Journal of Biochemical and Molecular Toxicology最新文献

{"title":"Study on the Role of microRNA-138-5p Through Sorbin and SH3 Domain-Containing Protein 2 in Breast Cancer","authors":"LiGong Zhang,&nbsp;Chao Zhu,&nbsp;Chenxu Guo,&nbsp;FaXiang Yin,&nbsp;Qiang Xie,&nbsp;Min Tao","doi":"10.1002/jbt.70081","DOIUrl":"10.1002/jbt.70081","url":null,"abstract":"<div>\u0000 \u0000 <p>Breast cancer (BRCA) is one of the major threats to women's health worldwide. This study focuses on the roles of sorbin and SH3 domain-containing protein 2 (SORBS2) protein and microRNA-138-5p in the progression of BRCA, analyzing their regulatory effects on cancer cell proliferation, cell cycle, and migration ability. Using bioinformatics tools and experimental methods, the study found that SORBS2 is commonly underexpressed in BRCA. Additionally, it demonstrated that microRNA-138-5p can significantly inhibit tumor growth by suppressing SORBS2 expression, providing new molecular targets for BRCA treatment.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 12","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142800869","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":"Innovation in CRC Research: Targeting SPACA6P-AS for Progression","authors":"Tianyi Ma,&nbsp;Yinghu Jin,&nbsp;Song Wang,&nbsp;Hanqing Hu,&nbsp;Meng Wang,&nbsp;Guoqing Yan,&nbsp;Qingchao Tang,&nbsp;Rui Huang,&nbsp;Guiyu Wang","doi":"10.1002/jbt.70039","DOIUrl":"10.1002/jbt.70039","url":null,"abstract":"<div>\u0000 \u0000 <p>The purpose of this research was to provide light on the functional role that the long noncoding RNA SPACA6P-AS plays in the biology of colorectal cancer (CRC). The presence of elevated SPACA6P-AS expression in colorectal cancer tissues is linked to advanced stages of the disease as well as a decreased overall survival rate. It has been demonstrated through knockdown tests conducted on CRC cell lines that SPACA6P-AS stimulates cell growth in both in vitro and in vivo settings. By acting as a competing endogenous RNA, SPACA6P-AS is able to modulate the levels of miR-339-5p and promote the proliferation of colorectal cancer cells by way of the miR-339-5p/FAM167AFAM167A signaling axis. Based on these findings, SPACA6P-AS is a promising candidate for both a prognostic marker and a therapeutic target in colorectal cancer.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 12","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11629451/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142800851","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":"“Polyethylene Terephthalate Nanoplastics Caused Hepatotoxicity in Mice Can be Prevented by Betaine: Molecular and Immunohistochemical Insights”","authors":"Nehal A. Kamel,&nbsp;Dina W. Bashir,&nbsp;Ebtihal M. M. EL-Leithy,&nbsp;Adel F. Tohamy,&nbsp;Maha M. Rashad,&nbsp;Ghada E. Ali,&nbsp;Abdel Aleem A. El-Saba","doi":"10.1002/jbt.70088","DOIUrl":"10.1002/jbt.70088","url":null,"abstract":"<div>\u0000 \u0000 <p>Polyethylene terephthalate nanoplastics (PET-NPs) are one of the most frequently distributed nanoplastics in daily life. Betaine is thought to be a promising hepatoprotective agent. The current investigation focused on whether orally administered PET-NPs caused hepatotoxicity and ameliorative effect of betaine. Forty adult male Swiss albino mice were randomly split into four groups: group I control, group II betaine (1000 mg/kg I/P), group III PET-NPs (200 mg/kg orally), and group IV betaine plus PET-NPs at doses similar to group II&amp; III respectively. After 30 days, blood sample were collected then animals were euthanized and liver specimens were dissected out for biochemical and histopathological examination. PET-NPs induced a significant elevation in alanine aminotransferase (ALT), aspartate aminotransferase (AST), and malondialdehyde (MDA), as well as an increase in the inflammatory genes a proto-oncogene (c-FOS) and cyclooxygenase 2 (COX2) (<i>p</i> ≤ 0.05), with a substantial