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METTL3-mediated m6A modification of pri-miR-148a-3p affects prostate cancer progression by regulating txnip

ENVIRONMENTAL TOXICOLOGY 2023年第10期38卷 2377-2390页

作者： Li, Guoqiang Liu, Junwen Wang, Yinhuai Liu, Hanqi Fu, Jianhan Zhao, Yuanqiao Huang, Yanqing Cent South Univ Xiangya Hosp 2 Dept Urol Changsha Peoples R China Cent South Univ Xiangya Sch Med Dept Histol & Embryol 172 Tongzipo Rd Changsha 410000 Peoples R China

ObjectiveProstate cancer (PCa) severely affects men's health worldwide. The mechanism of methyltransferase-like 3 (METTL3) in affecting PCa development by regulating miR-148a-3p expression via N6-methyladenosine (m6A) modification was investigated. MethodsMETTL3, miR-148a-3p, and thioredoxin interacting protein (txnip) levels were determined using RT-qPCR and Western blotting. The m6A modification level of miR-148a-3p was observed by Me-RIP assay. Bioinformatics website predicted miR-148a-3p and txnip levels in PCa and their correlation, and the binding site between them was verified by dual-luciferase assay. The proliferation, migration, invasion, and apoptosis of PCa cells were examined by CCK-8 assay, Transwell assay, and flow cytometry. A transplanted tumor model was established in nude mice to observe the tumor growth ability, followed by determination of txnip levels in tumor tissues by immunohistochemistry. ResultsMETTL3 interference restrained the proliferation, migration, and invasion and promoted apoptosis of PCa cells. METTL3 up-regulated miR-148a-3p by promoting the m6A modification of pri-miR-148a-3p in PCa cells. miR-148a-3p overexpression nullified the inhibitory actions of silencing METTL3 on PCa cell growth. miR-148a-3p facilitated PCa cell growth by silencing txnip. METTL3 interference inhibited tumor growth by down-regulating miR-148a-3p and up-regulating txnip. ConclusionMETTL3 promoted miR-148a-3p by mediating the m6A modification of pri-miR-148a-3p, thereby targeting txnip, interfering with METTL3 to inhibit the proliferation, migration and invasion of PCa cells, promote apoptosis, and inhibit tumor growth in nude mice.

关键词： epigenetics m6A METTL3 miR-148a-3p pri-miR-148a-3p prostate cancer txnip

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Ginsenoside Compound K Ameliorates Osteoarthritis by Inhibiting the Chondrocyte Endoplasmic Reticulum Stress-Mediated IRE1α-txnip-NLRP3 Axis and Pyroptosis

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JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY 2023年第3期71卷 1499-1509页

作者： Tian, Yicheng Feng, Xinyuan Zhou, Zimo Qin, Sen Chen, Senxiang Zhao, Jihui Hou, Jianglin Liu, Da China Med Univ Dept Orthoped Shengjing Hosp Shenyang 110004 Liaoning Peoples R China

Osteoarthritis (OA) is a common joint disease, and studies have reported that the endoplasmic reticulum stress (ERS) in chondrocytes caused by the cartilage tissue damage could mediate the activation of Nod-like receptor protein 3 (NLRP3) inflammasomes through inositol-requiring enzyme 1 alpha (IRE1a) and thioredoxin interacting protein (txnip). Ginsenoside compound K (CK) has an inhibitory effect on IRE1a activation. However, the role of IRE1 alpha-txnip and its interaction with CK are still unclear. In this study, we examined the role and mechanism of action of CK in OA. We found that CK ameliorated OA and ERS in IL-1 beta-treated chondrocytes and a monoiodoacetate-induced rat OA model. The effect of CK on inflammation, pyroptosis, and ERS was blocked by the ERS inducer tunicamycin. In conclusion, CK hindered OA progression by inhibiting the ERS-IRE1atxnip-NLRP3 axis. Overall, our data indicate that CK could be useful in the treatment of OA and other chronic inflammatory diseases.

