Journal of Biochemical and Molecular Toxicology最新文献

{"title":"The Protective Effects of Chrysin on Acrylamide-Induced Hepatotoxicity: Insights Into Oxidative Stress, Inflammation, Apoptosis, Autophagy, and Histological Evaluation in Rats","authors":"Selman Gencer,&nbsp;Nurhan Akaras,&nbsp;Hasan Şimşek,&nbsp;Cihan Gür,&nbsp;Mustafa İleritürk,&nbsp;Sefa Küçükler,&nbsp;Fatih Mehmet Kandemir","doi":"10.1002/jbt.70334","DOIUrl":"https://doi.org/10.1002/jbt.70334","url":null,"abstract":"<p>Acrylamide (ACR) is a toxic chemical with a high carcinogenic risk that is released as a result of heating or processing foods at high temperatures. Chrysin (CHR) is a flavonoid that is naturally found in foods such as honey and passionflower and stands out with its antioxidant, anticancer, and anti-inflammatory properties. This study aims to determine the protective effects of CHR in ACR-induced hepatotoxicity. ACR was administered orally at a dose of 38.27 mg/kg; CHR (25 or 50 mg/kg) was administered orally for ten days. Biochemical and molecular methods were used to investigate oxidative stress, inflammation, and apoptotic markers in liver tissue. Additionally, histological methods were used to determine the liver tissue's structural and functional characteristics and autophagy. CHR treatment alleviated ACR-induced oxidative stress by increasing antioxidants (SOD, CAT, GPx, GSH) and reducing increased oxidant MDA. CHR reduced inflammatory activity by inactivating NF-κB and pro-inflammatory cytokines. ACR-induced increases in apoptotic Casp-3, Casp-6, Casp-9, and Bax were reduced by CHR, while the decreased level of antiapoptotic Bcl-2 was increased. It was also determined immunohistochemically that CHR inhibited autophagic Beclin-1 activity. CHR was effective in reducing ACR-induced hepatotoxicity damage and may be an effective treatment option.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 6","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jbt.70334","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144244322","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}

{"title":"PTPRC Knockdown Inhibits Inflammation in Gouty Arthritis by Blocking the JAK2/STAT3 Signaling Pathway","authors":"Hong Mo,&nbsp;Fengxia Li,&nbsp;Zhongying Zheng,&nbsp;Zongbo Ma,&nbsp;Shuyue Liu,&nbsp;Lian Wen,&nbsp;Xubo Su","doi":"10.1002/jbt.70340","DOIUrl":"https://doi.org/10.1002/jbt.70340","url":null,"abstract":"<div>\u0000 \u0000 <p>Gouty arthritis (GA) is a prevalent inflammatory arthropathy triggered by the deposition of monosodium uric acid (MSU) crystals. However, the molecular mechanism underlying GA pathogenesis is still unclear. GA-related differentially expressed genes (DEGs) were identified from the GSE242872 and GSE190138 datasets. A rat model of GA was established by injecting MSU crystals. The lipopolysaccharide (LPS) and MSU-stimulated THP-1 cells were used for In Vitro studies. The severity of GA was assessed by joint swelling, dysfunction, and hematoxylin and eosin staining. Inflammatory cytokine levels were detected by enzyme-linked immunosorbent assay. The downstream target of protein tyrosine phosphatase receptor type C (PTPRC) was explored by bioinformatics analysis and western blot. Four key genes, including IL 6, PTPRC, CXCL1, and CCR7, were overexpressed in GA. PTPRC knockdown attenuated GA, accompanied by reduced joint swelling, dysfunction index, and inflammatory cell infiltration in GA rats. The levels of pro-inflammatory cytokines were lowered after PTPRC knockdown. Bioinformatics analysis demonstrated a significant relationship between PTPRC and the Janus Kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathways and PTPRC knockdown reduced the phosphorylation levels of the JAK2 and STAT3 in vivo and In Vitro. Treatment with CA1, an activator of the JAK2/STAT3 pathway, significantly counteracted the effects of PTPRC knockdown on GA. PTPRC knockdown attenuates inflammation in GA by suppressing the JAK2/STAT3 pathway, which provides a new insight into the treatment of GA.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 6","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144244854","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}

