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Luteolin alleviates sorafenib-induced ferroptosis of BRL-3A cells through modulation of the Nrf2/GPX4 signaling pathway

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Traditional Medicine Research 2024年第10期9卷 1-9页

作者： Bo-Wen Zhang Di Yang jin-tao li Mei-Hao Peng Jia-Qing liao Qi Zhao Yi-Xi Yang Qiu-Xia Lu Engineering Research Center of Sichuan-Tibet Traditional Medicinal Plant Chengdu UniversityChengdu 610106China School of Food and Biological Engineering Chengdu UniversityChengdu 610106China School of Pharmacy Chengdu UniversityChengdu 610106China

Background:Luteolin is a flavonoid chemical that exists in a variety of medicinal and edible plants and holds many biologically active properties in liver protection,anti-cancer,antioxidants,anti-inflammatory,neuroprotective,etc.According to its hepatoprotective properties,luteolin was selected to co-treat with sorafenib,one of the approved protein kinase inhibitors,to reduce sorafenib-induced normal liver cell damage.Methods:The BRL-3A cell line was treated with sorafenib to establish a liver injury model,followed by luteolin treatment.The cell viability was detected,and the mechanism of action was detected by immunofluorescence,western blotting,and real-time quantitative PCR.Results:The research findings demonstrated that luteolin could increase cystine/glutamate transporter xCT(SLC7A11)and glutathione peroxidase 4(GPX4)expression and display a chelating effect on iron,which led to increased glutathione and decreased malondialdehyde,Fe^(2+) and lipid reactive oxygen species contents in BRL-3A cells,and the sorafenib-induced mitochondrial membrane potential decrease was also inhibited.In addition,when sorafenib caused the accumulation of lipid reactive oxygen species,luteolin could help release this oxidative stress by activating nuclear factor E2-related factor 2(Nrf2)and up-regulating the expression of the associated genes heme oxygenase 1(HO-1)and quinone oxidoreductase 1(NQO1).Conclusion:Therefore,luteolin may ameliorate sorafenib-induced ferroptosis by activating the Nrf2-associated pathway without any impact on sorafenib anti-cancer activity.It can be used as an adjuvant to sorafenib to reduce liver injury in patients with hepatocellular carcinoma.

关键词： luteolin sorafenib liver injury ferroptosis Nrf2/GPX4

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The flavonoids from Pentorum chinense Pursh.mediates ferroptosis to alleviate sorafenib-induced liver injury in BRL-3A cells

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Traditional Medicine Research 2024年第2期9卷 18-26页

作者： Di Yang Bo-Wen Zhang Shan Lei jin-tao li Mei-Hao Peng Jia-Qing liao Xue Tang Qi Zhao Qiu-Xia Lu Engineering Research Center of Sichuan-Tibet Traditional Medicinal Plant Chengdu UniversityChengdu 610106China School of Food and Biological Engineering Chengdu UniversityChengdu 610106China School of Pharmacy Chengdu UniversityChengdu 610106China Chengdu Analytical Applications Center Shimadzu(China)Co.Ltd.Chengdu 610023China

Background:Drug-induced liver damage is a severe medical issue that affects people all over the world.Sorafenib has some side effects that cause liver injury.A dietary medicinal plant called Penthorum chinense Pursh.(PCP)has hepatoprotective properties.There are currently few reports on PCP’s protective impact and mechanism against sorafenib-induced liver injury.Methods:To create a liver injury model,sorafenib was administered to BRL-3A cells.Cell viability assays,immunofluorescence tests,Western blotting,real-time quantitative PCR,and high-content imaging systems were utilized to examine PCP’s effect and mechanism.Results:In this study,PCP treatment mitigated the liver damage caused by sorafenib by enhancing cell survival,lowering lipid reactive oxygen species and malondialdehyde levels,and elevating glutathione levels.In addition,PCP can enhance the protein expression of cystine/glutamate transporter xCT and glutathione peroxidase 4,reduce iron content and alleviate mitochondrial toxicity.Further mechanism studies revealed that PCP inhibited ferroptosis by promoting the production of nuclear factor E2-related factor 2 nuclear translocation and subsequently affecting target genes(HO-1 and NQO1).Conclusion:Together,PCP regulates the nuclear factor E2-related factor 2 pathway,which helps to lessen ferroptosis brought on by sorafenib.