关键词： compound K osteoarthritis endoplasmic reticulum stress txnip

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Epigallocatechin-3-Gallate Ameliorates Diabetic Kidney Disease by Inhibiting the txnip/NLRP3/IL-1β Signaling Pathway

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FOOD SCIENCE & NUTRITION 2024年第12期12卷 10800-10815页

作者： Wang, Yinghui Wang, Qimeng Wang, Mingming Wang, Xueling Liu, Qingzhen Lv, Shasha Nie, Huibin Liu, Gang Shandong Univ Multidisciplinary Innovat Ctr Nephrol Dept Nephrol Hosp 2 Jinan Shandong Peoples R China Shandong Univ Nephrol Res Inst Jinan Shandong Peoples R China Chengdu Univ TCM Chengdu Peoples Hosp 1 Dept Nephrol Integrated TCM & Western Med Hosp Chengdu Sichuan Peoples R China Shandong Univ Key Lab Reprod Endocrinol Minist Educ Jinan Shandong Peoples R China

Recent research indicates that the activation of the NLRP3 inflammasome is crucial in the development of diabetic kidney disease (DKD). Epigallocatechin-3-gallate (EGCG), the predominant catechin in green tea, has been noted for its anti-inflammatory properties in DKD. However, the specific mechanisms are not yet fully understood. In this study, our objective was to explore the effects of EGCG on podocytes and in diabetic kidney disease (DKD) mice and investigate how EGCG modulates the txnip/NLRP3/IL-1 beta signaling pathway in DKD, both in podocytes and animal models. In vitro, we co-cultured podocytes with EGCG and detected the viability, apoptosis, inflammation and the txnip/NLRP3/IL-1 beta signaling pathway. In vivo, DKD mice were given EGCG via oral gavage, followed by evaluations of renal function, inflammation, and the aforementioned signaling pathway. Our findings revealed that oxidative stress, inflammatory cytokines, and the txnip/NLRP3/IL-1 beta pathway were upregulated in podocytes exposed to high glucose (HG) and in the kidneys of DKD mice. However, EGCG treatment reduced the expression of the NLRP3 inflammasome and its associated proteins, including txnip, ASC, caspase-1, and IL-1 beta, as well as the levels of ROS and inflammatory factors such as TNF-alpha, IL-6, and IL-18. Furthermore, in vivo, EGCG improved kidney function, reduced albuminuria and body weight, and alleviated renal pathological damage. In summary, our study suggests that EGCG mitigates inflammation in podocytes and DKD through the txnip/NLRP3/IL-1 beta signaling pathway, indicating potential benefits of EGCG or green tea in managing DKD.

关键词： diabetic kidney disease EGCG green tea inflammation NLRP3 txnip

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Resveratrol improves diabetes-induced cognitive dysfunction in part through the miR-146a-5p/txnip axis

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KAOHSIUNG JOURNAL OF MEDICAL SCIENCES 2023年第4期39卷 404-415页

作者： Hu, Ying Zhang, Qin Wang, Jian-Cheng Wang, Jiao Liu, Ying Zhu, Ling-Yan Xu, Ji-Xiong Nanchang Univ Affiliated Hosp 1 Dept Endocrinol & Metab 17 Yongwaizheng St Nanchang 330006 Jiangxi Peoples R China Jiangxi Clin Res Ctr Endocrine & Metab Dis 17 Yongwaizheng St Nanchang 330006 Jiangxi Peoples R China Natl Clin Res Ctr Metab Dis Jiangxi Branch 17 Yongwaizheng St Nanchang 330006 Jiangxi Peoples R China Med Ctr Anesthesiol & Pain Dept Anesthesiol & Operat Med Nanchang Peoples R China

