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

Targeting CD36 With EP 80317 Reduces Remote Inflammatory Response to Hind Limb Ischemia-Reperfusion in Mice 用 EP 80317 靶向 CD36 可降低小鼠后肢缺血再灌注的远端炎症反应

IF 3.2 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2024-11-18 DOI: 10.1002/jbt.70057

Hanan Elimam, Jade Gauvin, David N. Huynh, Liliane Ménard, Marie-Lynn Al-Hawat, Diala Harb, William D. Lubell, André C. Carpentier, Huy Ong, Sylvie Marleau

{"title":"Targeting CD36 With EP 80317 Reduces Remote Inflammatory Response to Hind Limb Ischemia-Reperfusion in Mice","authors":"Hanan Elimam, Jade Gauvin, David N. Huynh, Liliane Ménard, Marie-Lynn Al-Hawat, Diala Harb, William D. Lubell, André C. Carpentier, Huy Ong, Sylvie Marleau","doi":"10.1002/jbt.70057","DOIUrl":"10.1002/jbt.70057","url":null,"abstract":"<p>Reperfusion of ischemic skeletal muscle triggers oxidative stress and an immediate inflammatory reaction, leading to damage of distant organs such as the lungs. The inflammatory process implicates numerous mediators, including cytokines, chemokines, and arachidonic acid metabolites. In the orchestration of the inflammatory cascade, a critical role is played by the cluster of differentiation-36 receptor (CD36), a scavenger receptor class B protein (SR<i>-</i>B2) which is expressed on macrophages and functions as a Toll-like receptor coreceptor. A mouse model of hind limb ischemia-reperfusion has been used to investigate the interplay between CD36 signaling and remote inflammation: leukocyte recruitment, regulation of the nucleotide-binding domain leucin-rich repeat and pyrin-containing receptor 3 (NLRP3) inflammasome, and release of nuclear factor-kappa B (NF-ĸB) and arachidonic acid metabolites. Levels of reactive oxygen species, inflammatory mediators, and gene expression were measured in blood and lung tissue samples collected from anesthetized mice on which unilateral hind limb ischemia was induced by rubber band constriction for 30 min followed by reperfusion for 3 h. The CD36 modulator EP 80317, a member of the growth hormone releasing peptide 6 family, was employed as a pharmacological agent to mitigate distant lung injury following skeletal limb ischemia-reperfusion. Targeting CD36 on monocytes/macrophages, EP 80317 abated pro-inflammatory signaling and transcriptional activity encompassing lipid and cytokine mediators. Targeting CD36 was shown to offer promise for curtailing tissue injury following hind limb ischemia-reperfusion.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 12","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jbt.70057","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142648159","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

In Vitro and Vivo Experiments Revealing Astragalin Inhibited Lung Adenocarcinoma Development via LINC00582/miR-140-3P/PDPK1 体外和体内实验揭示黄芪通过 LINC00582/miR-140-3P/PDPK1 抑制肺腺癌发展

IF 3.2 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2024-11-18 DOI: 10.1002/jbt.70042

Juncheng Bai, Yuxin Chen, Geyu Zhao, Rong Gui

{"title":"In Vitro and Vivo Experiments Revealing Astragalin Inhibited Lung Adenocarcinoma Development via LINC00582/miR-140-3P/PDPK1","authors":"Juncheng Bai, Yuxin Chen, Geyu Zhao, Rong Gui","doi":"10.1002/jbt.70042","DOIUrl":"10.1002/jbt.70042","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 <p>This study aimed to explore the mechanism of the development of lung adenocarcinoma (LUAD) treated by astragalin. Transcriptome sequencing was performed to obtain the gene profile of LUAD treated by astragalin. Combining with bioinformatics analysis including differential gene screening, function enrichment analysis (gene ontology and KEGG), and ceRNA construction, we obtained the novel mechanism of lncRNA mediated miRNA/mRNA axis. Then, the cell experiments were performed to examine the role of lncRNA in cell proliferation, migration and invasion, and apoptosis for LUAD treated with astragalin. Moreover, the tumor formation in nude mice was carried out to detect the ceRNA mechanism in LUAD treated by astragalin in vivo. The lncRNA mediated ceRNA network was obtained, that is, LINC00852 LINC00582/miR-140-3p/PDPK1 played an important role in LUAD treated by astragalin. Function experiments indicated that si-LINC00852 inhibited LUAD cell proliferation, migration and invasion, and promoted cell apoptosis via miR-140-3p/PDPK1 (<i>p</i> < 0.05, <i>p</i> < 0.01). The animal experiments further confirmed that si-LINC00852 inhibited tumor growth through miR-140-3p/PDPK1 in vivo. Conversely, this study provides comprehensive insights into the diagnostic and therapeutic implications of LINC00582 in LUAD, LINC00582 mediated miR-140-3p/PDPK1 axis was the novel drug target of astragalin for treating LUAD.</p>\u0000 </section>\u0000 </div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 12","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142648042","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Identification of the Oncogenic Role of the Circ_0001326/miR-577/VDAC1 Cascade in Prostate Cancer 确定 Circ_0001326/miR-577/VDAC1 级联在前列腺癌中的致癌作用