decrease in glutathione (GSH) (<i>p</i> ≤ 0.05). Furthermore, on the level of histopathological analysis PET-NPs caused alterations in hepatic tissue architecture as vascular dilatation and congestion with hepatocytes degeneration, bile duct epithelial hyperplasia and inflammatory cell infiltrations While on the level of immunohistochemistry, PET-NPs trigger positive tumor necrosis factor-alpha (TNF-α) and nuclear factor-kappa B (NF-ҠB) expression in comparison to control. Meanwhile, betaine treatment reduced the deleterious effects of PET-NPs. To summarize, PET-NPs may cause hepatotoxicity in mice, with a belief that betaine could mitigate the detrimental impact.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 12","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142800847","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":"MiR-200a-3p Attenuates Neuropathic Pain by Suppressing the Bromodomain-Containing Protein 3-Nuclear Factor-κB Pathway","authors":"Chao Deng,&nbsp;Xuequan Yuan,&nbsp;Xuezheng Lin,&nbsp;Sitong Liu","doi":"10.1002/jbt.70041","DOIUrl":"10.1002/jbt.70041","url":null,"abstract":"<div>\u0000 \u0000 <p>MicroRNAs (miRNAs) have key roles in the pathological processes of neuropathic pain. Here, our aim was to elucidate the function of miR-200a-3p as well as its related regulatory mechanism in neuropathic pain. An animal model of neuropathic pain was established by chronic constriction injury (CCI) induction. The knockdown experiments are performed by injecting a lentiviral construct intrathecally. MiR-200a-3p and bromodomain-containing protein 3 (BRD3) expression in rat spinal cord was determined using RT-qPCR. The mechanical, thermal, and cold responses in animals were assessed at the indicated time after surgery. The levels of inflammatory cytokines in rat spinal cord were measured by ELISA. The changes in NF-κB signaling-related molecules in rat spinal cord were determined using western blot and immunofluorescence. MiR-200a-3p was underexpressed in CCI rats in a time-dependent manner. Overexpression of miR-200a-3p decreased mechanical hyperalgesia and thermal sensitivity to attenuate neuropathic pain in rats. BRD3 was targeted by miR-200a-3p. Additionally, downregulation of BRD3 inhibited neuropathic pain progression. Moreover, overexpression of BRD3 rescued the effect of miR-200a-3p on NF-κB signaling and neuropathic pain in CCI rats. MiR-200a-3p attenuates neuropathic pain via downregulating BRD3 to block NF-κB signaling.</p>\u0000 </div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 12","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142800867","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":"LncRNA 93358 Aggravates the Apoptosis of Myocardial Cells After Ischemia-Reperfusion by Mediating the PI3K/AKT/mTOR Pathway","authors":"Jiumei Cai,&nbsp;Zhiwei Zhang,&nbsp;Lingling Chen,&nbsp;Xiaoping Wang,&nbsp;Yiming Zhong,&nbsp;Dongyang Xie,&nbsp;Wei Liao","doi":"10.1002/jbt.70085","DOIUrl":"10.1002/jbt.70085","url":null,"abstract":"<div>\u0000 \u0000 <p>To investigate the impact of LncRNA 93358 on ischemia-reperfusion induced myocardial cell apoptosis and the underlying mechanism. After being subjected to hypoxia for 4 h, three models of hypoxia-reoxygenation (H/R) with reoxygenation times of 8, 16, and 24 h were established. The expression of LncRNA 93358 was detected by qPCR, and the most suitable conditions were selected for subsequent experiments. The LncRNA 93358 knockout rat myocardial cells were established by transfecting with shRNA-93358 and identified by the RT-PCR assay, followed by constructing the in vitro H/R model. H/R myocardial cells were treated with blank medium (Model), shRNA-NC (LncRNA 93358 NC), shRNA-93358 (LncRNA 93358 knock), and shRNA-93358 + LY294002 (LncRNA 93358 knockout+LY294002), respectively. Normal myocardial cells treated with blank medium was taken as the control group. The cell cycle and apoptosis were analyzed by the flow