Resveratrol (RSV) has been shown to have a neuroprotective effect in various central nervous system disorders, although the role of RSV in diabetes-induced cognitive dysfunction is still not fully elucidated. Here, we investigated whether RSV improved diabetes-related cognitive dysfunction in vivo and in vitro. We induced a rat diabetic model with a high-fat and high-sucrose diet followed by intraperitoneal injection of streptozotocin and a diabetic neuron cell model by stimulation with high levels of glucose. We observed that RSV improved impairment in spatial learning and memory in the Morris water maze test (MWM) and novel object recognition test (ORT) in diabetic rats. RSV reversed the reduced miR-146a-5p and upregulated thioredoxin-interacting protein (txnip) and inhibited the diabetes-induced increase in interleukin (IL)-1 beta and tumor necrosis factor (TNF)-alpha levels in vivo and in vitro. RSV also inhibited diabetes-induced endoplasmic reticulum stress (ESR) by reducing ESR-related protein expression in vivo and in vitro. Moreover, inhibition of miR-146a-5p partially abolished the protective effects of RSV in HG-treated primary neurons. Additionally, we used starBase to predict that miR-146a-5p interacts with txnip, which we then verified using a luciferase reporter gene assay. We further observed that miR-146a-5p regulates the mRNA and protein expression of txnip in vitro, indicating that the miR-146a-5p/txnip axis is involved in the regulation of cognitive dysfunction in a rat diabetic model. Collectively, these results demonstrate that RSV plays a neuroprotective role in diabetes-associated cognitive dysfunction at least in part through regulation of the miR-146a-5p/txnip axis.

关键词： diabetes-induced cognitive dysfunction miR-146a-5p resveratrol txnip

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ChREBP-?/txnip aggravates frucose-induced renal injury through triggering ferroptosis of renal tubular epithelial cells

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FREE RADICAL BIOLOGY AND MEDICINE 2023年 199卷 154-165页

作者： Guo, Hang Fang, Ting Cheng, Ying Li, Ting Qu, Jing-Ru Xu, Chao-fei Deng, Xiao-qing Sun, Bei Chen, Li -Ming Tianjin Med Univ Chu Hsien I Mem Hosp Tianjin Key Lab Metab Dis NHC Key Lab Hormones & Dev Tianjin 300134 Peoples R China Tianjin Med Univ Tianjin Inst Endocrinol Tianjin 300134 Peoples R China

High fructose intake is an essential risk factor for kidney injury. However, the specific mechanism underlying high fructose-induced kidney injury remains unclarified. Carbohydrate response element-binding protein (ChREBP) is a key transcriptional activator that regulates fructose metabolism. ChREBP-beta exhibits sustained activity due to the lack of a low glucose inhibitory domain, and is thus described as the active form of ChREBP. In this study, a mouse model with specific overexpression of ChREBP-beta in the renal tubule was established by using the Cre/LoxP method. Quantitative proteomic analysis and experimental verification results suggest that ChREP-beta overexpression leads to ferroptosis of renal tubular epithelial cells and kidney injury. ChREPB-beta promotes the gene transcription of thioredoxin-interacting protein (txnip) and thereby increases its expression level. txnip is associated with activation of ferroptosis. txnip can initiate ferroptosis and eventually contribute to high fructose-induced renal tubular epithelial cell damage. Through down-regulating ChREBP-beta, metformin can inhibit gene transcription of txnip, attenuate high fructose-induced ferroptosis in renal tubular epithelial cells, and alleviate kidney injury. In conclusion, ChREBP-beta mediates fructose-induced ferroptosis of renal tubular epithelial cells, and metformin with a ChREBP-beta inhibitory effect may be a potential treatment for ferroptosis of renal tubular epithelial cells.