{"title":"Antagonism of 5-HT7 Receptors as a Promising Target for Gastric Cancer via Apoptotic Pathway","authors":"Irfan Cinar,&nbsp;Busra Dincer,&nbsp;Elif Cadirci,&nbsp;Salih Kara,&nbsp;Mehmet Ilhan Yildirgan,&nbsp;Zekai Halici,&nbsp;Saziye Sezin Palabiyik-Yucelik","doi":"10.1002/jbt.70326","DOIUrl":"https://doi.org/10.1002/jbt.70326","url":null,"abstract":"<p>Although current treatment strategies have improved clinical outcomes for gastric cancer, they present a challenging prognosis that necessitates novel therapeutic approaches. The 5-HT7 receptor, a member of the serotonin receptor family, plays a significant role in influencing the pathogenesis of various cancer types. This study seeks to investigate the complex interactions among 5-HT7 receptors, gastric cancer, and apoptotic processes. A comprehensive set of experimental techniques was employed, including in vitro staining assays for apoptosis assessment, real-time PCR, and cell proliferation assays. The findings indicate that the 5-HT7 receptor agonist enhances the proliferation of primary gastric tissue cancer cells and KATO-III cells, whereas treatment with the 5-HT7 receptor antagonist significantly inhibits cellular proliferation. Analysis of 5-HT7 receptor mRNA expression in gastric cancer patient populations indicated significantly elevated levels in cancerous tissues when compared to those in healthy tissues. The administration of a 5-HT7 receptor agonist (LP44) resulted in increased cell proliferation in primary gastric cancer cells and KATO-III cell lines, whereas treatment with a 5-HT7 receptor antagonist (SB-269970) significantly inhibited proliferation. Additionally, KATO-III cells treated with the 5-HT7 receptor antagonist demonstrated a marked upregulation of caspase-3, caspase-9, and BAX gene mRNA levels. In contrast, treatment with the 5-HT7 receptor antagonist was associated with a significant reduction in the expression of nuclear factor kappa B and 5-HT7 receptor mRNA levels. Annexin V-FITC/PI and Hoechst 33342 staining demonstrated a pronounced apoptotic effect through antagonism of 5-HT7 receptors compared to other groups. Collectively, the findings of this study suggest that the enhanced expression of 5-HT7 receptors influences gastric cancer formation by regulating the apoptotic axis. This provides a novel perspective for understanding the molecular mechanisms underlying the potential of 5-HT7 receptors as a targeted approach for combating gastric cancer via the apoptotic pathway.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 6","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jbt.70326","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144245050","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}

{"title":"Involvement of IL-6/JAK/STAT3/SOCS3, SIRT1, and Cytoglobin Signaling in Diacerein Protective Effect against Intestinal Injury Induced by Methotrexate","authors":"Gaber F. Ali,&nbsp;Emad H. M. Hassanein,&nbsp;Mustafa Ahmed Abdel-Reheim,&nbsp;El-shaimaa A. Arafa,&nbsp;Wafaa R. Mohamed","doi":"10.1002/jbt.70339","DOIUrl":"https://doi.org/10.1002/jbt.70339","url":null,"abstract":"<div>\u0000 \u0000 <p>Despite its wide applications, methotrexate (MTX) causes significant intestinal toxicity by inducing oxidative stress, inflammatory cascades, and apoptosis. Diacerein (DIA) is a pain-relieving and anti-inflammatory medication with favorable antioxidant properties. We investigated DIA protective effects on MTX-induced intestinal toxicity. Rats were divided into five groups: Control, DIA (50 mg/kg), MTX (single dose of 20 mg/kg; i.p. on 5th day), DIA (25 mg/kg) + MTX, and DIA (50 mg/kg) + MTX. Compared to the MTX-treated group, DIA alleviated MTX-induced intestinal histopathological abrasions and inflammatory cell infiltration, improving average villous length and crypt depth. Furthermore, DIA exhibited potent antioxidative properties, evident by decreasing lipid peroxidation and increasing SOD activity and GSH content, and upregulating the expression of SIRT1 and cytoglobin. In addition, DIA ameliorated MTX-induced intestinal inflammation demonstrated by decreasing IL-6 and TNF-α mediated via suppressing NF-κBp65, phosphorylation of JAK1/STAT3, and upregulation of SOCS3 expression compared to the MTX-treated group. Furthermore, DIA inhibited intestinal apoptotic alterations by reducing cleaved caspase-3 protein expression. These results suggest that DIA, in a dose-dependent manner, could be an effective treatment for reducing intestinal toxicity by MTX via exerting an antioxidant effect, anti-inflammatory properties, and antiapoptotic activity with possible involvement of NF-κBp65, IL-6/JAK1/STAT3/SOCS3, SIRT1, and cytoglobin signaling.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 6","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144245049","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}

