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txnip contributes to induction of pro-inflammatory phenotype and caspase-3 activation in astrocytes during Alzheimer's diseases

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REDOX BIOLOGY 2023年 63卷 102735页

作者： Kim, Junhyung Lim, Jaejoon Yoo, Ik Dong Park, Samel Moon, Jong-Seok Soonchunhyang Univ Soonchunhyang Inst Med bio Sci SIMS Dept Integrated Biomed Sci Cheonan 31151 Chungcheongnam South Korea CHA Univ Bundang CHA Med Ctr Dept Neurosurg Yatap dong 59 Seongnam 13496 South Korea Soonchunhyang Univ Hosp Cheonan Dept Nucl Med Cheonan 31151 Chungcheongnam South Korea Soonchunhyang Univ Hosp Cheonan Dept Internal Med Cheonan 31151 Chungcheongnam South Korea Soonchunhyang Univ Soonchunhyang Inst Med bio Sci SIMS Dept Integrated Biomed Sci Cheonan Chungcheongnam South Korea

Neuroinflammation and oxidative stress have been implicated in the pathogenesis of Alzheimer's disease (AD). Neuroinflammation and oxidative stress are associated with neuronal death in AD. Astrocytes are linked to neuroinflammation during AD. Astrocytes are important contributors to AD progression. Although the role of thioredoxin-interacting protein (txnip) has been identified in inflammation and oxidative stress, the mechanism by which txnip regulates inflammation and oxidative stress in astrocytes during AD remains unclear. In the present study, we found that txnip gene levels were elevated in cerebral cortex of patients with AD. The protein levels of txnip were elevated in GFAP-positive astrocytes of cerebral cortex from patients with AD and APP/PS1 double-transgenic mouse model of AD. Our results showed that txnip increased expression of genes related to pro-inflammatory reactive astrocytes and pro-inflammatory cytokines and chemokines in human astrocytes. Moreover, txnip increased production of pro-inflammatory cytokines and chemokines in human astrocytes. txnip induced activation of NK-kB signaling and over-production of mitochondrial reactive oxygen species (mtROS) in human astrocytes. txnip also induced mitochondrial oxidative stress by reduction of mitochondrial respiration and ATP production in human astrocytes. Furthermore, elevated txnip levels are correlated with caspase-3 activation of GFAP-positive astrocytes in patients with AD and mouse AD. txnip induced mitochondria-dependent apoptosis via caspase-9 and caspase-3 activation in human astrocytes. These results suggest that txnip contributes to induction of pro-inflammatory phenotype and caspase-3 activation in astrocytes during AD.

关键词： txnip Astrocytes Inflammation Mitochondrial oxidative stress Caspase-3 Alzheimer 's disease

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Notoginsenoside R1 Protects against Diabetic Nephropathy through txnip-NLRP3 Signaling Pathway

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Clinical Complementary Medicine and Pharmacology 2023年第4期3卷 34-48页

作者： Chunting Zhang Renyikun Yuan Siyuan Li Guodong Huang Kaili Sun Jiaping Pan Qiuxia Liu Xiang Gao Zhijing Wang Tongyu Li Shilong Lu Jianzhen Lv Liting Huang Hongwei Gao College of Pharmacy Guangxi University of Chinese MedicineNanning 530200GuangxiChina Guangxi Engineering Technology Research Center of Advantage Chinese Development Nanning 530200GuangxiChina Guangxi International Zhuang Medicine Hospital Nanning 530200GuangxiChina The First Affiliated Hospital of Guangxi University of Chinese Medicine Nanning 530200GuangxiChina Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine Nanning 530001GuangxiChina