关键词： High fructose Ferroptosis Kidney injury ChREBP-? txnip

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miR-20b attenuates airway inflammation by regulating txnip and NLRP3 inflammasome in ovalbumin-induced asthmatic mice

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JOURNAL OF ASTHMA 2023年第11期60卷 2040-2051页

作者： Huang, Jieyuan Ruan, Xingya Tian, Tian Xu, Yingchen Hu, Lin Sun, Yun Nanjing Med Univ Affiliated Changzhou Peoples Hosp No 2 Dept Emergency Changzhou Peoples R China Kunshan Hosp Chinese Med Dept Pulm Dis Dept Pulm & Crit Care Med Kunshan Peoples R China Nanjing Med Univ Affiliated Changzhou Peoples Hosp No 2 Dept Pulm & Crit Care Med Changzhou Peoples R China Nanjing Med Univ Affiliated Changzhou Peoples Hosp No 2 Dept Resp & Crit Care Med Changzhou Peoples R China Nanjing Med Univ Affiliated Changzhou Peoples Hosp No 2 Dept Resp & Crit Care Med 29 Xinglong Rd Changzhou 213164 Peoples R China

ObjectivesAsthma is a chronic inflammatory disorder of the airway and is associated with pyroptosis. microRNAs (miRNAs) underlie pathogenic mechanism in asthma. This study is expected to evaluate the role of miR-20b in asthma-induced airway inflammation via regulating thioredoxin-interacting protein (txnip) and NOD-like receptor family pyrin domain containing 3 (NLRP3) *** asthmatic mouse model was established via ovalbumin (OVA) induction. Expressions of miR-20b, txnip, and NLRP3 in lung tissues were determined. Bronchial hyperresponsiveness was appraised, cells in bronchoalveolar lavage fluid were counted and categorized, and histopathological damage was observed. Levels of inflammatory and pyroptotic cytokines were measured. The binding relationship of miR-20b and txnip was testified. Co-location and interaction between txnip and NLRP3 were detected. Mice were infected with the lentivirus packaged with pcDNA3.1-txnip or pcDNA3.1-NLRP3 for joint experiments to observe the pathological changes of ***-20b was poorly expressed, while txnip and NLRP3 were highly expressed in OVA-induced mice. miR-20b overexpression attenuated airway inflammation and pyroptosis, manifested by alleviation of histopathological damage, declined numbers of total cells and inflammatory cells, lowered bronchial hyperresponsiveness, decreased levels of pro-inflammatory and pyroptotic cytokines, and increased anti-inflammatory cytokines. miR-20b targeted txnip and inhibited txnip expression, and txnip can bind to NLRP3 and upregulated NLRP3 expression. Upregulation of txnip or NLRP3 could reverse the protecting role of miR-20b overexpression in OVA-induced ***-20b inhibited txnip expression to reduce the binding of txnip and NLRP3, thus restricting pyroptosis and airway inflammation of asthmatic mice.

关键词： Asthma airway inflammation miR-20b txnip NLRP3 pyroptosis hematoxylin-eosin staining bronchoalveolar lavage fluid

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Ferulic acid relieved ulcerative colitis by inhibiting the txnip/NLRP3 pathway in rats

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CELL BIOLOGY INTERNATIONAL 2023年第2期47卷 417-427页

作者： Yu, Sheng Qian, Haihua Zhang, Dan Jiang, Zhenzhen Anhui Med Univ Affiliated Hosp 1 Dept Tradit Chinese Med Hefei Anhui Peoples R China Jiangsu Prov Hosp Tradit Chinese Med Dept Anorectal Dis 155 Hanzhong Rd Nanjing 210000 Jiangsu Peoples R China

