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Neuroprotective potential of tranilast in streptozotocin-induced sporadic Alzheimer's disease model targeting txnip-NLRP3 inflammasome pathway

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INTERNATIONAL IMMUNOPHARMACOLOGY 2025年 156卷

作者： Padhy, Dibya Sundar Vesmaker, Kushal Banerjee, Sugato Natl Inst Pharmaceut Educ & Res NIPER Dept Pharmacol & Toxicol Kolkata 700054 W Bengal India

Sporadic Alzheimer's disease (sAD) is a progressive neurodegenerative disorder characterised by oxidative stress, neuroinflammation, mitochondrial dysfunction and cerebral insulin resistance. Even though approximately 95 % of AD cases are reported as sporadic, the exact pathogenesis remains sparse. Tranilast, an analogue of tryptophan metabolite, was initially endowed as an anti-allergic agent and used in multiple inflammatory ailments. Still, the molecular mechanisms targeting sAD are yet to be investigated. In the present study, we investigated the neuroprotective potential of tranilast by performing biochemical, molecular and histopathological assessments using both in vivo and in vitro experimental sAD models. Streptozotocin (STZ;3 mg/kg) was bilaterally injected on day 1 and 3 through the intracerebroventricular (ICV) route to Sprague Dawley rats for the in vivo model induction. Spontaneous alternation test, novel object recognition test, and passive avoidance test were performed to assess the altered behavioural patterns in animals. Furthermore, human neuroblastoma cells (SHSY5Y) were exposed to STZ (1 mM) and tranilast for 24 h to validate the in vivo results. Three weeks of tranilast (30 and 100 mg/kg, p. o.) treatment improved neurobehavioural anomalies in ICV-STZ-treated rats by halting neuroinflammation and NLRP3 inflammasome activation caused by enhanced reactive oxygen species (ROS) and thioredoxin interaction protein (txnip) overexpression. The phosphorylated tau (p-tau S416) level was also increased in the ICV-STZ rat's hippocampus and reversed upon tranilast treatment. A high dose of tranilast (100 mg/kg) treatment sensitised hippocampal insulin signalling in ICV-STZ-treated rats. Furthermore, in cell culture studies, 24-h tranilast (30 and 100 mu M) treatment reduced the mitochondrial ROS production and attenuated inflammasome activation in STZ-treated SHSY5Y cells. In summary, the findings of the study proclaim the neuroprotective potential of tran

关键词： Streptozotocin Sporadic Alzheimer's disease Neuroinflammation Tranilast txnip NLRP3

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Ginsenoside Rg1 attenuates T2DM-induced renal damage and fibrosis by inhibiting TRPC6-ChREBP-txnip signaling

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JOURNAL OF ETHNOPHARMACOLOGY 2025年 348卷 119863页

作者： Zhang, Hui Liang, Haoyu Fan, Lei Zhu, Xing Ji, Pengmin Su, Yong Li, Weiping Li, Weizu Anhui Med Univ Sch Basic Med Sci Dept Pharmacol Key Lab Antiinflammatory & ImmunopharmacolMinist Hefei 230032 Peoples R China Anhui Med Univ Affiliated Hosp 1 Dept Pharm Hefei 230032 Peoples R China