Background:Diabetic nephropathy(DN)is a microvascular complication of diabetes mellitus(DM).DN results from many factors,including changes in glomerular hemodynamics,oxidative stress and inflammation,and in-terstitial fibrosis and tubular *** notoginseng,a commonly used Chinese medicine,has been used in the treatment of kidney *** R1(NGR1),the main compound isolated from ***,has been reported to have a renoprotective role in ***,the therapeutic effect and mechanism of NGR1 in DN remain ***:The present study aimed to investigate the therapeutic effect and mechanism of NGR1 in ***:In this study,mouse podocytes(MPC-5 cells)and db/db mice were used to investigate the effect of NGR1 on DN in vitro and in vivo,*** glucose,renal function,inflammatory factors,and PI3K/AKT-Nrf2-NLRP3 signaling pathway proteins were ***:The study results indicated that NGR1 reversed cell viability induced by high glucose(HG,30 mM).The related mechanism results showed that NGR1 decreased oxidative stress by inhibiting reactive oxygen species(ROS)level and upregulating the expression of Nrf2,NQO1,and HO-1 via txnip *** addition,NLRP3 inflammasome and PI3K/AKT were engaged in NGR1-based protection against HG-stimulated *** db/db mice,NGR1 significantly decreased blood glucose,urine protein,urine output,blood urea nitrogen,and other parameters as well as reversed kidney injury by inhibiting oxidative stress and proinflammatory ***:Taken together,this study revealed that NGR1 exerted a significant therapeutic effect on DN both in vitro and in vivo via a mechanism related to the txnip-Nrf2 pathway and NLRP3 inflammasome,suggesting that NGR1 is a potential therapeutic option for DN.

关键词： Diabetic nephropathy NGR1 PI3K/AKT NRF2 txnip NLRP3 inflammasome

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Long non-coding RNA NEAT1 promotes lipopolysaccharide-induced injury in human tubule epithelial cells by regulating miR-93-5p/txnip axis

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MEDICAL MICROBIOLOGY AND IMMUNOLOGY 2021年第2-3期210卷 121-132页

作者： Yang, Jing Wu, Lin Liu, Shanshou Hu, Xiaomin Wang, Qianmei Fang, Liying Xijing Hosp Dept Emergency Xian Shaanxi Peoples R China Fourth Peoples Hosp Shaanxi Prov Dept Resp & Crit Care Med 512 Xianning East Rd Xian 710043 Shaanxi Peoples R China

Many long non-coding RNAs (lncRNAs) have been found to play crucial roles in sepsis-induced acute kidney injury (AKI), including lncRNA nuclear-enriched abundant transcript 1 (NEAT1). We aimed to further elucidate the functions and molecular mechanism of NEAT1 in sepsis-induced AKI. Sepsis-induced AKI cell model was established by treatment with lipopolysaccharide (LPS) in human tubule epithelial (HK2) cells. Cell viability and apoptosis were determined by Cell Counting Kit-8 (CCK-8) assay and flow cytometry, respectively. Western blot assay was performed to measure all protein levels. The concentrations of inflammatory factors were evaluated using enzyme-linked immunosorbent assay (ELISA). The expression levels of inflammatory factors, NEAT1, microRNA-93-5p (miR-93-5p), and thioredoxin-interacting protein (txnip) were measured by quantitative real-time polymerase chain reaction (qRT-PCR). The oxidative stress factors were detected using corresponding kits. The interaction between miR-93-5p and NEAT1 or txnip was predicted by bioinformatics analysis and verified by dual-luciferase reporter and RNA Immunoprecipitation (RIP) assays. NEAT1 was upregulated in serum of sepsis patients and LPS-induced HK2 cells. NEAT1 silence alleviated LPS-induced HK2 cell injury by inhibiting apoptosis, inflammation and oxidative stress. Moreover, miR-93-5p was a direct target of NEAT1, and suppression of NEAT1 weakened LPS-induced injury by upregulating miR-93-5p in HK2 cells. Furthermore, txnip was a downstream target of miR-93-5p, and miR-93-5p attenuated LPS-induced HK2 cell injury by downregulating txnip. In addition, NEAT1 regulated txnip expression by acting as a sponge of miR-93-5p. NEAT1 might aggravate LPS-induced injury in HK2 cells by regulating miR-93-5p/txnip axis, providing a potential therapeutic strategy for sepsis-associated AKI.