cytometry. The level of cellular SOD and MDA was measured by the ELISA assay. The expression level of LncRNA 93358 was determined by the RT-PCR assay and Western blot assay was utilized to evaluate the expression level of AKT1, p-AKT1, mTOR, p-mTOR, bcl-2, and Bax. Compared to control, the expression of LncRNA 93358 in H9C2 cells was significantly increased under hypoxic conditions for 4 h followed by reoxygenation for 8 h/16 h. Moreover, the expression of LncRNA 93358 was relatively higher under hypoxic conditions for 4 h followed by reoxygenation for 16 h. Compared to control, significantly lower p-mTOR/mTOR and p-AKT1/AKT1 level was observed in the model group, accompanied by the elevated MDA level, declined SOD level, increased apoptotic rate, enhanced arrest at S phase, upregulated Bax, and downregulated Bcl-2. Compared to the model and LncRNA 93358 NC group, the expression level of p-mTOR/mTOR and p-AKT1/AKT1 was significantly promoted in the LncRNA 93358 knock group, accompanied by the declined MDA level, increased SOD level, reduced apoptotic rate, increased arrest at G0/G1 phase, downregulated Bax, and upregulated Bcl-2, which were dramatically reversed in the LncRNA 93358 knockout+LY294002 group. LncRNA 93358 aggravated the apoptosis of myocardial cells after ischemia-reperfusion by mediating the PI3K/AKT/mTOR pathway.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 12","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11626694/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142800853","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":"Vitamin D3 Exerts a Neuroprotective Effect in Metabolic Syndrome Rats: Role of BDNF/TRKB/Akt/GS3Kβ Pathway","authors":"Noha Aladdin,&nbsp;Salah A. Ghareib","doi":"10.1002/jbt.70082","DOIUrl":"10.1002/jbt.70082","url":null,"abstract":"<div>\u0000 \u0000 <p>Metabolic syndrome (MetS) is usually associated with cognitive impairment, neuropathic pain, and reduced brain-derived neurotrophic factor (BDNF) levels. BDNF via tropomyosin receptor kinase B (TrkB) exerts neuroprotection by activating protein kinase B (Akt) to inhibit glycogen synthase kinase-3β (GSK3β). Although Vitamin D3 (VitD3) has demonstrated favorable metabolic and neuronal outcomes in MetS, the precise molecular mechanisms underlying its neuroprotective effects remain poorly elucidated. We aimed to test the hypothesis that VitD3 mitigates MetS-induced cognition deficits and neuropathic pain via modulating the BDNF/TRKB/Akt/GS3Kβ signaling pathway. MetS was induced in male rats by 10% fructose-supplemented water and 3% salt-enriched diet. After 6 weeks, normal and MetS rats received either vehicle or VitD3 (10 µg/kg/day) for an additional 6 weeks. Glycemic status, lipid profile, and behavioral changes were assessed. The advanced glycation end products (AGEs), and markers of inflammation (TNF-α and NF-κB), oxidative stress (malondialdehyde), and apoptosis (caspase3), as well as BDNF, TrkB, PI3K, Akt, GSK3β, phosphorylated tau, and amyloid beta (Aβ) were assessed in the cerebral cortex. MetS rats had deteriorated glycemic and lipid profiles, higher AGEs, reduced levels of BDNF, TrkB, PI3K, and active Akt, along with increased GSK3β levels, inflammation, oxidative stress, and apoptosis. These changes were associated with higher levels of cognitive impairment markers phosphorylated tau and Aβ, as well as behavioral changes indicative of cognitive impairment and neuropathic pain. VitD3 improved the cognitive and behavioral alterations, while mitigating the associated molecular derangements. Our results indicate that VitD3 may exert neuroprotective effects by modulating the BDNF/TrkB/PI3K/Akt/GSK3β signaling pathway.