IF 3.2 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2024-11-18 DOI: 10.1002/jbt.70034

Zhirong Zhu, Guiliang Tang, Mengqi Shi, Mengjie Fang, Xiaolong Zhang, Huali Xu

{"title":"Identification of the Oncogenic Role of the Circ_0001326/miR-577/VDAC1 Cascade in Prostate Cancer","authors":"Zhirong Zhu, Guiliang Tang, Mengqi Shi, Mengjie Fang, Xiaolong Zhang, Huali Xu","doi":"10.1002/jbt.70034","DOIUrl":"10.1002/jbt.70034","url":null,"abstract":"<div>\u0000 \u0000 <p>Prostate cancer (PCa) is one of the leading causes of cancer death among men worldwide. Circular RNAs (circRNAs) have been implicated in the pathogenesis of PCa. However, the precise action of circ_0001326 in PCa malignant progression is still unknown. The levels of circ_0001326, miR-577 and voltage dependent anion channel 1 (VDAC1) were determined by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. Cell proliferation, colony formation, apoptosis, migration and invasion were evaluated by the Cell Counting Kit-8 (CCK-8), EdU staining, colony formation, flow cytometry, wound-healing and transwell assays, respectively. Targeted relationships among circ_0001326, miR-577 and VDAC1 were confirmed by dual-luciferase reporter assays. Xenograft experiments were performed to detect the role of circ_0001326 in tumor growth. Our data revealed that circ_0001326 was overexpressed in PCa tissues and cells. Circ_0001326 depletion repressed PCa cell proliferation, migration, and invasion and enhanced apoptosis in vitro, as well as hampered tumor growth in vivo. Mechanistically, circ_0001326 directly targeted miR-577, and VDAC1 was directly targeted and suppressed by miR-577. Moreover, the effects of circ_0001326 knockdown on PCa cell functional behaviors were mediated by miR-577. VDAC1 silencing phenocopied miR-577 overexpression in regulating PCa cell functional behaviors in vitro. Furthermore, circ_0001326 regulated VDAC1 expression through sponging miR-577. Our findings showed that circ_0001326 regulated PCa cell functional behaviors at least partly through targeting the miR-577/VDAC1 axis.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 12","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142647998","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Targeted therapy: P2X3 receptor silencing in bone cancer pain relief 靶向治疗：抑制 P2X3 受体，缓解骨癌疼痛。

IF 3.2 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2024-11-11 DOI: 10.1002/jbt.70026