Ulcerative colitis (UC) is a disorder of the bowel that is characterized by a chronic inflammatory response. The traditional Chinese herbal medicine ferulic acid (FA) is known for its antioxidant, antiapoptotic, and antiinflammatory properties. However, its role in UC is still unclear. Thus, the current study was conducted to investigate the role of FA in UC. Rats were treated with 2,4,6-triabrobenzene sulfonic acid to induce UC and subjected to FA. Human intestinal microvascular endothelial cells (HIMECs) were treated with tumor necrosis factor-alpha (TNF-alpha) and pretreated with FA. Pathological changes in colonic tissues were visualized via hematoxylin-eosin staining. Enzyme linked immunosorbent assay was conducted to detect interleukin (IL)-6, IL-12, and IL-1 beta levels. Cell morphology was visualized by using a microscope, and viability was detected by using MTT. The percentage of apoptosis was detected via flow cytometry. Western blot analysis was performed to detect the expression of the apoptosis-related proteins thioredoxin-interacting protein (txnip) and NOD-like receptor pyrin domain-containing 3 (NLRP3). In vivo FA administration alleviated intestinal injury in UC rats and inhibited inflammatory factor levels (IL-6, IL-12, and IL-1 beta), apoptosis-related protein expression (caspase-1 and caspase-3) and the txnip/NLRP3 signaling pathway. In vitro, TNF-alpha treatment reduced HIMEC viability, increased cell apoptosis and inflammatory factor levels and activated the txnip/NLRP3 signaling pathway. However, FA treatment restored the viability of HIMECs, reduced TNF-alpha-induced cell apoptosis and inflammation and inhibited the txnip/NLRP3 signaling pathway. Furthermore, with increasing FA concentration, the effects were stronger. In summary, FA inhibits the inflammatory injury of endothelial cells in ulcerative colitis or alleviates TNF-alpha-induced HIMEC injury by inhibiting the txnip/NLRP3 signaling pathway.

关键词： ferulic acid inflammatory NLRP3 txnip ulcerative colitis

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Circ_0001806 relieves LPS-induced HK2 cell injury by regulating the expression of miR-942-5p and txnip

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JOURNAL OF BIOENERGETICS AND BIOMEMBRANES 2023年第4期55卷 301-312页

作者： Chen, Mingjin Zhang, Lefeng Lishui Second Peoples Hosp Dept Emergency Med 69 North Ring Rd Lishui City 323000 Zhejiang Peoples R China

Sepsis is a systemic inflammatory disease that can cause a variety of diseases, including septic acute kidney injury (AKI). Circular RNAs (circRNAs) are believed to be involved in the development of this disease. This study aims to clarify the function of circ_0001806 in lipopolysaccharide (LPS)-induced HK2 cell model and its related mechanisms. Circ_0001806 was up-regulated in septic AKI serum specimens and LPS-induced HK2 cells. Circ_0001806 knockdown promoted cell proliferation and restrained apoptosis, inflammation and oxidative stress in LPS-induced HK2 cells. In mechanism, circ_0001806 can be used as a sponge for miR-942-5p, and miR-942-5p can directly target txnip. Functional experiments revealed that the miR-942-5p inhibitor could reverse the alleviating effect of circ_0001806 knockdown on LPS-induced HK2 cell injury, and txnip addition can also reverse the inhibitory effect of miR-942-5p overexpression on LPS-induced HK2 cell injury. In addition, circ_0001806 regulated txnip expression through sponging miR-942-5p. Besides, exosome-derived circ_0001806 was upregulated in LPS-induced HK2 cells, while was downregulated by GW4869. The results showed that circ_0001806 knockdown could reduce LPS-induced HK2 cell injury by regulating txnip expression via targeting miR-942-5p, indicating that circ_0001806 might be an important biomarker for alleviating sepsis-related AKI. This might provide therapeutic strategy for the treatment of sepsis.

关键词： Sepsis AKI circ_0001806 miR-942-5p txnip

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Chrysophanol exerts a protective effect against Aβ25-35-induced Alzheimer's disease model through regulating the ROS/txnip/NLRP3 pathway

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INFLAMMOPHARMACOLOGY 2023年第3期31卷 1511-1527页

作者： Zhang, Meng Ding, Zhi-xian Huang, Wei Luo, Jing Ye, Shu Hu, Sheng-lin Zhou, Peng Cai, Biao Anhui Univ Chinese Med Dept Integrated Tradit Chinese & Western Med Key Lab Xinan Med Minist Educ Hefei 230012 Peoples R China