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 12","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142800871","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":"Exosomal miR-20b-5p Induces EMT and Enhances Progression in Non-Small Cell Lung Cancer Via TGFBR2 Downregulation","authors":"Hui Ma,&nbsp;Bo Jiang,&nbsp;Qiu Ren,&nbsp;Yajiao Sun,&nbsp;Mengyao Wang,&nbsp;Siyu Xia,&nbsp;Dong Wang,&nbsp;Wei Zhang","doi":"10.1002/jbt.70080","DOIUrl":"10.1002/jbt.70080","url":null,"abstract":"<div>\u0000 \u0000 <p>The mechanism by which specific miRNAs in NSCLC exosomes regulate NSCLC progression remains unclear. First, exosomes were isolated and identified. Exosomes were labeled with PKH26 for cell tracking studies. Subsequently, BEAS-2B cells and BEAS-2B cell exosomes were transfected with miR-20b-5p mimics or miR-20b-5p inhibitors, and cell proliferation was measured by EdU and CCK-8. cell migration and invasion were detected by wound healing tests and Transwell. The potential target of miR-20b-5p was predicted and verified by luciferase assay. Relative expression levels of miR-20b-5p and TGFBR2 were detected by qRT-PCR. Protein expression level was detected by Western blot. In addition, A549 cell exosomes were injected into mice through the tail vein and the pathological changes of lung tissue were detected by HE staining. Expression levels of E-cadherin and Vimentin in lung tissues were detected by immunohistochemistry. Our results also showed that high levels of miR-20b-5p in exosomes generated from NSCLC cells conceivably enter the cytoplasm of their own cells and by downregulating TGFBR2, accelerate NSCLC invasion, migration and EMT while promoting NSCLC cell proliferation. Exosome analysis using clinical plasma specimens revealed that miR-20b-5p expression was considerably improved in exosomes from NSCLC patients compared with those from healthy controls. In vitro and in vivo, exosomes with high levels of miR-20b-5p were linked to the progression of NSCLC. Our data suggest that exosomes with high levels of miR-20b-5p can increase development and metastasis of NSCLC cells by downregulating TGFBR2, which would serve as a predictive and diagnostic marker for NSCLC.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 12","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142785720","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":"Protective Effects of NRF2 Activator Sulforaphane in Polyinosinic:Polycytidylic Acid-Induced In Vitro and In Vivo Model","authors":"Shailesh Vilas Matsagar,&nbsp;Rakesh Kumar Singh","doi":"10.1002/jbt.70086","DOIUrl":"10.1002/jbt.70086","url":null,"abstract":"<div>\u0000 \u0000 <p>NRF2 is a nuclear transcription factor involved in the cellular protection against oxidative stress and inflammatory signaling. Sulforaphane is a known NRF2 activator used for its strong antioxidant and anti-inflammatory activity through regulation of Keap-1-HO-1 pathway. However, there is a limited exploration about the role of NRF2 activator, sulforaphane in regulation of poly(I:C)-induced oxidative stress, inflammation and injury in lung. Therefore, we aimed to evaluate the therapeutic effect of sulforaphane in poly(I:C)-induced responses using in vitro as well as in vivo model. We evaluated oxidative stress and inflammatory cytokines in poly(I:C)-induced RAW264.7 cells. We also employed in vivo animal study to evaluate tissue oxidative–antioxidative balance along with expression of NRF2, Keap-1, histopathological assessment by hematoxylin–eosin staining and picrosirius red staining to explore the protective mechanisms of sulforaphane in poly(I:C)-induced mouse model. Our results indicated that sulforaphane increased the expression of NRF2 and its downstream proteins. In addition, sulforaphane alleviated poly(I:C)-induced activation of the oxidative and pro-inflammatory pathways, histopathological changes, depleted expression of GSH and superoxide dismutase in lung tissue. This study suggested that sulforaphane may be one of the useful therapeutic alternatives for poly(I:C) induced lung injury and inflammation.