Ethnopharmacological relevance: As a traditional Chinese medicine, ginseng has many benefits, including regulating blood sugar, blood pressure and so on. Ginsenoside Rg1 is the main active component of ginseng and has been found to significantly improve renal pathological injury in type 2 diabetes mellitus (T2DM) mice. However, the effects and mechanisms of Rg1 in attenuating T2DM are not fully understood. Aim of the study: This study aims to investigate the role of Rg1 in the treatment of renal damage and fibrosis induced by T2DM and its molecular mechanism. Materials and methods: T2DM models were constructed on mice and cells respectively and were administered with corresponding drugs. SA-beta-Gal and Oil Red O were used to observe cell senescence and lipid droplet deposition;H&E and PAS were used to observe pathological changes in the kidney;masson and sirius red were used to evaluate the level of renal fibrosis. Immunohistochemistry, immunofluorescence and Western blotting were performed to analyze the relevant indexes which resulted in the detection of ROS levels in vitro and in vivo. Calcium imaging was used to test the level of [Ca2+]i . Results: Rg1 and Trpc6 knockout could significantly improve kidney dysfunction, attenuate renal injury and fibrosis and also decrease the expression levels of TRPC6, CaN, txnip, ChREBP, p-ASK1 and NLRP3 inflammasome. Meanwhile, Rg1 and Trpc6 knockout significantly inhibited mitochondrial damage and apoptosis protein release. Additionally, Rg1 treatment has been shown to markedly reduce lipid deposition and ROS accumulation in T2DM, while Trpc6 knockout exhibited no effect on these parameters. Conclusion: Rg1 treatment can inhibit the TRPC6-ChREBP-txnip pathway, thereby improving chronic T2DMinduced renal injury and fibrosis.

关键词： Diabetic kidney disease Ginsenoside Rg1 TRPC6 txnip NLRP3 inflammasome

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CYP3A5 unexpectedly regulates glucose metabolism through the AKT-txnip-GLUT1 axis in pancreatic cancer

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Genes & Diseases 2024年第4期11卷 381-399页

作者： Ming Shao Qingfei Pan Haiyan Tan Jing Wu Ha Won Lee Andrew D.Huber William C.Wright Ji-Hoon Cho Jiyang Yu Junmin Peng Taosheng Chen Department of Chemical Biology and Therapeutics St.Jude Children's Research HospitalMemphisTN 38105USA Department of Computational Biology St.Jude Children's Research HospitalMemphisTN 38105USA Center for Proteomics and Metabolomics St.Jude Children's Research HospitalMemphisTN 38105USA Department of Structural Biology St.Jude Children's Research HospitalMemphisTN 38105USA Department of Developmental Neurobiology St.Jude Children's Research HospitalMemphisTN 38105USA

CYP3A5 is a cytochrome P450(CYP)enzyme that metabolizes drugs and contributes to drug resistance in ***,it remains unclear whether CYP3A5 directly influences cancer *** this report,we demonstrate that CYP3A5 regulates glucose metabolism in pancreatic ductal ***-omics analysis showed that CYP3A5 knockdown re-sults in a decrease in various glucose-related metabolites through its effect on glucose trans-port.A mechanistic study revealed that CYP3A5 enriches the glucose transporter GLUT1 at the plasma membrane by restricting the translation of txnip,a negative regulator of ***,CYP3A5-generated reactive oxygen species were proved to be responsible for atten-uating the AKT-4EBP1-txnip signaling ***3A5 contributes to cell migration by maintaining high glucose uptake in pancreatic *** together,our results,for the first time,reveal a role of CYP3A5 in glucose metabolism in pancreatic ductal adenocarcinoma and identify a novel mechanism that is a potential therapeutic target.

关键词： Cell migration CYP3A5 Glucose metabolism GLUT1 Pancreatic cancer txnip

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FOXO regulation of txnip induces ferroptosis in satellite cells by inhibiting glutathione metabolism, promoting Sarcopenia

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CELLULAR AND MOLECULAR LIFE SCIENCES 2025年第1期82卷 1-24页

作者： Maimaiti, Yasenjiang Abulitifu, Mukedasi Ajimu, Zulifeiya Su, Ting Zhang, Zhanying Yu, Zhichao Xu, Hong Peoples Hosp Xinjiang Uygur Autonomous Reg Gerontol Ctr 91 Tianchi Rd Urumqi Xinjiang Peoples R China