Yuge Jiang, Xuan Liu, Hong Zhang, Longhe Xu

{"title":"Targeted therapy: P2X3 receptor silencing in bone cancer pain relief","authors":"Yuge Jiang, Xuan Liu, Hong Zhang, Longhe Xu","doi":"10.1002/jbt.70026","DOIUrl":"10.1002/jbt.70026","url":null,"abstract":"<p>Bone cancer pain remains a significant clinical challenge, often refractory to conventional treatments. The upregulation of the P2X3 receptor in the dorsal root ganglia has been implicated in the pathogenesis of bone cancer pain. This study aimed to elucidate the role of the P2X3 receptor in this context and assess the therapeutic potential of receptor silencing. Utilizing a rat model with Walker 256 cells to simulate bone cancer pain, researchers conducted molecular analyses, including semi-quantitative RT-PCR and Western Blot, to investigate P2X3 receptor expression in the dorsal root ganglia. Results demonstrated a marked increase in P2X3 receptor levels in the dorsal root ganglia of the bone cancer pain model. Targeted silencing of the P2X3 receptor using specific shRNA delivered via lentiviral vectors significantly reduced pain sensitivity, underscoring the receptor's potential as a valuable therapeutic target. In addition, a comprehensive gene expression analysis leveraging the GEO data set GSE249443 was performed to explore the underlying biological pathways linked to bone cancer pain. This analysis provided insights into the intricate interplay between bone cancer pain and associated biological processes, offering a deeper understanding of the mechanisms involved in pain modulation and progression. In conclusion, this research identifies the P2X3 receptor as a critical molecular target for mitigating bone cancer pain. The selective silencing of the P2X3 receptor emerges as a promising and innovative therapeutic strategy, presenting novel avenues for managing bone cancer pain and potentially revolutionizing treatment approaches in this challenging domain.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 11","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142620850","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Synergistic Effect of Salinomycin With Budesonide on TNBC Regression via EMT Reversal and Autophagy Induction 沙林霉素与布地奈德通过EMT逆转和自噬诱导对TNBC消退的协同效应

IF 3.2 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2024-11-11 DOI: 10.1002/jbt.70045

Shilpi Sarkar, Siddhartha Sankar Ghosh

{"title":"Synergistic Effect of Salinomycin With Budesonide on TNBC Regression via EMT Reversal and Autophagy Induction","authors":"Shilpi Sarkar, Siddhartha Sankar Ghosh","doi":"10.1002/jbt.70045","DOIUrl":"10.1002/jbt.70045","url":null,"abstract":"<div>\u0000 \u0000 <p>Triple-negative breast cancer (TNBC) poses a significant clinical challenge due to its aggressive nature, lack of specific therapeutic targets, and drug resistance. Chemotherapy resistance in TNBC is largely driven by the abnormal activation of epithelial-to-mesenchymal transition (EMT) and the associated cancer stem cell-like characteristics. The combination of multiple chemotherapeutic drugs has shown promise as a treatment approach for TNBC. This study evaluates the efficacy of a novel combination therapy involving the anti-inflammatory drug Budesonide and Salinomycin, which targets cancer stem cells. Co-administration of Budesonide and Salinomycin demonstrated a synergistic effect in inhibiting TNBC cell growth by activating the intrinsic apoptosis pathway. It induced a 2- to 3-fold increase in intracellular reactive oxygen species (ROS) generation and a 25%–30% rise in mitochondrial membrane depolarization. Additionally, extensive signaling studies revealed that the co-treatment specifically targeted multiple signaling nodes, limiting downstream crosstalk. The combination also enhanced autophagic activity by inhibiting the AKT/mTOR pathway and reduced cell migration and stemness by suppressing the EMT process. Therefore, the combination of Budesonide and Salinomycin offers a novel therapeutic approach for TNBC.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 11","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142620849","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Lactoperoxidase Inhibition of Celecoxib Derivatives Containing the Pyrazole Linked-Sulfonamide Moiety: Antioxidant Capacity, Antimicrobial Activity, and Molecular Docking Studies 含吡唑连接磺酰胺分子的塞来昔布衍生物的乳过氧化物酶抑制作用：抗氧化能力、抗菌活性和分子对接研究。

IF 3.2 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2024-11-11 DOI: 10.1002/jbt.70055

Songül Bayrak, Serpil Gerni, Cansu Öztürk, Züleyha Almaz, Çetin Bayrak, Namık Kılınç, Hasan Özdemir