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 12","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142779997","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":"Synthesis, Biological Evaluation and in Silico Studies of Novel Urea/Thiourea Derivatives of Lenalidomide","authors":"Fatih Tok,&nbsp;Burçin İrem Abas,&nbsp;Faika Başoğlu,&nbsp;Özge Çevik,&nbsp;Sevgi Karakuş,&nbsp;Abdulilah Ece","doi":"10.1002/jbt.70079","DOIUrl":"https://doi.org/10.1002/jbt.70079","url":null,"abstract":"<div>\u0000 \u0000 <p>Designing new compounds from existing chemotherapeutic drugs to enhance inhibitory effects on tumor cells while overcoming multidrug resistance is one of the important strategies for new drug discovery in medicinal chemistry. A new series of urea and thiourea derivatives based on Lenalidomide as potential anticancer agents have been designed and synthesized. <i>In vitro</i> anticancer activity assay against Caki cancer cells and HUVEC endothelial cells revealed that 1-(4-methylphenyl)-3-[2-(2,6-dioxopiperidin-3-yl)-1-oxoisoindolin-4-yl]urea (<b>11</b>) exhibited the highest anticancer activity and selectivity in the series with IC₅₀ values of 9.88 and 179.03 µM, respectively. Among the compounds, <b>11</b> showed significant HDAC1 inhibiton of 68.02 ± 2.44% at 10 µM concentration. TGF-β, Bax, Bcl-2 protein levels and scratch assay were analyzed in Caki cells. As a result, compound <b>11</b> induced apoptosis in Caki cells. In this study, it has been demonstrated that compound <b>11</b> can be a lead compound for further detailed investigation in renal cancer treatment. Through molecular docking studies, it was determined that the most active compound, <b>11</b>, forms stable interactions with key residues in the enzyme's active site, particularly engaging in hydrogen bonds with GLY149 and coordinating with the zinc ion in the HDAC1 active site. These interactions are crucial for the observed inhibitory activity. Molecular dynamics simulation revealed the binding event of the most active compound with class I histone deacetylase and the stability of the complex in a biological environment.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 12","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142759848","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":"Silent Information Regulator 1/Peroxisome Proliferator-Activated Receptor-γ Coactivator-1α Axis: A Promising Target for Parkinson's and Alzheimer's Disease Therapies","authors":"Ahsas Goyal,&nbsp;Anshika Kumari,&nbsp;Aanchal Verma,&nbsp;Vandana Chaudhary,&nbsp;Vaibhav Agrawal,&nbsp;Harlokesh Narayan Yadav","doi":"10.1002/jbt.70078","DOIUrl":"https://doi.org/10.1002/jbt.70078","url":null,"abstract":"<div>\u0000 \u0000 <p>One of the key challenges in medical research is developing safe medications to treat neurodegenerative disorders. Increased oxidative stress, mitochondrial dysfunction, and neuroinflammation are common features of Alzheimer's disease (AD) and Parkinson's disease (PD). Silent information regulator 1 (SIRT-1), part of the sirtuin family, plays a critical role in various physiological processes by binding to histones and nonhistone proteins. SIRT-1 primarily mitigates oxidative stress and regulates mitochondrial activity by maintaining the deacetylated form of peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α), ensuring stable PGC-1α levels. Research has shown reduced SIRT-1/PGC-1α expression in AD and PD models. Targeting this pathway presents a promising therapeutic approach for managing AD and PD, potentially leading to disease-modifying treatments and improved outcomes. This review highlights the findings of various studies suggesting that the SIRT-1/PGC-1α pathway promotes mitochondrial biogenesis, synaptic plasticity, and cognitive function, as well as exerts antioxidant, anti-inflammatory, and anti-apoptotic effects, offering a potential method for AD and PD treatment.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"38 12","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142762516","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}