关键词： Sepsis Acute kidney injury NEAT1 miR-93-5p txnip

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Upregulation of txnip contributes to granulosa cell dysfunction in polycystic ovary syndrome via activation of the NLRP3 inflammasome

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MOLECULAR AND CELLULAR ENDOCRINOLOGY 2023年 561卷 111824页

作者： Wang, Ying Yang, Jiyu Wang, Yu Chen, Yao Wang, Yiran Kuang, Hongying Feng, Xiaoling Heilongjiang Univ Chinese Med Affiliated Hosp 1 Dept Gynecol 2 Harbin Peoples R China Heilongjiang Univ Chinese Med Grad Sch Harbin Peoples R China Heilongjiang Univ Chinese Med Sch Pharm Harbin Peoples R China

Polycystic ovary syndrome (PCOS) is a complex endocrine disease. Thioredoxin-interacting protein (txnip) promotes oxidative stress and triggers inflammation. Herein, we investigated the role and potential mechanism of txnip in PCOS. In a mouse model of dehydroepiandrosterone (DHEA)-induced PCOS, we found that txnip was upregulated in the ovaries, especially in granulosa cells (GCs). txnip was also upregulated in testosterone (T)-treated GCs in vitro. Knockdown of txnip by lentivirus-constructed shRNA attenuated T-induced GC injury and oxidative stress, as well as inflammation and the NLRP3 inflammasome. The mechanism by which txnip promotes inflammation may involve txnip dissociation from the txnip-TRX complex and binding to NLRP3 to form the inflammasome. Additionally, we verified that knockdown of txnip ameliorated ovarian injury and inflammation in mice with DHEA-induced PCOS in vivo. Collectively, we demonstrated that txnip is involved in GC inflammation by promoting NLRP3 inflammasome activation in PCOS.

关键词： txnip PCOS Granulosa cells NLRP3 inflammasome

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硫氧还原蛋白互作蛋白txnip在胚胎干细胞中抑制早期胚胎基因表达

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南开大学学报（自然科学版） 2024年第3期57卷 26-29,34页

作者：李晓敏周莎吕鑫屹南开大学药物化学生物学全国重点实验室天津300350

胚胎干细胞是一种具有高发育潜能的多能干细胞.虽然胚胎干细胞中有极少量细胞高表达2细胞早期胚胎相关基因,但是这些2细胞基因却在大部分胚胎干细胞中被沉默.2细胞胚胎相关基因被哪些因子所沉默仍不完全清楚.发现硫氧还原蛋白互作蛋白Tx... 详细信息

胚胎干细胞是一种具有高发育潜能的多能干细胞.虽然胚胎干细胞中有极少量细胞高表达2细胞早期胚胎相关基因,但是这些2细胞基因却在大部分胚胎干细胞中被沉默.2细胞胚胎相关基因被哪些因子所沉默仍不完全清楚.发现硫氧还原蛋白互作蛋白txnip是胚胎干细胞中抑制2细胞早期胚胎标志基因如Zscan4与MERVL的关键因素.使用shRNA干扰txnip的表达或者用CRISPR/Cas9敲除txnip不影响胚胎干细胞多能性维持却可以激活Zscan4与MERVL等2细胞早期胚胎标志基因的表达.为后续研究txnip在胚胎干细胞中的作用机制奠定了基础.

关键词：胚胎干细胞基因敲除 txnip 2细胞基因

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Pharmacological activation of pyruvate kinase M2 reprograms glycolysis leading to txnip depletion and AMPK activation in breast cancer cells

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CANCER & METABOLISM 2021年第1期9卷 5页

作者： Almouhanna, Fadi Blagojevic, Biljana Can, Suzan Ghanem, Ali Woelfl, Stefan Heidelberg Univ Inst Pharm & Mol Biotechnol Neuenheimer Feld 364 D-69120 Heidelberg Germany

BackgroundAerobic glycolysis, discovered by Otto Warburg, is a hallmark of cancer metabolism even though not yet fully understood. The low activity of the cancerous pyruvate kinase isozyme (M2) is thought to play an important role by facilitating the conversion of glycolytic intermediates to other anabolic pathways to support tumors' high proliferation *** breast cancer cell lines representing different molecular subtypes were used in this study where real time measurements of cellular bioenergetics and immunoblotting analysis of energy- and nutrient-sensing pathways were employed to investigate the potential effects of PKM2 allosteric activator (DASA-58) in glucose *** this study, we show that DASA-58 can induce pyruvate kinase activity in breast cancer cells without affecting the overall cell survival. The drug is also able to reduce txnip levels (an intracellular glucose sensor) probably through depletion of upstream glycolytic metabolites and independent of AMPK and ER signaling. AMPK shows an induction in phosphorylation (T172) in response to treatment an effect that can be potentiated by combining DASA-58 with other metabolic ***, the multifaceted metabolic reprogramming induced by DASA-58 in breast cancer cells increases their susceptibility to other therapeutics suggesting the suitability of the intracellular glucose sensor txnip as a marker of PK activity.