{"title":"Lactoperoxidase Inhibition of Celecoxib Derivatives Containing the Pyrazole Linked-Sulfonamide Moiety: Antioxidant Capacity, Antimicrobial Activity, and Molecular Docking Studies","authors":"Songül Bayrak, Serpil Gerni, Cansu Öztürk, Züleyha Almaz, Çetin Bayrak, Namık Kılınç, Hasan Özdemir","doi":"10.1002/jbt.70055","DOIUrl":"10.1002/jbt.70055","url":null,"abstract":"<p>Celecoxib derivatives that contain the pyrazole-linked sulfonamide moiety were synthesized, and the in vitro inhibitory impacts of the aforesaid compounds against the lactoperoxidase (LPO) enzyme were researched. To this end, LPO was purified using the affinity chromatography technique with a yield of 12.63% (319.23-fold). The results showed that the aromatic pyrazole compound (compound <b>1</b>) containing 2,3-dimethoxyphenyl functional groups was the most effective LPO inhibitor with a K<sub>i</sub> value of 3.2 ± 0.7 nM and noncompetitive inhibition type. The second section of the study tested the previously synthesized compounds to reveal their antioxidant and antimicrobial properties. The above-mentioned compound also displayed high activity levels compared to standard antibiotics and antifungals, while all other compounds also showed antibacterial activity. In the three antioxidant methods we used, the compound with 2,5-dimethoxy phenyl groups obtained from the reaction of the aromatic pyrazole compound with propionic anhydride in the presence of NEt<sub>3</sub> displayed the highest activity. Furthermore, molecular docking and molecular mechanics studies were conducted to complement and validate the experimental findings. The results obtained from these computational analyses are highly consistent with the experimental data.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 11","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jbt.70055","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142620936","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Anti-Proliferation Effect of Nodosin on Hepatocellular Carcinoma Cells Via The ERCC6L/PI3K/AKT/Axis Nodosin 通过 ERCC6L/PI3K/AKT/Axis 对肝细胞癌细胞的抗增殖作用

IF 3.2 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2024-11-06 DOI: 10.1002/jbt.70049

Qingling Wang, Qingquan Gong, Chun Zhang, Jianyuan Lin, Dexian Xiao, Dianlian Li, Feng Lin, Dengfang Guo

{"title":"Anti-Proliferation Effect of Nodosin on Hepatocellular Carcinoma Cells Via The ERCC6L/PI3K/AKT/Axis","authors":"Qingling Wang, Qingquan Gong, Chun Zhang, Jianyuan Lin, Dexian Xiao, Dianlian Li, Feng Lin, Dengfang Guo","doi":"10.1002/jbt.70049","DOIUrl":"10.1002/jbt.70049","url":null,"abstract":"<div>\u0000 \u0000 <p>Nodosin, a prominent diterpenoid derived from <i>Rabdosia serra</i> [Maxim] Hara extracts, exhibits notable antitumor activity in various cancers. However, its effect on hepatocellular carcinoma (HCC) and the underlying molecular mechanism remain inadequately understood, which is important for its clinical prescription. This study aims to reveal the mechanism through which nodosin exerts its effects, thereby providing further insights for its application. Nodosin was prepared in concentrations of 0, 0.2, 0.4, 0.6, 0.8, 1.0, and 2.0 μM. The effect of nodosin on the viability of SNU378 and HCCLM3 cells was evaluated using CCK8 and flow cytometry assays. Furthermore, the regulation of PI3K/AKT signaling was assessed by Western blot analysis. The results demonstrated that nodosin significantly suppressed the viability of SNU378 and HCCLM3 cells, yielding IC<sub>50</sub> values of 0.890 and 0.766 μM, respectively. Notably, ERCC6L was downregulated in cells treated with nodosin. Overexpressing ERCC6L was found to reverse the proliferation inhibition and the apoptosis enhancement by nodosin in HCC cells. Additionally, ERCC6L was observed to mitigate the inhibitory effects of nodosin on PI3K/AKT signaling in both SNU378 and HCCLM3 cells. Conversely, the inhibition of PI3K/Akt signaling could counteract the effect of ERCC6L. Thus, the anti-proliferation effects of nodosin on HCC cells are mediated by the ERCC6L/PI3K/AKT axis.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 11","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142583325","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

NK Cell-Based Cancer Immunotherapies: Current Progress, Challenges and Emerging Opportunities 基于 NK 细胞的癌症免疫疗法：当前的进展、挑战和新机遇》。

IF 3.2 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2024-11-06 DOI: 10.1002/jbt.70044

Mohammad Y. Alshahrani, Subasini Uthirapathy, Abhinav Kumar, Enwa Felix Oghenemaro, Roopashree R., Madan Lal, Isha Arora, Ashish Singh Chauhan, Mahmood Jumaa Saud, Hanen Mahmod Hulail