关键词： sorafenib Pentorum chinense Pursh. ferroptosis oxidative stress Nrf2

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Ethanol extract of Herpetospermum caudigerum Wall ameliorates psoriasis-like skin inflammation and promotes degradation of keratinocyte-derived ICAM-1 and CXCL9

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Journal of Integrative Medicine 2023年第6期21卷 584-592页

作者： Ya Zhong Bo-wen Zhang jin-tao li Xin Zeng Jun-xia Pei Ya-mei Zhang Yi-xi Yang Fu-lun li Yu Deng Qi Zhao Engineering Research Center of Sichuan-Xizang Traditional Medicinal Plant Chengdu UniversityChengdu 610106Sichuan ProvinceChina Institute of Cancer Biology and Drug Discovery Chengdu UniversityChengdu 610106Sichuan ProvinceChina School of Food and Biological Engineering Chengdu UniversityChengdu 610106Sichuan ProvinceChina School of Pharmacy Chengdu UniversityChengdu 610106Sichuan ProvinceChina Key Laboratory of Clinical Genetics Affiliated Hospital of Chengdu UniversityChengdu 610106Sichuan ProvinceChina Department of Dermatology Yueyang Hospital of Integrated Traditional Chinese and Western MedicineShanghai University of Traditional Chinese MedicineShanghai 200437China School of Basic Medical Sciences Chengdu UniversityChengdu 610106Sichuan ProvinceChina

Objective:To explore whether the ethanol extract of Herpetospermum caudigerum Wall(EHC),a Xizang medicinal plant traditionally used for treating liver diseases,can improve imiquimod-induced psoriasis-like skin inflammation.Methods:Immunohistochemistry and immunofluorescence staining were used to determine the effects of topical EHC use in vivo on the skin pathology of imiquimod-induced psoriasis in mice.The protein levels of interferon-γ(IFN-γ),tumor necrosis factor-a(TNF-a),and interleukin-17A(IL-17A)in mouse skin samples were examined using immunohistochemical staining.In vitro,IFN-γ-induced HaCaT cells with or without EHC treatment were used to evaluate the expression of keratinocyte-derived intercellular cell adhesion molecule-1(ICAM-1)and chemokine CXC ligand 9(CXCL9)using Western blotting and reverse transcription-quantitative polymerase chain reaction.The protein synthesis inhibitor cycloheximide and proteasome inhibitor MG132 were utilized to validate the EHC-mediated mechanism underlying degradation of ICAM-1 and CXCL9.Results:EHC improved inflammation in the imiquimod-induced psoriasis mouse model and reduced the levels of IFN-γ,TNF-a,and IL-17A in psoriatic lesions.Treatment with EHC also suppressed ICAM-1 and CXCL9 in epidermal keratinocytes.Further mechanistic studies revealed that EHC suppressed keratinocyte-derived ICAM-1 and CXCL9 by promoting ubiquitin–proteasome-mediated protein degradation rather than transcriptional repression.Seven primary compounds including ehletianol C,dehydrodiconiferyl alcohol,herpetrione,herpetin,herpetotriol,herpetetrone and herpetetrol were identified from the EHC using ultra-performance liquid chromatography-quadrupole-time of flight-mass spectrometry.Conclusion:Topical application of EHC ameliorates psoriasis-like skin symptoms and improves the inflammation at the lesion sites.