Aging-related sarcopenia represents a significant health concern due to its impact on the quality of life in the elderly. This study elucidates the molecular mechanisms underlying sarcopenia by employing single-cell sequencing and public transcriptome databases to compare young and aged mouse skeletal muscles. Cellular classification and pseudotime analyses differentiated cell types and their interrelationships, revealing a marked reduction in satellite cell numbers and a consistent upregulation of txnip (Thioredoxin interacting protein) across various muscle cell populations in aged mice. Further transcriptomic data integration and batch correction from the GEO (Gene Expression Omnibus) database highlighted key differentially expressed genes. The role of txnip and its transcriptional regulation by FOXO1 (Forkhead box O1) was confirmed through in vitro experiments, which demonstrated FOXO1's influence on txnip expression and its subsequent suppression of glutathione metabolism, leading to satellite cell ferroptosis. Additionally, in vivo studies showed that overexpression of txnip in young mice's muscle tissues significantly reduced muscle mass, suggesting its potential role in the initiation of sarcopenia. Our findings suggest that FOXO1-mediated regulation of txnip and the disruption of glutathione metabolism are central to the process of sarcopenia, offering new insights into its pathogenesis.

关键词： Sarcopenia Single-cell sequencing txnip FOXO1 Muscle satellite cells Ferroptosis

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Exosomal OIP5-AS1 attenuates cerebral ischemia-reperfusion injury by negatively regulating txnip protein stability and inhibiting neuronal pyroptosis

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INTERNATIONAL IMMUNOPHARMACOLOGY 2024年 127卷 111310页

作者： Li, Zhongchen Pang, Yuejiu Hou, Lei Xing, Xiaohui Yu, Fuhua Gao, Mingxu Wang, Jiyue Li, Xueyuan Zhang, Liyong Xiao, Yilei Liaocheng Peoples Hosp Dept Neurosurg Liaocheng 252000 Shandong Peoples R China Shandong Univ Dept Neurosurg Qilu Hosp Jinan 250063 Shandong Peoples R China Shandong First Med Univ Prov Hosp Dept Healthcare Neurol Jinan 250021 Shandong Peoples R China Liaocheng Peoples Hosp Dept Neurosurg 67 Dongchang West Rd Liaocheng 252000 Shandong Peoples R China

Background: Cerebral ischemia-reperfusion injury (CIRI) can cause neuronal apoptosis and lead to irreversible brain injury. Numerous lncRNAs have been reported to play important roles in CIRI, but it is unclear whether these lncRNAs can function through exosomes. Methods: In this study, we utilized the middle cerebral artery occlusion/reperfusion (MCAO/R) animal model and the oxygen-glucose deprivation/ reoxygenation (OGD/R) cell model. RNA sequencing was performed to screen for differentially expressed lncRNAs in M2 microglia-derived exosomes (M2-Exos). RNA pull-down, RNA immunoprecipitation, co-immunoprecipitation and ubiquitination assays were used to explore the molecular mechanism of OIP5-AS1 in alleviating CIRI. Results: M2-Exos could alleviate nerve injury and pyroptosis after CIRI in vitro and in vivo. OIP5-AS1 was found to be significantly up-regulated in M2-Exos and down-regulated in OGD/R neurons, MCAO/R mice and ischemic stroke patients. In MCAO/R mice, OIP5-AS1 could reduce cerebral infarct size, cerebral edema and mNSS scores, and inhibit the expression levels of pyroptosis-related proteins in brain tissue. txnip was confirmed to be a reliable binding protein of OIP5-AS1. OIP5-AS1 overexpression significantly attenuated MCAO/R-induced upregulation of txnip at the protein level, but not at the mRNA level. OIP5-AS1 promoted the txnip degradation process and increased the ubiquitination of txnip. ITCH could bind to txnip. ITCH overexpression or knockdown did not alter the mRNA level of txnip, but negatively regulated txnip expression at the protein level. ITCH accelerated the degradation and ubiquitination of txnip, which could be attenuated by OIP5-AS1 knockdown. OIP5-AS1 could improve neuronal damage and inhibit neuronal pyroptosis through txnip. Conclusions: M2-Exo-derived OIP5-AS1 can induce txnip ubiquitination and degradation by recruiting ITCH, negatively regulate txnip protein stability, inhibit neuronal pyroptosis, and attenuate CIRI.