{"title":"Cardiac Fibroblast Receptors: A Preclinical Dive Into Their Regulatory Influence on Cardiovascular Diseases","authors":"Nandini Dubey,&nbsp;Vishal Kumar Vishwakarma,&nbsp;Aanchal Verma,&nbsp;Ahsas Goyal,&nbsp;Harlokesh Narayan Yadav,&nbsp;K. H. Reeta,&nbsp;Subhash Chandra Yadav,&nbsp;Neeraj Parakh","doi":"10.1002/jbt.70347","DOIUrl":"https://doi.org/10.1002/jbt.70347","url":null,"abstract":"<div>\u0000 \u0000 <p>Cardiac fibroblasts contribute to the heart's structural, electrical, and chemical integrity. Research has shown that cardiac fibroblasts have a variety of receptors that play an essential role in heart healing and function by maintaining control of autophagy, cell growth, breakdown and renewal of extracellular matrix, as well as signalling molecule production such as growth factors, cytokines, and chemokines. Receptors like endothelin, angiotensin, and DDR2 contribute to the development of cardiac fibrosis. When these receptors are triggered by their specific binding molecules (ligands), they activate fibroblasts and promote their transformation into myofibroblasts, which is marked by higher levels of collagen and α-smooth muscle actin. Cardiovascular diseases are among the top causes of illness, disability, and death around the world, affecting both the public and private sectors. It's fascinating that the transformation of cardiac fibroblasts into cardiac myofibroblasts could play a crucial role in the development of cardiovascular diseases. Since it's been challenging to differentiate between these two cell types, gaining a better understanding of their activity might lead to therapies that support heart healing. Therefore, this review highlights the role of cardiac fibroblast receptors and their contributions to the progression of cardiac fibrosis which leads to several heart diseases.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 6","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144244321","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}

{"title":"Copper Chlorophyllin as an Antioxidant and Photosensitizer: Mitigating Ifosfamide Toxicity and Enhancing Photodynamic Therapy","authors":"Lamia M. Elashry,&nbsp;Nashwah I. Zaki,&nbsp;Einas Yousef,&nbsp;Omar A. Ahmed-Farid,&nbsp;Tarek A. El-Tayeb","doi":"10.1002/jbt.70330","DOIUrl":"https://doi.org/10.1002/jbt.70330","url":null,"abstract":"<div>\u0000 \u0000 <p>Copper chlorophyllin (Cu-Chl) is known for its antioxidant and anticancer properties, particularly as a photosensitizer in photodynamic therapy (PDT). This study aimed to explore the protective effects of Cu-Chl against ifosfamide (IFO)-induced toxicity. Moreover, it aimed to assess the anticancer activity of Cu-Chl as a photosensitizing agent in PDT when used alone or when combined with IFO against Ehrlich solid tumors in mice. To achieve our objectives, we conducted two experiments. The first assessed the potential protective effects of orally administered Cu-Chl in a rat model of IFO-induced toxicity. The liver and kidney tissues underwent biochemical, oxidative stress, inflammatory markers, and histological analyses. The second experiment evaluated the combined effects of IFO and Cu-Chl as part of PDT on Ehrlich solid tumors in mice. The Ehrlich tumor, liver, and kidney tissues underwent histological and biochemical analyses. The results of the present study demonstrated that Cu-Chl administration significantly mitigated IFO-induced liver and kidney damage, as evidenced by improved liver enzyme profiles, reduced levels of oxidative stress and inflammatory markers, and improved histological outcomes. Higher doses of Cu-Chl (100 mg/kg) demonstrated significant protective effects. In the second experiment, Cu-Chl in PDT exerts an antitumorigenic effect by reducing tumor cell viability and promoting necrosis; however, its effect appears weaker than that of IFO. Our histological analysis revealed extensive necrotic regions in tumor tissues treated with Cu-Chl, highlighting its antitumorigenic effect, which was weaker than IFO. Our findings suggest that Cu-Chl, as part of PDT, exerts a dose-dependent apoptotic-modulating effect, as evidenced by reduced caspase-3 and restored Bcl-2 levels when combined with IFO. Combinations of higher Cu-Chl ratios relative to IFO minimized systemic toxicity while maintaining antitumor efficacy. The 3IFO+2Cu-Chl group, in which the rats were treated with IFO for 3 days, followed by 30 min of red light exposure per day for 2 days after the oral administration of Cu-Chl (50 mg/kg), demonstrated an optimal balance between antitumor effects and organ protection. Cu-Chl protects against IFO-induced toxicity and is an effective photosensitizer in PDT. This combination offers a promising approach for enhancing cancer treatment efficacy while minimizing adverse effects on vital organs.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 6","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144244853","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}