BackgroundThe primary pathogenic factors of Alzheimer's disease (AD) have been identified as oxidative stress, inflammatory damage, and apoptosis. Chrysophanol (CHR) has a good neuroprotective effect on AD, however, the potential mechanism of CHR remains *** this study, we focused on the ROS/txnip/NLRP3 pathway to determine whether CHR regulates oxidative stress and ***-galactose and A beta(25-35) combination were used to build an in vivo model of AD, and the Y-maze test was used to evaluate the learning and memory function of rats. Morphological changes of neurons in the rat hippocampus were observed using hematoxylin and eosin (HE) staining. AD cell model was established by A beta(25-35) in PC12 cells. The DCFH-DA test identified reactive oxygen species (ROS). The apoptosis rate was determined using Hoechst33258 and flow cytometry. In addition, the levels of MDA, LDH, T-SOD, CAT, and GSH in serum, cell, and cell culture supernatant were detected by colorimetric method. The protein and mRNA expressions of the targets were detected by Western blot and RT-PCR. Finally, molecular docking was used to further verify the in vivo and in vitro experimental *** could significantly improve learning and memory impairment, reduce hippocampal neuron damage, and reduce ROS production and apoptosis in AD rats. CHR could improve the survival rate, and reduce the oxidative stress and apoptosis in the AD cell model. Moreover, CHR significantly decreased the levels of MDA and LDH, and increased the activities of T-SOD, CAT, and GSH in the AD model. Mechanically, CHR significantly reduced the protein and mRNA expression of txnip, NLRP3, Caspase-1, IL-1 beta, and IL-18, and increase *** exerts neuroprotective effects on the A beta(25-35)-induced AD model mainly by reducing oxidative stress and neuroinflammation, and the mechanism may be related to ROS/txnip/NLRP3 signaling pathway.

关键词： Chrysophanol Alzheimer's disease ROS txnip NLRP3 pathway Oxidative stress Neuroinflammation

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Phytochemicals as potential target on thioredoxin-interacting protein (txnip) for the treatment of cardiovascular diseases

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INFLAMMOPHARMACOLOGY 2023年第1期31卷 207-220页

作者： Zhou, Peng Ma, Yao-yao Zhao, Xiao-ni Hua, Fang Anhui Univ Chinese Med Dept Integrated Tradit Chinese & Western Med Hefei Anhui Peoples R China Anhui Xinhua Univ Sch Pharm Hefei Anhui Peoples R China

Cardiovascular diseases (CVDs) are currently the major cause of death and morbidity on a global scale. Thioredoxin-interacting protein (txnip) is a marker related to metabolism, oxidation, and inflammation induced in CVDs. The overexpression of txnip is closely related to the occurrence and development of CVDs. Hence, txnip inhibition is critical for reducing the overactivation of its downstream signaling pathway and, as a result, myocardial cell damage. Due to the chemical variety of dietary phytochemicals, they have garnered increased interest for CVDs prevention and therapy. Phytochemicals are a source of medicinal compounds for a variety of conditions, which aids in the development of effective and safe txnip-targeting medications. The objective of this article is to find and virtual screen novel safe, effective, and economically viable txnip inhibitors from flavonoids, phenols, and alkaloids derived from foods and plants. The results of the docking study revealed that silibinin, rutin, luteolin, baicalin, procyanidin B2, hesperetin, icariin, and tilianin in flavonoids, polydatin, resveratrol, and salidroside in phenols, and neferine in alkaloids had the highest Vina scores, indicating that these compounds are the active chemicals on txnip. In particular, silibinin can be utilized as a lead chemical in the process of structural alteration. These dietary phytochemicals may aid in the discovery of lead compounds for the development of innovative txnip agents for the treatment of cardiovascular disease.

关键词： Cardiovascular disease txnip Flavonoids Phenols Alkaloids Molecular docking

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