关键词： Cerebral ischemia reperfusion injury M2 microglial exosomes Pyroptosis OIP5-AS1 txnip

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METTL14 drives growth and metastasis of non-small cell lung cancer by regulating pri-miR-93-5p maturation and txnip expression

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GENES & GENOMICS 2024年第2期46卷 213-229页

作者： Qian, Shuai Liu, Jun Liao, Wenliang Wang, Fengping Wenzhou Med Univ Quzhou Affiliated Hosp Quzhou Peoples Hosp Dept Clin Lab 100 Minjiang Ave Quzhou 324000 Zhejiang Peoples R China

BackgroundNon-small cell lung cancer (NSCLC) is a prevalent and aggressive malignancy responsible for a significant number of cancer-related deaths worldwide. Unraveling the molecular mechanisms governing NSCLC growth and metastasis is crucial for the identification of novel therapeutic targets and the development of effective anti-cancer strategies. One such mechanism of interest is the involvement of METTL14, an RNA methyltransferase implicated in various cellular processes, in NSCLC *** objective of this study was to investigate the role of METTL14 in NSCLC development and metastasis and to elucidate the underlying molecular mechanisms. By understanding the impact of METTL14 on NSCLC pathogenesis, the study aimed to identify potential avenues for targeted therapies in NSCLC *** used bioinformatics and high-throughput transcriptome sequencing analyses to screen regulatory mechanisms affecting NSCLC. The Kaplan-Meier method assessed the correlation between METTL14 expression and the prognosis of NSCLC patients. The effects of manipulated METTL14 on malignant phenotypes of NSCLC cells were examined by colony formation assay, flow cytometry, scratch assay, and Transwell assay. The tumorigenic capacity and metastatic potential of NSCLC cells in vivo were evaluated in nude ***14 was overexpressed in NSCLC tissues and cell lines. Its high expression indicated a poor prognosis for NSCLC patients. METTL14 silencing promoted apoptosis and repressed proliferation, migration, and invasion of NSCLC cells. miR-93-5p targeted and inhibited txnip. METTL14 increased miR-93-5p expression and matured pri-miR-93-5p through m6A alteration to inhibit txnip, thereby inhibiting NSCLC cell apoptosis. By controlling the miR-93-5p/txnip axis, METTL14 increased the tumorigenic potential and lung metastasis of NSCLC cells in nude *** study revealed a role for METTL14 in the contribution to NSCLC development and metastasis and

关键词： Non-small cell lung cancer m6A methyltransferase METTL14 m6A modification Pri-miR-93-5p miR-93-5p txnip

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Ginsenoside Rg1 improves hypoxia-induced pulmonary vascular endothelial dysfunction through txnip/NLRP3 pathway-modulated mitophagy

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JOURNAL OF GINSENG RESEARCH 2025年第1期49卷 80-91页

作者： Zhang, Ru Lu, Meili Ran, Chenyang Niu, Linchao Qi, Qi Wang, Hongxin Jinzhou Med Univ Key Lab Cardiovasc & Cerebrovascular Drug Res Liao Jinzhou Peoples R China

Background: Vascular endothelial dysfunction (VED) is one of the main pathogenic events in pulmonary arterial hypertension (PAH). Previous studies have demonstrated that the ginsenoside Rg1 (Rg1) can ameliorate PAH, but the mechanism by which Rg1 affects pulmonary VED in hypoxia-induced PAH remains unclear. Methods: Network pharmacology, molecular docking and other experiments were used to explore the mechanisms by which Rg1 affects PAH. A PAH mouse model was established via hypoxia combined with the vascular endothelial growth factor (VEGFR) inhibitor su5416 (SuHx), and a cell model was established via hypoxia. The functions of Rg1 in VED, oxidative stress, inflammation, mitophagy, and txnip and NLRP3 expression were examined. Results: In hypoxia-induced VED, progressive exacerbation of oxidative stress, inflammation, and mitophagy were observed, and were associated with elevated txnip and NLRP3 expression in vivo and in vitro. Rg1 improved hypoxia-induced impaired endothelium-dependent vasodilation and increased nitric oxide (NO) and endothelial NO synthase (eNOS) expression. Rg1, SRI37330 (a txnip inhibitor), MCC950 (an NLRP3 inhibitor), and Liensinine (a mitophagy inhibitor) attenuated oxidative stress, inflammation, and mitophagy by reducing the expression of txnip and NLRP3 in mice and cells. Furthermore, the combination of SB203580 (a mitophagy agonist) with Rg1 disrupted the protective effect of Rg1 on hypoxia-induced pulmonary artery and human pulmonary artery endothelial cells (HPAECs). Conclusion: Rg1 improves hypoxia-induced pulmonary vascular endothelial dysfunction through txnip/NLRP3 pathway-modulated oxidative stress, inflammation and mitophagy.