关键词： Pyruvate kinase M2 AMPK txnip Glycolysis Cancer metabolism Breast cancer

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High txnip expression accelerates the migration and invasion of the GDM placenta trophoblast

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BMC PREGNANCY AND CHILDBIRTH 2023年第1期23卷 235-235页

作者： Sa, Rina Ma, Jing Yang, Jie Li, Dong Fang Du, Jie Jia, Jian Chao Li, Zhi Ying Huang, Na Lamusi, A. Sha, Rula Nai, Gal Hexig, Bayar Meng, Ji Qing Yu, Lan Inner Mongolia Peoples Hosp Dept Clin Med Res Ctr Hohhot 010010 Peoples R China Mongolia Matern & Child Hlth Care Hosp Dept Clin Lab Hohhot 010000 Peoples R China Inner Mongolia Peoples Hosp Dept Gynecol & Obstet Hohhot 010010 Peoples R China Inner Mongolia Int Mongolian Hosp Dept Ophthalmol Hohhot 010000 Peoples R China Inner Mongolia Peoples Hosp Dept Pharmacol Hohhot 010000 Peoples R China Inner Mongolia Univ Sch Life Sci Dept Genet Dev & Cell Biol Hohhot 010000 Peoples R China Inner Mongolia Univ Sch Life Sci State Key Lab Reprod Regulat & Breeding Grassland Hohhot 010000 Peoples R China Inner Mongolia Peoples Hosp Dept Endocrine & Metab Dis Hohhot 010010 Peoples R China

IntroductionOur previous study has proofed the glucose sensitive gene-thioredoxin-interacting protein (txnip) expression was up in the placenta of the patients with gestational diabetes mellitus (GDM), but the pathological mechanisms underlying abnormal txnip expression in the placenta of patients with GDM is completely unclear and additional investigations are required to explain the findings we have observed. In the present study, we simulated the high txnip expression via introducing the Tet-On "switch" in vitro, approximate to its expression level in the real world, to explore the following consequence of the abnormal *** expression and localization of txnip in the placenta of GDM patients and the health control was investigated via immunofluorescent staining, western blot and RT-qPCR. Overexpression of txnip was achieved through transfecting Tet-on system to the human trophoblastic cell line-HTR-8/Svneo cell. txnip knockout was obtained via CRISPR-Cas9 method. The cell phenotype was observed via IncuCyte Imaging System and flow cytometry. The mechanism was explored via western blot and *** expression level of txnip in the GDM placenta was nearly 2-3 times higher than that in the control. The txnip located at trophoblastic cells of the placenta. When the expression of txnip was upregulated, the migration and invasion of the cells accelerated, but cell apoptosis and proliferation did not changed compared with the control group. Furthermore, the size of the Tettxnip cells became larger, and the expression level of Vimentin and p-STAT3 increased in the Tettxnip cells. All the changes mentioned above were opposite in the txnip-KO *** expression of txnip might be related to the impairment of the GDM placental function, affecting the migration and invasion of the placental trophoblast cells through STAT3 and Vimentin related pathway;thus, txnip might be the potential therapeutic target for repairing the placental dysfu

关键词： GDM Placenta txnip Migration Invasion

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DNMT1 regulates miR-20a/txnip-mediated pyroptosis of retinal pigment epithelial cells through DNA methylation

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MOLECULAR AND CELLULAR ENDOCRINOLOGY 2023年第1期577卷 112012页

