed that Ori could significantly decrease hyperoxia-induced alveolar injury, inhibit neutrophil recruitment, myeloperoxidase concentrations, and release inflammatory factors in BPD neonatal rats. Taken together, the experimental results suggested that Ori can significantly improve BPD in neonatal rats by inhibiting inflammatory response.</p></div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 9","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141626836","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}