关键词： Ginsenoside Rg1 Vascular endothelial dysfunction Pulmonary arterial hypertension txnip NLRP3

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Inhibition of the Foxo3/txnip Axis Alleviates Ventilator-Induced Diaphragmatic Dysfunction by Downregulating MuRF1

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APPLIED BIOCHEMISTRY AND BIOTECHNOLOGY 2025年 1-20页

作者： Shen, Jia Ma, Xiaojun Ningxia Med Univ Gen Hosp Dept Intens Care Unit 804 Shengli South St Yinchuan 750002 Peoples R China Peoples Hosp Ningxia Hui Autonomous Reg Dept Orthoped Yinchuan 750004 Peoples R China

Ventilator-induced diaphragm dysfunction (VIDD) is one of the main causes of weaning from mechanical ventilation (MV). The forkhead box O3 (Foxo3) has been identified as being involved in regulating the contractile function of skeletal muscle. This study aimed to figure out the regulatory role and mechanism of Foxo3 on VIDD. The mouse myoblast C2C12 cells were stimulated using different intensities of stress to mimic the in-vitro VIDD model. 3- (4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and TdT-mediated dUTP nick end labeling (TUNEL) assays were applied to check cell viability and apoptosis, respectively. Cellular inflammation and oxidative stress levels were evaluated by measuring cellular inflammatory factors (IL-1 beta and TNF-alpha) and oxidative stress markers (SOD and MDA). The release of oxygen species (ROS) was assayed by cellular immunofluorescence. The expression of apoptosis-associated proteins (Bax and Bcl-2), Gpx4, Slc7a11, Ptgs2, Foxo3, txnip, Murf1, Atrogin-1, Nlrp3, Asc, and Caspase1 was gauged using Western blot. The rats with or without MV therapy were treated with the Foxo3 inhibitor Carbenoxolone (CBX) to characterize the impact of Foxo3 on VIDD. Stress stimulation dampened myogenic cell viability, boosted apoptosis, inflammation, oxidative stress, and ROS release, and activated the expression of Foxo3 and txnip pathways. Overexpression of txnip or Murf1 lessened the protective effect of FOxO3 inhibition on myoblasts. Downregulation of txnip or Murf1 mitigated myoblasts dysfunction that was induced by Foxo3 overexpression. In vivo, inhibition of Foxo3 mitigated MV-induced diaphragmatic atrophy and reduced contractility, inflammation, and oxidative stress in rats. Inhibition of Foxo3 eased VIDD by downregulating txnip and Murf1.

关键词： Foxo3 txnip MuRF1 Myoblast Ventilator-induced diaphragm dysfunction

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Hydrogel PCDME creates pancreatic cancer stem cells in OXPHOS metabolic state with txnip elevation

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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 2025年 751卷 151416页

作者： Aoki, Yuma Wang, Lei Tsuda, Masumi Saito, Yusuke Kubota, Takenori Oda, Yoshitaka Hirano, Satoshi Gong, Jian Ping Tanaka, Shinya Hokkaido Univ Grad Sch Med Dept Canc Pathol Sapporo Japan Hokkaido Univ Grad Sch Med Dept Gastroenterol Surg 2 Sapporo Japan Hokkaido Univ Fac Med Dept Canc Pathol Sapporo Japan Hokkaido Univ Inst Chem React Design & Discovery WPI ICReDD World Premier Int Res Ctr Initiat Sapporo Japan Hokkaido Univ Hosp Div Clin Canc Genom Sapporo Japan Hokkaido Univ Fac Med Dept Gastroenterol Surg 2 Sapporo Japan Hokkaido Univ Fac Adv Life Sci Sapporo Japan Hokkaido Univ Hosp Dept Surg Pathol Sapporo Japan