关键词： Psoriasis Herpetospermum caudigerum wall Cytokines Degradation

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Diet high in branched-chain amino acid promotes PDAC development by USP1-mediated BCAT2 stabilization

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National Science Review 2022年第5期9卷 119-128页

作者： jin-tao li Kai-Yue li Ying Su Yuan Shen Ming-Zhu Lei Fan Zhang Miao Yin Zheng-Jun Chen Wen-Yu Wen Wei-Guo Hu Dan Su Jia Qu Qun-Ying Lei Fudan University Shanghai Cancer Center and Institutes of Biomedical Sciences Cancer Institutes Key Laboratory of Breast Cancer in ShanghaiShanghai Key Laboratory of Medical EpigeneticsInternational Co-Laboratory of Medical Epigenetics and MetabolismMinistry of Science and Technology Shanghai Medical College Fudan University State Key Laboratory of Cell Biology Shanghai Institute of Biochemistry and Cell Biology Center for Excellence in Molecular Cell ScienceChinese Academy of Sciences Cancer Research Institute Zhejiang Cancer Hospital and Key Laboratory Diagnosis and Treatment Technology on Thoracic Oncology of Zhejiang Province Department of Oncology Shanghai Medical College Fudan University State Key Laboratory of Medical Neurobiology Fudan University

BCAT2-mediated branched-chain amino acid(BCAA) catabolism is critical for pancreatic ductal adenocarcinoma(PDAC) development,especially at an early stage.However,whether a high-BCAA diet promotes PDAC development in vivo,and the underlying mechanism of BCAT2 upregulation,remain undefined.Here,we find that a high-BCAA diet promotes pancreatic intraepithelial neoplasia(PanIN)progression in LSL-KrasG12 D/+; Pdx1-Cre(KC) mice.Moreover,we screened with an available deubiquitylase library which contains 31 members of USP family and identified that USP1 deubiquitylates BCAT2 at the K229 site.Furthermore,BCAA increases USP1 protein at the translational level via the GCN2-eIF2α pathway both in vitro and in vivo.More importantly,USP1 inhibition recedes cell proliferation and clone formation in PDAC cells and attenuates pancreas tumor growth in an orthotopic transplanted mice model.Consistently,a positive correlation between USP1 and BCAT2 is found in KC;LSL-KrasG12D/+;p53flox/+;Pdx1-Cre mice and clinical samples.Thus,a therapeutic targeting USP1-BCAT2-BCAA metabolic axis could be considered as a rational strategy for treatment of PDAC and precisive dietary intervention of BCAA has potentially translational significance.

关键词： USP1 deubiquitylation BCAT2 PanIN PDAC

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Palmitoylation of MDH2 by ZDHHC18 activates mitochondrial respiration and accelerates ovarian cancer growth

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Science China(life Sciences) 2022年第10期65卷 2017-2030页

作者： Xuan Pei Kai-Yue li Yuan Shen jin-tao li Ming-Zhu Lei Cai-Yun Fang Hao-Jie Lu Hui-Juan Yang Wenyu Wen Miao Yin Jia Qu Qun-Ying Lei Fudan University Shanghai Cancer Center&Institutes of Biomedical Sciences Cancer InstitutesKey Laboratory of Breast Cancer in ShanghaiShanghai Key Laboratory of Radiation OncologyThe Shanghai Key Laboratory of Medical EpigeneticsShanghai Medical CollegeFudan UniversityShanghai 200032China Department of Oncology Shanghai Medical CollegeFudan UniversityShanghai 200032China Department of Gynecological Oncology Fudan University Shanghai Cancer CenterShanghai 200032China State Key Laboratory of Medical Neurobiology Fudan UniversityShanghai 200032China

Epithelial ovarian cancer(EOC) exhibits strong dependency on the tricarboxylic acid(TCA) cycle and oxidative phosphorylation to fuel anabolic process.Here,we show that malate dehydrogenase 2(MDH2),a key enzyme of the TCA cycle,is palmitoylated at cysteine 138(C138) residue,resulting in increased activity of MDH2.We next identify that ZDHHC18 acts as a palmitoyltransferase of MDH2.Glutamine deprivation enhances MDH2 palmitoylation by increasing the binding between ZDHHC18 and MDH2.MDH2 silencing represses mitochondrial respiration as well as ovarian cancer cell proliferation both in vitro and in vivo.Intriguingly,re-expression of wild-type MDH2,but not its palmitoylation-deficient C138 S mutant,sustains mitochondrial respiration and restores the growth as well as clonogenic capability of ovarian cancer cells.Notably,MDH2 palmitoylation level is elevated in clinical cancer samples from patients with high-grade serous ovarian cancer.These observations suggest that MDH2 palmitoylation catalyzed by ZDHHC18 sustains mitochondrial respiration and promotes the malignancy of ovarian cancer,yielding possibilities of targeting ZDHHC18-mediated MDH2 palmitoylation in the treatment of EOC.

