Journal of Biochemical and Molecular Toxicology最新文献

{"title":"miR-186-5p Down-Regulates PD-L1 Level in Acute Myeloid Leukemia Cells and Inhibits Tumorigenesis and Immune Escape","authors":"Cheng Lian,&nbsp;Yanhui Liu,&nbsp;Pingchong Lei","doi":"10.1002/jbt.70278","DOIUrl":"https://doi.org/10.1002/jbt.70278","url":null,"abstract":"<div>\u0000 \u0000 <p>Acute myeloid leukemia (AML) is a malignant tumor of blood cells, which seriously interferes with the generation of normal cells. Although miR-186-5p is diminished in AML, its exact mechanism is not well understood. miR-186-5p and PD-L1 levels in AML cells (HL-60, KG-1, TF-1a, MOLT-3) and subcutaneous tumor tissue were discovered through qRT-PCR and Western blot. miR-186-5 p and PD-L1 combining sites were foreseen by the database and verified by dual luciferase and immunoprecipitation experiments. AML cells with miR-186-5p overexpression or knockdown and PD-L1 overexpression were cocultured with CD4⁺ and CD8⁺ T cells. The proliferation, migration, invasion and apoptosis of AML cells, CD8⁺ and CD4⁺ T cell growth and apoptosis, and activated markers (Perforin and Granzyme B) and secreted cytokines (IFN-γ, IL-4 and TNF-α) levels were detected by CCK8, Transwell, flow cytometry, CFSE, Western blot and ELISA, respectively. Subcutaneous xenograft magnitude and mass in nude mice were measured. Ki67 level was identified through immunohistochemistry. CD4⁺ and CD8⁺ T cell level and infiltration were detected by immunofluorescence and flow cytometry. miR-186-5p was downregulated, and PD-L1 was boosted in AML cells and subcutaneous tumor tissues (<i>p</i> &lt; 0.05), while miR-186-5p targeted down-regulate PD-L1. miR-186-5p upregulation hindered AML cell multiplication, migration, invasion and facilitate cell death, and enhanced the proliferation activity, activation markers (Perforin and Granzyme B) and secreted cytokines (IFN-γ, IL-4, TNF-α) of CD8⁺ and CD4⁺ T cells, inhibited apoptosis, and inhibited immune escape (<i>p</i> &lt; 0.05). Knockdown of miR-186-5p can promote AML progression, but PD-L1 upregulation weakens the antitumor impact of miR-186-5p overexpression (<i>p</i> &lt; 0.05). Transplanted tumor mice experiments also found that miR-186-5p hindered PD-L1 and tumor growth (<i>p</i> &lt; 0.05). In conclusion, miR-186-5p can target inhibit PD-L1, suppress AML cells multiplication, movement, invasion and immune escape, and then reduce AML, aiming to provide support and basis for the pathological mechanism and prevention and treatment strategy of AML.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 5","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143875649","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":"RETRACTION: The Pyrethroid Insecticide Permethrin Confers Hepatotoxicity Through DNA Damage and Mitochondria-Associated Apoptosis Induction in Rat: Palliative Benefits of Fumaria Officinalis","authors":"","doi":"10.1002/jbt.70250","DOIUrl":"https://doi.org/10.1002/jbt.70250","url":null,"abstract":"<p><b>RETRACTION:</b> N. Aoiadni, N. Chiab, H. Jdidi, R.G. Bouzid, A. El Feki, H. Fetoui, and F.G. Koubaa, “The Pyrethroid Insecticide Permethrin Confers Hepatotoxicity Through DNA Damage and Mitochondria-Associated Apoptosis Induction in Rat: Palliative Benefits of <i>Fumaria officinalis, ” Journal of Biochemical and Molecular Toxicology</i> 36, no. 10 (2022): e23172, http://doi.org/10.1002/jbt.23172.</p><p>The above article, published online on 21 July 2022 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Hari K. Bhat, and Wiley Periodicals, LLC. The retraction has been agreed due to unattributed reuse of data and images in Table 4, Table 5, Figure 2A, and Figure 4 from the authors' previously published work. The authors were not able to provide a satisfactory explanation for this reuse and therefore, the article must be retracted. The authors did not respond to this decision.