作者： Xi, Xiaoting Wang, Min Chen, Qianbo Ma, Jia Zhang, Junyan Li, Yan Kunming Med Univ Affiliated Hosp 1 Dept Ophthalmol Kunming 650032 Yunnan Peoples R China Fudan Univ Eye & ENT Hosp Dept Ophthalmol Shanghai 200031 Peoples R China Shanxi Bethune Hosp Shanxi Acad Med Sci Dept Clin Epidemiol & Evidence based Med Taiyuan 030032 Peoples R China Kunming Med Univ Affiliated Hosp 1 295 Xichang Rd Kunming 650032 Yunnan Peoples R China

Background: Pyroptosis of retinal pigment epithelium (RPE) cells is associated with the etiology of diabetic retinopathy (DR). In this study, we investigated the effect of DNMT1 on RPE cell pyroptosis by regulating miR20a/txnip expression through DNA methylation. Methods: High glucose (HG)-induced ARPE-19 cells and mice were injected with streptozotocin (STZ) to generate DR cells and animal models. RT-qPCR was used to detect the expression of miR-20a, and methylation-specific PCR (MS-PCR) was used to determine the occurrence of methylation of miR-20a. The expression of pyroptosisrelated proteins (caspase-1 and NLRP3) and DNA methyltransferase (DNMT1) was detected by western blotting, and the expression of inflammatory factors (IL-1 & beta;and IL-18) was detected by ELISA. Apoptosis was detected by flow cytometry and TUNEL. HE staining was used to observe the pathological changes in retinal tissue in ***: In HG-induced DR cell models, the expression of miR-20a was significantly downregulated, while the expression of inflammatory factors (IL-1 & beta;, IL-18) and pyroptosis-associated proteins (caspase-1, NLRP3) was significantly upregulated. Transfection of miR-20a mimic can effectively reverse HG-induced pyroptosis and release of inflammatory factors. DNMT1 promotes miR-20a methylation and inhibits the expression of miR-20a. DNMT1-mediated methylation is involved in the pyroptosis process of high glucose-induced RPE cells, and silencing DNMT1 can promote the expression of miR-20a, thereby inhibiting the release of IL-1 & beta;and IL-18 and reducing the occurrence of cell pyroptosis. miR-20a targets negative regulation of txnip expression, and overexpression of txnip can effectively reverse the inhibitory effect of miR-20a on pyroptosis. The methylation inhibitor 5-AZ can inhibit the occurrence of pyroptosis and DR processes, while treatment with a miR-20a inhibitor or OE-txnip can reverse the effect of 5-AZ. Conclusion: DNMT1 promotes DNA methylation, decre

关键词： Diabetic retinopathy Pyroptosis Retinal pigment epithelium cells DNMT1 miR-20a txnip

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1,8-Cineole ameliorates diabetic retinopathy by inhibiting retinal pigment epithelium ferroptosis via PPAR-?/txnip pathways

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BIOMEDICINE & PHARMACOTHERAPY 2023年第1期164卷 114978-114978页

作者： Liu, Zhangnian Gan, Shiquan Fu, Lingyun Xu, Yini Wang, Shengquan Zhang, Guangqiong Pan, Di Tao, Ling Shen, Xiangchun Guizhou Med Univ State Key Lab Funct & Applicat Med Plants Guiyang Peoples R China Guizhou Med Univ High Efficacy Applicat Nat Med Resources Engn Ctr Dept Pharmacol Mat Med Guiyang Peoples R China Guizhou Med Univ Sch Pharmaceut Sci High Educ Key Lab Guizhou Prov Nat Med Pharmacol & Guiyang Peoples R China Guizhou Med Univ Union Key Lab Guiyang City Guizhou Med Univ Sch Pharmaceut Sci Key Lab Optimal Utilizat Nat Med Resources Guiyang Peoples R China Guizhou Med Univ Key Lab Endem & Ethn Dis Minist Educ Guiyang Peoples R China