关键词： EOC MDH2 cysteine palmitoylation ZDHHC18 glutamine

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Improvement of Bonding Strength of Horizontal Twin-Roll Cast Steel/Aluminum Clad Sheet by Electromagnetic Fields

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Acta Metallurgica Sinica(English Letters) 2018年第1期31卷 55-62页

作者： Gang Chen jin-tao li Guang-Ming Xu Key Laboratory of Electromagnetic Processing of Materials(Ministry of Education) Northeastern University School of Mechanical Materials and Mechatronic Engineering University of Wollongong

Electromagnetic field is an available online method to increase bonding strength of clad sheet manufactured by horizontal twin-roll casting （HTRC）. In this paper, an electric current pulse （ECP） and a complex field （static magnetic field （SMF） together with ECP） are exerted during HTRC of steel/aluminum clad sheet. The produced clad sheet has good appearance, and no visible defects exist at the bonding interface. The inter-diffusion zone at Fe/A1 interface in ECP and SMF＋ECP sheets is 3 and 4 μm, respectively, and the latter increases slightly compared with that in non-field sheet. The average peel strengths （APS） of ECP and SMF＋ECP sheet are 14 and 21 N/mm, respectively, which increase by 2 and 9 N/mm compared with 12 N/mm of non-field sheet. The APS increment in SMF＋ECP sheet is resulted from the increment of interface bonding spots and the enhancement of inter-diffusion zone width.

关键词： Clad sheet Twin-roll casting Electromagnetic field Bonding strength

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Dietary folate drives methionine metabolism to promote cancer development by stabilizing MAT IIA

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Signal Transduction and Targeted Therapy 2022年第7期7卷 2581-2592页

作者： jin-tao li Hai Yang Ming-Zhu Lei Wei-Ping Zhu Ying Su Kai-Yue li Wen-Ying Zhu Jian Wang Lei Zhang Jia Qu Lei Lv Hao-Jie Lu Zheng-Jun Chen Lu Wang Miao Yin Qun-Ying Lei Fudan University Shanghai Cancer Center&Institutes of Biomedical Sciences Cancer Institutes Key Laboratory of Breast Cancer in Shanghai Shanghai Key Laboratory of Radiation Oncology the Shanghai Key Laboratory of Medical EpigeneticsDepartment of OncologyShanghai Medical CollegeFudan UniversityShanghai 200032People’s Republic of China Department of Hepatic Surgery Fudan University Shanghai Cancer CenterShanghai Medical CollegeFudan UniversityShanghai 200032People’s Republic of China

Folic acid,served as dietary supplement,is closely linked to one-carbon metabolism and methionine metabolism.Previous clinical evidence indicated that folic acid supplementation displays dual effect on cancer development,promoting or suppressing tumor formation and progression.However,the underlying mechanism remains to be uncovered.Here,we report that high-folate diet significantly promotes cancer development in mice with hepatocellular carcinoma(HCC)induced by DEN/high-fat diet(HFD),simultaneously with increased expression of methionine adenosyltransferase 2A(gene name,MAT2A;protein name,MATIIα),the key enzyme in methionine metabolism,and acceleration of methionine cycle in cancer tissues.In contrast,folate-free diet reduces MATIIαexpression and impedes HFD-induced HCC development.Notably,methionine metabolism is dynamically reprogrammed with valosin-containing protein p97/p47 complex-interacting protein(VCIP135)which functions as a deubiquitylating enzyme to bind and stabilize MATIIαin response to folic acid signal.Consistently,upregulation of MATIIαexpression is positively correlated with increased VCIP135 protein level in human HCC tissues compared to adjacent tissues.Furthermore,liver-specific knockout of Mat2a remarkably abolishes the advocating effect of folic acid on HFD-induced HCC,demonstrating that the effect of high or free folate-diet on HFD-induced HCC relies on Mat2a.Moreover,folate and multiple intermediate metabolites in one-carbon metabolism are significantly decreased in vivo and in vitro upon Mat2a deletion.Together,folate promotes the integration of methionine and one-carbon metabolism,contributing to HCC development via hijacking MATIIαmetabolic pathway.This study provides insight into folate-promoted cancer development,strongly recommending the tailor-made folate supplement guideline for both sub-healthy populations and patients with cancer expressing high level of MATIIαexpression.