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 5","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jbt.70250","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143871872","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":"Therapeutic Potential of Exosomal miRNAs: New Insights and Future Directions","authors":"Haili Duan,&nbsp;Seyedeh Helya Siadat,&nbsp;Saade Abdalkareem Jasim,&nbsp;Pooja Bansal,&nbsp;Harpreet Kaur,&nbsp;Maytham T. Qasim,&nbsp;Munther Kadhim Abosaoda,&nbsp;Raed Fanoukh Aboqader Al-Aouadi,&nbsp;Muath Suliman,&nbsp;payam Ali khiavi","doi":"10.1002/jbt.70270","DOIUrl":"https://doi.org/10.1002/jbt.70270","url":null,"abstract":"<div>\u0000 \u0000 <p>Modern advancements in medicine include developing targeted drug delivery systems in the medical field, which are designed to unravel the potential of therapeutic products and overcome the barriers to the effectiveness of current approaches. Various nanopolymer carrier systems have been introduced in this regard, and the simple characteristics of extracellular vesicles have drawn special attention to their application as an effective drug delivery tool. Exosomes are very similar to transport vesicles and have a lipid-biomembrane covering an aqueous core. They also contain both hydrophilic and lipophilic substances and deliver their cargo to the desired targets. These properties enable exosomes to overcome some of the limitations of liposomes. Exosomes can easily diffuse into body fluids and remain in the bloodstream for a long time, crossing physiological barriers and entering cells. Exosomes, which contain a large volume of biomolecules, do not stimulate immune responses and do not accumulate in the liver or lungs instead of target tissues. Recent advancements in regenerative medicine have enabled scientists to utilize exosomes extracted from mesenchymal stem cells (MSCs), which possess significant regenerative abilities, for treating various diseases. The contents of these exosomes are crucial for both diagnosis and treatment, as they influence disease progression. Numerous in vitro studies have confirmed the safety, effectiveness, and therapeutic promise of exosomes in conditions such as cancer, neurodegenerative disorders, cardiovascular issues, and orthopedic ailments. This article explores the therapeutic potential of MSC-derived exosomes and outlines the essential procedures for their preparation.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 5","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143865627","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":"Salvianolic Acid A Attenuates Lipopolysaccharide-Induced Acute Lung Injury by Activating AMPK/SIRT1/Nrf2 Signaling Pathway","authors":"Pengwei Wang,&nbsp;Yu Sun,&nbsp;Ru Zhang,&nbsp;Yongli Guo,&nbsp;Yongheng Zhang,&nbsp;Shengjie Guo,&nbsp;Yemin Wang,&nbsp;Jianlian Gao,&nbsp;Pengfei Yang,&nbsp;Zhijian Deng","doi":"10.1002/jbt.70282","DOIUrl":"https://doi.org/10.1002/jbt.70282","url":null,"abstract":"<div>\u0000 \u0000 <p>Salvianolic acid A (Sal A) has been reported to have anti-inflammatory and antioxidant properties. The present study aimed to explore the potential mechanisms of Sal A on lipopolysaccharide (LPS)-induced acute lung injury (ALI). The results indicated that Sal A pretreatment attenuated LPS induced lung injury, shown by alleviated histopathological damage and alveolar-capillary barrier dysfunction, as well as reduced inflammatory response and oxidative stress. Moreover, Sal A pretreatment effectively increased the expression of p-AMPK and SIRT1 and promoted Nrf2 nuclear translocation in lung tissues. However, these effects were remarkably blunted by Compound C. Molecular docking experiments further confirmed that Sal A bound well to the active sites of AMPK and SIRT1. In conclusion, these results indicated that Sal A exerted its protective effects on LPS-induced ALI through suppressing inflammation and oxidative stress, which was mainly dependent on the activation of AMPK/SIRT1/Nrf2 signaling pathway.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 5","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143865628","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":"Sevoflurane Preconditioning Protects Against Myocardial Ischemia Reperfusion Injury in Mice via PI3K/AKT/GSK3β-mediated Upregulation of Syntaxin1a","authors":"Meng Liu,&nbsp;Fengying Xu,&nbsp;Jinjin Lv,&nbsp;Xiaofeng Liu,&nbsp;Eerdun Wang","doi":"10.1002/jbt.70260","DOIUrl":"https://doi.org/10.1002/jbt.70260","url":null,"abstract":"<div>\u0000 \u0000 <p>Preconditioning with volatile anesthetics, such as isoflurane and sevoflurane, can protect the myocardium against ischemia/reperfusion injury (IRI). Syntaxin1A (Stx1A) is cardioprotective and regulated by volatile anesthetics. However, is the mechanism by which sevoflurane preconditioning (SPC) induces Stx1A to exert myocardial protection remains unclear. The study investigates whether SPC induces upregulation of Stx1A through the