{"title":"Taurine Mitigates Metaflumizone-Induced Hepatonephrotoxicity in Rats by Inhibiting Oxidative Stress, Inflammation, and Apoptosis","authors":"Hasan Huseyin Demirel,&nbsp;Sinan Ince,&nbsp;Fahriye Zemheri-Navruz,&nbsp;Sevim Feyza Erdogmus,&nbsp;Nilay Isitez","doi":"10.1002/jbt.70335","DOIUrl":"https://doi.org/10.1002/jbt.70335","url":null,"abstract":"<p>Metaflumizone (MTF) is a pyrazoline sodium channel blocker (SBI) insecticide, and data on its toxicity are limited. Taurine (2-aminoethanesulfonic acid) is a sulfur-containing β-amino acid that is naturally found in high concentrations in cells. In this study, we thoroughly evaluated the impact of taurine on MTF-induced hepatonephrotoxicity in a rat model, focusing on oxidative stress, inflammatory responses, and programmed cell death. In the present study, MTF (500 mg/kg, orally) to induce hepatonephrotoxicity was delivered to male rats for 30 days, and taurine at different concentrations (50, 100, and 200 mg/kg, orally) was used for protective effect for the same period. Taurine treatment alleviated the elevated levels of AST, ALT, ALP, BUN, and creatinine caused by MTF. It further suppressed malate dehydrogenase levels and enhanced antioxidant defense by elevating SOD, GSH, and CAT levels. Additionally, taurine increased the mRNA expression levels of <i>Bcl-2</i>, which had been reduced due to oxidative stress, inflammatory, and apoptotic pathways, while suppressing the elevated gene expression levels of <i>NFκB</i>, <i>TNF-α</i>, <i>Bax</i>, and <i>Cas-3</i>. Furthermore, taurine regulated the altered protein expression levels of <i>Bcl-2</i>, <i>Bax</i>, and <i>TNF-α</i> induced by MTF. Microscopically, taurine also mitigated liver and kidney tissue damage caused by MTF. In conclusion, taurine significantly reduced MTF-induced hepatonephrotoxicity by suppressing oxidative stress, inflammatory responses, and programmed cell death. These findings indicate that taurine has the potential to be a treatment option in the case of the prevention of liver and kidney damage caused by SBI.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 6","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jbt.70335","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144244323","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}

{"title":"Update on Application of Oncolytic Virus-Based Combination Therapy in the Treatment of Hepatocellular Carcinoma","authors":"Mariam Ayad Abd,&nbsp;Mohammed Asiri,&nbsp;Shahd Rajab Farhan,&nbsp;Gaurav Sanghvi,&nbsp;Rangaswamy Roopashree,&nbsp;Aditya Kashyap,&nbsp;D. Alex Anand,&nbsp;Rajashree Panigrahi,&nbsp;Yasser Fakri Mustafa,&nbsp;Baneen C. Gabaal","doi":"10.1002/jbt.70327","DOIUrl":"https://doi.org/10.1002/jbt.70327","url":null,"abstract":"<div>\u0000 \u0000 <p>Hepatocellular carcinoma (HCC) is the fifth most common cancer worldwide and the fourth leading cause of cancer-related mortality. Despite the development of several therapeutic strategies to treat HCC, the highly refractory nature of this disease limits therapeutic outcomes and patient survival. Oncolytic viruses (OVs) are a type of natural virus that can specifically infect and kill human tumor cells in HCC and have been extensively investigated as attractive live therapeutic agents for the treatment of HCC. Engineered OVs are capable of inhibiting HCC progression through direct tumor lysis, perpetuation of apoptosis and infection-destruction cycle, activation of antitumor innate immunity and autoimmunity, disruption of tumor vasculature, induction of immunogenic cell death, and regulation of tumor microenvironment. However, HCC is a heterogeneous tumor and further preclinical or clinical studies are needed to focus on optimizing the route of administration and combination of OVs with other conventional therapies and, more importantly, to develop targeted delivery systems for better treatment of HCC while avoiding liver toxicity, as reviewed in this study.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 6","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144244849","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}