关键词： metabolism cancer methionine

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Integration of human papillomavirus 18 DNA in esophageal carcinoma 109 cells

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World Journal of Gastroenterology 2011年第37期17卷 4242-4246页

作者： Ke Zhang jin-tao li Shu-Ying li li-Hua Zhu ling Zhou Yi Zeng College of Basic Medicine Hebei United University Tangshan 063000 Hebei Province China College of life Science and Bio-engineering Beijing University of Technology Beijing 10024 China National Institute for Viral Disease Control and Prevention Chinese Center for Disease Control and Prevention and State Key Laboratory for Infectious Disease Prevention and Control Beijing 100052 China

AIM:To detect human papillomavirus(HPV) DNA in esophageal carcinoma(EC) 109 cells and investigate the relationship between HPV and EC.METHODS:Genomic DNA and total RNA from EC109 cells were isolated.HPV DNA was detected by polymerase chain reaction(PCR) with the general primer sets of My09/11 and GP5 +/6 + for the HPV L1 gene and type-specific primer sets for HPV18 E6 and HPV18 E6-E7.Reverse transcription(RT) of mRNA isolated from EC109 cells was performed to produce a cDNA.And then a PCR-based protocol for the amplification of papillomavirus oncogene transcripts was used to analyze HPV18 DNA and integrated transcripts of HPV18 in the chromosomes of EC109 cells.The final nested PCR products were cloned into a pMD-18T vector and sequenced to analyze the chromosomal location of HPV integration.RESULTS:HPV18 DNA was detected in EC109 cells by PCR using the general primer sets of My09/11 and GP5 +/6 + for HPV L1 and the type-specif ic primer sets for HPV18 E6 and E6-E7 to generate products of 450 bp,150 bp,335 bp and 944 bp,respectively.Approximately 600 bp of integrated HPV18-specific transcript was identified.The final nested PCR product of integrated HPV18 DNA was cloned into a pMD-18T vector and sequenced to analyze the chromosomal location of HPV integration.Sequence alignment showed that the HPV18 sequence from EC109 cells was identical to that of the encoded early protein E7-E1 of the standard HPV18 strain X05015,and another partial gene sequence was identical to a partial sequence of human chromosome 8.CONCLUSION:Integration of the HPV genome into the host cell chromosome suggests that persistent HPV infection is vital for malignant cell transformation and carcinogenesis.

关键词：乳头状瘤病毒 DNA检测细胞染色食管癌人类癌组织 PCR产物基因组DNA

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MicroRNAs: a novel promising therapeutic target for cerebral ischemia/reperfusion injury?

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Neural Regeneration Research 2015年第11期10卷 1799-1808页

作者： Xiao-li Min Ting-yong Wang Yi Cao Jia liu jin-tao li Ting-hua Wang Institute of Neuroscience Kunming Medical University Faculty of Clinical Medicine Yunnan University of Traditional Chinese Medicine the First Affiliated Hospital of Yunnan University of Traditional Chinese Medicine School of Economics of Sichuan University Department of Neurosurgery the Second Affiliated Hospital of Kunming Medical University