1,8-Cineole, the main component of volatile oil in aromatic plants, has diverse pharmacological properties, including antioxidant, anti-inflammatory, and anti-cancer properties. Diabetic retinopathy (DR) is a common microvascular complication of diabetes mellitus (DM). Here, we investigated the protective effect of 1,8-cineole on DR and found that 1,8-cineole treatment could alter the expression of several genes in both high glucose (HG) -induced ARPE-19 cells and retinal tissues of DM mice, as well as inhibit ferroptosis. Subsequent investigations into the molecular mechanisms underlying this inhibition revealed that expression of thioredoxin-interacting protein (txnip) was significantly upregulated while that of peroxisome proliferator-activated receptor ? (PPAR-?) was significantly downregulated in HG-induced ARPE-19 cells, and treatment with 1,8-cineole could effectively reverse these changes. Treatment with a PPAR-? pharmacological agonist (rosiglitazone), alone or combined with 1,8-cineole, significantly inhibited the transcription of txnip and ferroptosis in HG-induced ARPE-19 cells. Conversely, pretreatment with GW9662, a PPAR-? inhibitor, upregulated the transcription and expression of txnip in HG-induced ARPE-19 cells;1,8-cineole failed to reverse this upregulated expression. To explore these relationships, we constructed a PPAR-? adenovirus shRNA to elucidate the effect of 1,8-cineole on the negative regulation of txnip by PPAR-?. Taken together, the present findings indicate that HG-induced ferroptosis in retinal tissue plays an essential role in the pathogenesis of DR, which can be ameliorated by 1,8-cineole.

关键词： 1,8-Cineole Diabetic retinopathy Retinal pigment epithelium Ferroptosis txnip PPAR-& gamma

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Caveolin-1 ameliorates acetaminophen-aggravated inflammatory damage and lipid deposition in non-alcoholic fatty liver disease via the ROS/txnip/NLRP3 pathway

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INTERNATIONAL IMMUNOPHARMACOLOGY 2023年 114卷 109558页

作者： Jiang, Xiangfu Li, Yu Fu, Dongdong You, Tingyu Wu, Shuai Xin, Jiao Wen, Jiagen Huang, Yan Hu, Chengmu Anhui Med Univ Anhui Inst Innovat Drugs Sch Pharm Anhui Prov Key Lab Major Autoimmune Dis Hefei 230032 Peoples R China Anhui Med Univ Sch Pharm Inst Liver Dis Hefei 230032 Peoples R China Minist Educ Key Lab Antiinflammatory & Immune Med Hefei 230032 Peoples R China

The overuse of acetaminophen (APAP) may cause more severe hepatotoxicity in patients with non-alcoholic fatty liver disease (NAFLD). Caveolin-1 (CAV1), is an essential regulator of metabolic function, which can alleviate liver damage by scavenging reactive oxygen species (ROS). Evidence suggests that the NOD-like receptor family pyrin domain-containing 3 (NLRP3) -mediated pyroptosis is involved in the development of NAFLD. Moreover, thioredoxin-interactive protein (txnip) activation is a key event linking ROS to NLRP3 inflammasome. However, whether CAV1 alleviates APAP-aggravated hepatotoxicity in NAFLD via the ROS/txnip/NLRP3 pathway remains unclear. An in vivo fatty liver model was established by feeding mice a high-fat diet for 56 days. Additionally, using in vitro approach, AML-12 cells were incubated with free fatty acids for 48 h and APAP was added during the last 24 h. We found that the overuse of APAP in NAFLD not only induced oxidative stress, but also increased txnip expression, NLRP3-mediated pyroptosis, and lipid deposition. In addition to inhibiting ROS generation and lipid deposition, overexpression of CAV1 reduced the elevated levels of txnip expression and NLRP3-mediated pyroptosis. However, the effect of CAV1 on txnip expression, NLRP3-mediated pyroptosis, and lipid deposition was reversed by CAV1 small interfering RNA (siRNA) intervention. Finally, N-acetyl cysteine (NAC) treatment reduced CAV1 siRNA-mediated changes in txnip expression and NLRP3-mediated pyroptosis levels. These results demonstrate that the inhibitory effect of CAV1 on NLRP3-mediated pyroptosis may be mediated through the ROS/txnip axis. Moreover, the current study provides novel mechanistic insights into the protective effects of CAV1 on APAP-aggravated hepatotoxicity in NAFLD.

关键词： Caveolin-1 Acetaminophen Pyroptosis Lipid deposition Non-alcoholic fatty liver disease ROS txnip NLRP3

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