{"title":"NK Cell-Based Cancer Immunotherapies: Current Progress, Challenges and Emerging Opportunities","authors":"Mohammad Y. Alshahrani, Subasini Uthirapathy, Abhinav Kumar, Enwa Felix Oghenemaro, Roopashree R., Madan Lal, Isha Arora, Ashish Singh Chauhan, Mahmood Jumaa Saud, Hanen Mahmod Hulail","doi":"10.1002/jbt.70044","DOIUrl":"10.1002/jbt.70044","url":null,"abstract":"<div>\u0000 \u0000 <p>Natural killer (NK) cells are vital innate immune cells that play a crucial role in cancer therapy. They are targeted by therapies designed to modulate, retain, and enhance their antitumor function in vivo. In addition to whole-cell therapy, NK cell-derived exosomes (NDEs) offer high immune safety and are easily subject to chemical, biological, and immunological modifications. This makes them suitable for use in combination with various current cancer therapies to enhance efficacy, treatment outcomes, and reduce side effects in vivo. This review aims to outline summarizes the antitumor potential of NK cells, as well as the current challenges and opportunities in NK cell-based immunotherapies such as allogeneic and autologous NK cell transplantation, CAR NK cell therapy, and the use of cytokines and monoclonal antibodies. The review also explores the dual regulatory effects of tumor exosomes on NK cells, and highlights the potential of NDEs, either alone or in combination with other antitumor therapies, to reprogram the immunosuppressive tumor microenvironment and expedite the therapeutic effects of cancer immunotherapy in future clinical research.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 11","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142583334","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Transcriptomic Analysis of the Protective Effect of Piperine on Orlistat Hepatotoxicity in Obese Male Wistar Rats 胡椒碱对肥胖雄性 Wistar 大鼠奥利司他肝毒性保护作用的转录组分析

IF 3.2 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2024-11-06 DOI: 10.1002/jbt.70040

Jessica Ledesma-Aparicio, Patrick Mailloux-Salinas, David Julian Arias-Chávez, Elihu Campos-Pérez, Sandra Calixto-Tlacomulco, Armando Cruz-Rangel, Juan Pablo Reyes-Grajeda, Guadalupe Bravo

{"title":"Transcriptomic Analysis of the Protective Effect of Piperine on Orlistat Hepatotoxicity in Obese Male Wistar Rats","authors":"Jessica Ledesma-Aparicio, Patrick Mailloux-Salinas, David Julian Arias-Chávez, Elihu Campos-Pérez, Sandra Calixto-Tlacomulco, Armando Cruz-Rangel, Juan Pablo Reyes-Grajeda, Guadalupe Bravo","doi":"10.1002/jbt.70040","DOIUrl":"10.1002/jbt.70040","url":null,"abstract":"<p>Obesity is a risk factor for the development of noncommunicable diseases that impair the quality of life. Orlistat is one of the most widely used drugs in the management of obesity due to its accessibility and low cost. However, cases of hepatotoxicity have been reported due to the consumption of this drug. On the other hand, piperine is an alkaloid found in black pepper that has demonstrated antiobesity, antihyperlipidemic, antioxidant, prebiotic, and hepatoprotective effects. The aim of this study was to evaluate the protective effect of piperine on the toxicity of orlistat in liver tissue. Obese male rats were administered piperine (30 mg/kg), orlistat (60 mg/kg), and the orlistat-piperine combination (30 mg/kg + 60 mg/kg) daily for 6 weeks. It was observed that the orlistat-piperine treatment resulted in greater weight loss, decreased biochemical markers (lipid profile, liver enzymes, pancreatic lipase activity), and histopathological analysis showed decreased hepatic steatosis and reduction of duodenal inflammation. Transcriptomic analysis revealed that the administration of piperine with orlistat increased the expression of genes related to the beta-oxidation of fatty acids, carbohydrate metabolism, detoxification of xenobiotics, and response to oxidative stress. Therefore, the results suggest that the administration of orlistat-piperine activates signaling pathways that confer a hepatoprotective effect, reducing the toxic impact of this drug.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 11","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jbt.70040","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142583342","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Correction to “WNT1/ROR2 Pathway Enhances the Triple-Negative Breast Cancer Invasion, Migration, and Epithelial-Mesenchymal Transition” 更正 "WNT1/ROR2 通路增强三阴性乳腺癌的侵袭、迁移和上皮-间质转化"。

IF 3.2 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2024-11-06 DOI: 10.1002/jbt.70054

引用次数: 0