To determine the molecular mechanism of cerebral ischemia/reperfusion injury, we examined the micro RNA（mi RNA） expression profile in rat cortex after focal cerebral ischemia/reperfusion injury using mi RNA microarrays and bioinformatic tools to systematically analyze Gene Ontology（GO） function classifications, as well as the signaling pathways of genes targeted by these differentially expressed mi RNAs. Our results show significantly changed mi RNA expression profiles in the reperfusion period after focal cerebral ischemia, with a total of 15 mi RNAs up-regulated and 44 mi RNAs down-regulated. Target genes of these differentially expressed mi RNAs were mainly involved in metabolic and cellular processes, which were identified as hub nodes of a mi RNA-GO-network. The most correlated pathways included D-glutamine and D-glutamate metabolism, the renin-angiotensin system, peroxisomes, the PPAR signaling pathway, SNARE interactions in vesicular transport, and the calcium signaling pathway. Our study suggests that mi RNAs play an important role in the pathological process of cerebral ischemia/reperfusion injury. Understanding mi RNA expression and function may shed light on the molecular mechanism of cerebral ischemia/reperfusion injury.

关键词： nerve regeneration microRNA therapeutic target cerebral ischemia/reperfusion injury miRNA expression profiles bioinformatics analysis Gene Ontology analysis molecular mechanism KEGG pathway neural regeneration

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Expression of NG2 and platelet-derived growth facto receptor alpha in the developing neonatal rat brain

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Neural Regeneration Research 2017年第11期12卷 1843-1852页

作者： Ping li Heng-xi li Hong-yan Jiang lie Zhu Hai-ying Wu jin-tao li Jiang-hua Lai College of Forensic Science Health Science CenterXi'an Jiaotong UniversityXi'anShaanxi ProvinceChina Department of Anatomy and Histology&Embryology Faculty of Basic Medical SciencesKunming Medical UniversityKunmingYunnan ProvinceChina Department of Plastic Surgery Changzheng HospitalShanghaiChina Department of Emergency and Intensive Care Unit First Affiliated HospitalKunming Medical UniversityKunmingYunnan ProvinceChina Neuroscience Institute Faculty of Basic Medical SciencesKunming Medical UniversityKunmingYunnan ProvinceChina

Platelet-derived growth factor receptor alpha （PDGFRct） is a marker of oligodendrocyte precursor cells in the central nervous system. NG2 is also considered a marker of oligodendrocyte precursor cells. However, whether there are differences in the distribution and morphol- ogy of oligodendrocyte precursor cells labeled by NG2 or PDGFRa in the developing neonatal rat brain remains unclear. In this study, by immunohistochemical staining, NG2 positive （NG2＋） cells were ubiquitous in the molecular layer, external pyramidal layer, internal pyramidal layer, and polymorphic layer of the cerebral cortex, and corpus callosum, external capsule, piriform cortex, and medial septal nucleus. NG2~ cells were stellate or fusiform in shape with long processes that were progressively decreased and shortened over the course of brain development. The distribution and morphology of PDGFRct positive （PDGFRa＋） cells were coincident with NG2＋ cells. The co- localization of NG2 and PDGFRu in the cell bodies and processes of some cells was confirmed by double immunofluorescence labeling. Moreover, cells double-labeled for NG2 and PDGFRa were predominantly in the early postnatal stage of development. The numbers of NG2＋/PDGFRa＋ cells and PDGFRa＋ cells decreased, but the number of NG2＋ cells increased from postnatal days 3 to 14 in the developing brain. In addition, amoeboid microglial cells of the corpus callosum, newborn brain macrophages in the normal developing brain, did not express NG2 or PDGFRu, but NG2 expression was detected in amoeboid microglia after hypoxia. The present results suggest that NG2 and PDGFRct are specific markers of oligodendrocyte precursor cells at different stages during early development. Additionally, the NG2 protein is involved in inflammatory and pathological processes of amoeboid microglial cells.

关键词： nerve regeneration NG2 platelet-derived growth factor receptor alpha oligodendrocyte precursor cells amoeboid microglial cells OX-42 hypoxia cerebral cortex corpus callosum neural regeneration

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