{"title":"Neurotoxic Effects of Airborne Particulate Matter: Mechanisms and Health Implications","authors":"Prakash Thangavel,&nbsp;Duckshin Park,&nbsp;Young-Chul Lee","doi":"10.1002/jbt.70322","DOIUrl":"https://doi.org/10.1002/jbt.70322","url":null,"abstract":"<div>\u0000 \u0000 <p>Exposure to particulate matter (PM) impacts various aspects of health. PM exposure has been increasingly associated with adverse neurological effects, including both neurodevelopmental disorders and neurodegenerative diseases. This review examines the pathways through which PM affects the central nervous system (CNS), including inhalation, systemic circulation, and direct olfactory translocation, leading to neuroinflammation, oxidative stress, and disruption of the blood-brain barrier (BBB). Epidemiological and experimental studies suggest a strong correlation between PM exposure and cognitive impairments, Alzheimer's disease (AD), Multiple sclerosis, and Parkinson's disease (PD). Investigating the PM-neurodegenerative disease relationship is a pressing public health priority, offering opportunities to protect vulnerable populations from the effects of neurodegenerative diseases. The potential of PM for long-term accumulation and neurotoxicity is further demonstrated by its toxicokinetics, which include its absorption, distribution, metabolism, and excretion. Understanding these pathways is essential for developing solutions to reduce PM-induced neurological hazards.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 6","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144214141","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}

{"title":"Study on the Effect of Naringenin on LPS-Induced Acute Lung Injury Based on NRF2/HO-1 Pathway","authors":"Xiao-wei Wang,&nbsp;Da-gui Chen,&nbsp;Ci-an Zhang,&nbsp;Mu-yan Sun,&nbsp;Hao-hao Song,&nbsp;Chen-xi Zhang,&nbsp;Fu-sheng Shang,&nbsp;Min Ye","doi":"10.1002/jbt.70333","DOIUrl":"https://doi.org/10.1002/jbt.70333","url":null,"abstract":"<div>\u0000 \u0000 <p>Acute lung injury (ALI) is a serious respiratory disease characterized by pulmonary inflammatory cell infiltration and oxidative stress and is the leading cause of human death. Naringenin (NAR) is a naturally active flavonoid widely present in citrus fruits and has been shown to have multiple pharmacological effects. In this study, we evaluated the potential mechanism of NAR in lipopolysaccharide (LPS)-induced ALI by constructing a mice model of ALI. It was found that NAR significantly increased the 7-day survival rate of mice after LPS stimulation, improved lung index, tissue inflammatory infiltration, and fibrosis levels, and found that it decreased Interleukin-1 beta(IL-1β), Interleukin-6(IL-6), Tumor Necrosis Factor-alpha(TNF-α), and Malondialdehyde(MDA) levels in bronchoalveolar lavage fluid (BALF), while increasing Glutathione(GSH) and Superoxide Dismutase(SOD) levels. In addition, naringenin suppressed the expression of apoptotic proteins BCL2-Associated X Protein(BAX), Cysteine-Aspartate Protease 3(Caspase 3)and Cleaved-Caspase 3, promoted the expression of B-Cell Lymphoma 2(Bcl-2), and upregulated the expression of Nuclear Factor Erythroid 2-Related Factor 2(NRF2) and Heme Oxygenase-1(HO-1) in lung tissue. These studies suggest that naringenin ameliorates LPS-induced acute lung injury in mice by activating the NRF2/HO-1 pathway.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 6","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144214137","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}