thymoma viral proto-oncogene (AKT)/Glycogen synthase kinase 3 β (GSK3β) signaling pathway. Myocardial IRI model in mice was established by surgically ligating the left anterior descending coronary followed by loosening of the occlusion. Regulation of signaling pathway by intraperitoneal administration of the phosphatidylinositol 3-kinase (PI3K) inhibitor, Ly294002 (30 mg/kg), and GSK3β inhibitor, TWS119 (30 mg/kg). The triphenyl tetrazolium chloride (TTC) staining method was used to measure the myocardial infarction area. Serum creatine kinase MB (CK-MB) and lactic dehydrogenase (LDH) concentration were measured by enzyme-linked immunosorbent assay (ELISA). Western blot was employed to examine AKT/GSK3β pathway activity, as well as expressions of Stx1A, small ubiquitin-like modifier 1 (SUMO1), growth hormone-releasing hormone (GHRH), or calcitonin gene-related peptide (CGRP), and brain natriuretic peptide (BNP). Both IRI and SPC induced upregulation of Stx1A in mice. However, the upregulation was abolished by treatment with Ly294002, while TWS119 further increased its expression (<i>p</i> &lt; 0.05). Myocardial infarct area, serum CK-MB, and LDH were elevated in the IRI group but were inhibited by SPC-induced (<i>p</i> &lt; 0.05); however, this inhibition by SPC was eliminated by Ly294002 (<i>p</i> &lt; 0.05). TWS119 causes the opposite effect (<i>p</i> &lt; 0.05). These findings demonstrated that SPC activated the AKT/GSK3β signaling pathway to upregulate Stx1A expression and provide protection to the myocardium.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 5","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143861831","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":"A Comparative Study of Quercetin/Rutin Loaded PEG Polymeric Nanoparticles: Controlled Drug Release and Its Biological Activity","authors":"Renuka Mani,&nbsp;Swethaa Viswaresh Babu,&nbsp;Nishanth Murugesan,&nbsp;Ramachandhiran Duraisamy,&nbsp;Palvannan Thayumanavan","doi":"10.1002/jbt.70269","DOIUrl":"https://doi.org/10.1002/jbt.70269","url":null,"abstract":"<div>\u0000 \u0000 <p>Flavonoids are natural polyphenolic compounds that primarily possess antioxidant properties and play a significant role in opposing various diseases. Current chemotherapeutic approaches are largely ineffective, thus calling for the development of alternative strategies to combat this disease. In this regard, numerous studies have reported the anticancer effect of flavonoids in different types of cancer. To enhance its therapeutic value, polymeric nanoparticles (PEG NPs) represent an ideal delivery system. Further, surface modification of NPs with PEG holds tremendous potential for improving the bioavailability and circulation time of native drugs in the blood. The present study aimed to develop Quercetin/Rutin-loaded PEG polymeric NPs (Qu-PEG/Ru-PEG NPs) with enhanced encapsulation efficiency and sustained drug release. The synthesized Qu-PEG NPs &amp; Ru-PEG NPs were characterized by UV-Vis Spectroscopy, FTIR spectrum, NMR, and XRD and SEM analysis. In-vitro drug release study exhibited a cumulative release of Quercetin &amp; rutin for 24 h at pH 7.4. Further, the polymeric nano-formulations of Quercetin &amp; Rutin showed enhanced antioxidant activity, leading to defense against oxidative stress. In-vitro cellular studies demonstrated that Qu-PEG NPs and Ru-PEG NPs significantly inhibit KB cell proliferation compared to free drugs alone. The current study also showed that Qu-PEG NPs &amp; Ru-PEG NPs enhance intracellular ROS generation compared to the drug alone. Hence, our research findings revealed that successful encapsulation of Quercetin &amp; Rutin in PEG NPs targets the tumor microenvironment and enhances the efficacy of drugs. Based on these preliminary results, flavonoid-loaded polymeric-based NPs might be potential therapeutic molecules against cancer in the future.