Pancreatic cancer is known as one of the poor prognostic cancers, and the most of patients are unable to undergo radical resection due to local progression or distant metastasis at initial diagnosis. In spite of the advancements in surgery and chemotherapy, there are many cases of recurrence after surgery or chemoradiotherapy mainly due to the presence of cancer stem cells (CSCs). CSCs are potential therapeutic target, but current issue is that an identification of CSCs is difficult since they are only present in a small number of tumor cells. Here we demonstrate that hydrogel PCDME can rapidly induce pancreatic cancer cell spheroids with elevated levels of stem cell markers including Sox2, Oct3/4, and Nanog, and the growth rate was reduced. CSCs showed activation of YAP/TAZ signaling, and microarray analysis showed markedly elevated expression of thioredoxin-interacting protein (txnip). Primary pancreatic cancer cells also increased txnip in addition to stemness markers on gel. In metabolic analysis, CSCs showed a shift of energy production from glycolysis to oxidative phosphorylation (OXPHOS). Furthermore, knockdown of txnip on PCDME gel using shRNAs decreased growth speed and in vivo tumorigenicity, suggesting that txnip may be involved in CSCs induction.

关键词： Pancreatic cancer Cancer stem cells OXPHOS txnip Quiescent Hydrogel HARP

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LncRNA AC005165.1 Alleviates IL-1β-Induced Osteoarthritis via miR-199a-3p/txnip Axis

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BIOCHEMICAL GENETICS 2025年第2期63卷 1551-1565页

作者： Gu, Xi Xie, Tian Wuhan Hosp Tradit Chinese Med Dept Orthoped 49 Lihuangpi Rd Wuhan 430014 Peoples R China

Osteoarthritis (OA) is a chronic musculoskeletal disease and often causes impaired joint mobility and disability. Long noncoding RNAs (lncRNAs) play pivotal roles in OA development. This study was done to explore the role and mechanism of the lncRNA AC005165.1 in the cell model of interleukin-1 beta (IL)-1 beta-treated chondrocytes. This study recruited 20 surgically treated OA patients and 12 age- and gender-matched controls. Real-time reverse transcription quantitative polymerase chain reaction was used to examine the expression levels of AC005165.1, miR-199a-3p, and thioredoxin-interacting protein (txnip) in articular cartilage of patients and IL-1 beta-treated human chondrocytes. Cell viability and apoptosis were evaluated by cell counting kit-8 and flow cytometry assays, respectively. The protein levels of inflammatory cytokines were assessed by western blotting. Enzyme-linked immunosorbent assay was conducted to detect the concentrations of the inflammatory cytokines in chondrocytes. Luciferase reporter assay and Pearson's correlation analysis were used for analyzing the interaction and the correlation among AC005165.1, miR-199a-3p, and txnip. AC005165.1 expression was downregulated in cartilage of OA patients and chondrocytes treated with IL-1 beta, compared to that in the control groups. AC005165.1 knockdown increased apoptosis and aggravated inflammatory response in IL-1 beta-treated chondrocytes. AC005165.1 interacted with miR-199a-3p, and txnip was targeted by miR-199a-3p. In rescue assay, miR-199a-3p knockdown and txnip overexpression significantly reduced apoptosis and mitigated inflammatory response in IL-1 beta-treated chondrocytes with AC005165.1 knockdown. AC005165.1 knockdown promoted apoptosis and inflammatory response in IL-1 beta-treated chondrocytes via the miR-199a-3p/txnip axis.

关键词： AC005165.1 Apoptosis Inflammation miR-199a-3p txnip

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