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 5","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143865864","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":"Auraptene Mitigates Cigarette Smoke and Lipopolysaccharide-Induced Chronic Obstructive Pulmonary Disease in Mice and BEAS-2B Cells via Regulating Keap1/Nrf2/HO-1 Pathway","authors":"Rui Qi,&nbsp;Yuwen Fei","doi":"10.1002/jbt.70253","DOIUrl":"https://doi.org/10.1002/jbt.70253","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 <p>Chronic obstructive pulmonary disease (COPD) is a most common respiratory condition characterized by airflow limitation, airway inflammation, and lung injury. The present study was undertaken to unveil the therapeutic potentials of the auroptene against lipopolysaccharide (LPS) and cigarette smoke (CS)-induced COPD in mice. The CS along with LPS was exposed to healthy C57BL/6 mice through the intranasal route to induce COPD. The exposure to CS was continued for 12 weeks. The LPS challenge was occurred on weeks 2, 4, 6, and 8. The auraptene was treated orally by gavage route 1 h before to CS exposure for last 4 weeks. After the completion of treatment, the respiratory function was assessed using a pulmonary function test equipment. The levels of mucin proteins, extracellular matrix (ECM) proteins, proliferative cytokine markers, epithelial marker protein E-cadherin, oxidative stress-related biomarkers, and inflammation-associated markers were assessed using respective commercial assay kits. An analysis of histopathology and histo-morphology was conducted on the pulmonary tissues. An in vitro assays were conducted on the CS condensate (CSC) and LPS-challenged BEAS-2B cells. The expressions of Keap1/Nrf2/HO-1 pathway associated proteins were assessed using assay kits. The findings of the current work has clearly proved that auraptene at 25 mg/kg concentrations significantly increased the pulmonary functions in the mice with COPD. The treatment of auraptene effectively reduced the ECM protein levels, proliferative cytokine marker levels, and inflammation-related cytokine levels in the COPD mice. In addition, the auraptene treatment effectively increased the antioxidants and mitigated the lung tissue injuries in the COPD mice. The Keap1/Nrf2/HO-1 signaling pathway expressions successfully regulated by the auraptene treatment in the CSC and LPS-induced BEAS-2B cells. Therefore, the current findings has highlighted that auraptene has the capability to be a beneficial intervention to treat COPD.</p>\u0000 </section>\u0000 </div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 5","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143865865","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":"N-Acety-L-Cysteine Alleviates Isoflurane-Triggered Neuronal Cell Parthanatos by Suppressing Reactive Oxygen Species Accumulation Through the Induction of c-Jun N-Terminal Kinase Signaling Pathway Inhibition","authors":"Nan Liu,&nbsp;Ya Liu,&nbsp;Xuedong Wang,&nbsp;Ming Liu,&nbsp;Yingying Wang,&nbsp;Chunsheng Feng,&nbsp;Meihua Piao","doi":"10.1002/jbt.70268","DOIUrl":"https://doi.org/10.1002/jbt.70268","url":null,"abstract":"<p>In recent years, the potential neurotoxicity of inhaled anesthetics on the developing brain has increasingly garnered attention, yet its mechanism remains unclear. Parthanatos is a newly discovered form of programmed cell death dependent on PARP-1, and it is believed to be closely associated with cellular oxidative stress response. However, it is still to be proven whether isoflurane, a commonly used clinical anesthetic, can induce parthanatos in developing brain neurons and whether it activates the oxidative stress signaling pathway in neuronal cells. In this study, we treated SH-SY5Y cells and rat hippocampus neuron cells (RN-h) with isoflurane, measured cell viability using the MTT assay, examined the activation of the parthanatos-related PARP-1/AIF/PAR signaling pathway using western blot analysis, detected the accumulation of ROS using DCFH-DA, detected mitochondrial membrane potential (Δψm) by a JC-1 assay, and assessed the activation of the oxidative stress-related JNK signaling pathway using western blot. In vivo, we examined the damaging effects of inhaled isoflurane on neonatal rat hippocampal neurons using HE staining. The results showed that 2% and 4% concentrations of isoflurane significantly inhibited cell survival and upregulated the expression levels of PARP-1, AIF, and PAR in both types of neuronal cells. Moreover, isoflurane significantly enhanced ROS levels and decreased Δψm, and activated the JNK signaling pathway in both cell types. Importantly, we found that pretreatment with N-Acetylcysteine (NAC) could inhibit isoflurane-induced parthanatos and the accumulation of ROS in cells, as well as the activation of the JNK pathway. The experimental results in neonatal rats also demonstrated that isoflurane led to significant neuronal death in the hippocampal CA1 region. However, pretreatment with NAC significantly increased the survival rate of pyramidal neurons in this region. In summary, through our experiments, we confirmed that isoflurane can induce parthanatos in neuronal cells, and NAC can decrease ROS accumulation in neuronal cells and thus mitigate the damage isoflurane causes to neuronal cells.</p>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 5","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jbt.70268","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143865793","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":"Indole-3-Carbinol Mechanisms Combating Chemicals and Drug Toxicities","authors":"Marian N. Gerges,&nbsp;Thoria Donia,&nbsp;Tarek M. Mohamed","doi":"10.1002/jbt.70280","DOIUrl":"https://doi.org/10.1002/jbt.70280","url":null,"abstract":"<div>\u0000 \u0000 <p>The toxicity of chemicals and drugs is a common crisis worldwide. Therefore, the search for protective compounds is growing. Natural compounds such as indole-3-carbinol (I3C) derived from cruciferous vegetables are preferred since they are safe for humans and the environment. This review focuses on I3C potential role in preventing and repairing damage caused by chemicals and drugs. Interestingly, I3C ameliorates hepatotoxicity induced by carbon tetrachloride (CCl₄), diethylnitrosamine (DENA), alcohol, gold nanoparticles, and microbial toxins. Additionally, it inhibits carcinogenesis induced by different chemicals and prevents the deleterious effects of different antineoplastic drugs including cisplatin, doxorubicin (DOX), and trabectidin on normal tissues. Moreover, it reduces fetal malformation and protects against micronuclei formation and calstogenecity induced by cyclophosphamide (CP) in bone marrow cells. It also attenuates methotrexate (MTX)-induced hepatotoxicity, mitigates neurotoxicity caused by thioacetamide and clonidine, and protects against aspirin side effects in gastric mucosa. Furthermore, its nanoparticles inhibit neuronal damage caused by glutamate and rotenone. Thus, I3C prevents the toxicities caused by chemicals in the surrounding environment as well as those of consumed drugs.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 5","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143865792","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":"Evaluation of Anti-Hyperlipidemic and Anti-Atherogenic Activity of Asiatic Acid and Its Effect on Lipid Peroxidation in Hyperlipidemic Rats","authors":"Aarti Tiwari,&nbsp;Amit Shukla,&nbsp;Pradeep Kumar Samal","doi":"10.1002/jbt.70255","DOIUrl":"https://doi.org/10.1002/jbt.70255","url":null,"abstract":"<div>\u0000 \u0000 <p>Atherosclerosis is associated with several illnesses, such as coronary heart disease (CHD), peripheral vascular disease, and ischemic cerebrovascular disease. Atherosclerosis development and accompanying complications are predominantly influenced by Hyperlipidemia, which plays a crucial role. These illnesses are the primary cause of most sickness and death among those who are in their middle age or older. The incidence of dyslipidemia among Chinese adults aged 18 and older is 18.6%, indicating that there are around 160 million individuals affected by this condition. This represents the smallest number of patients globally. This analysis was derived from research undertaken in the field of epidemiology. Hence, developing a comprehensive approach for early prevention and treatment of Hyperlipidemia is imperative. The reason for this is that Hyperlipidemia has the potential to deteriorate progressively. Despite the notable progress made in treating Hyperlipidemia with synthetic drugs, there has been a renewed interest in medicinal plants and phytoconstituents known for their therapeutic capabilities. Asiatic acid, primarily present in <i>Centella asiatica</i> (L.), is classified as one of the phytocompounds that can decrease plasma lipids and lipid peroxidation. This plant may include asiaticoside, asiatic acid, and other components. Asiatic acid has the potential to prevent Hyperlipidemia. The aim of our research is to explore the anti-Hyperlipidemic and anti-atherosclerosis potential of Asiatic acid, which will help to explore its potential mechanism of action and a possibility of its usefulness in this regard.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 5","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143861583","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}