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Melatonin alleviates alcoholic liver disease via EGFR-BRG1-TERT axis regulation

Acta Pharmaceutica Sinica B 2023年第1期13卷 100-112页

作者： Zhaodi Che Yali Song Chengfang Xu Wei li Zhiyong Dong Cunchuan Wang Yixing Ren Kwok-Fai So george l.tipoe Fei Wang Jia Xiao Clinical Medicine Research Institute and Department of Metabolic and Bariatric Surgery the First Affiliated Hospital of Jinan UniversityGuangzhou 510632China Department of Obstetrics the Third Affiliated HospitalSun Yat-sen UniversityGuangzhou 510630China Faculty of Pharmaceutical Sciences Toho UniversityChiba 2748510Japan Department of General Surgery and Institute of Hepato-Biliary-Pancreas and Intestinal DiseaseAffiliated Hospital of North Sichuan Medical CollegeNanchong 637000China GMH Institute of CNS Regeneration Guangdong Medical Key Laboratory of Brain Function and DiseasesJinan UniversityGuangzhou 510632China School of Biomedical Sciences LKS Faculty of Medicinethe University of Hong KongHong KongChina Division of Gastroenterology Seventh Affiliated Hospital of Sun Yat-sen UniversityShenzhen 518107China

Chronic alcohol consumption causes liver steatosis,cell death,and ***(MlT)is reported to alleviate alcoholic liver disease(AlD)-induced ***,its direct regulating targets in hepatocytes are not fully *** the current study,a cell-based screening model and a chronic ethanol-fed mice AlD model were used to test the protective mechanisms of *** ameliorated ethanol-induced hepatocyte injury in both cell and animal models(optimal doses of 10μmol/l and 5 mg/kg,respectively),including lowered liver steatosis,cell death,and ***-seq analysis and loss-of-function studies in AMl-12 cells revealed that telomerase reverse transcriptase(TERT)was a key downstream effector of *** assay found that epidermal growth factor receptor(EGFR)on the hepatocyte surface was a direct binding and regulating target of *** specific knock-down of Tert or Egfr in the AlD mice model impaired MlT-mediated liver protection,partly through the regulation of nuclear brahma-related gene-1(BRG1).long-term administration(90 days)of MlT in healthy mice did not cause evident adverse *** conclusion,MlT is an efficacious and safe agent for AlD *** direct regulating target in hepatocytes is EGFR and downstream BRG1-TERT *** might be used as a complimentary agent for alcoholics.

关键词： Alcoholic liver disease Melatonin Binding receptor TERT EGFR BRG1 Biophysics Safety

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Garlic-derived compound S-allylmercaptocysteine inhibits hepatocarcinogenesis through targeting lRP6/Wnt pathway

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Acta Pharmaceutica Sinica B 2018年第4期8卷 575-586页

作者： Jia Xiao Feiyue Xing Yingxia liu Yi lv Xiaogang Wang Ming-Tat ling Hao Gao Songying Ouyang Min Yang Jiang Zhu Yu Xia Kwok-Fai So george l.tipoe State Key Discipline of Infectious Diseases Shenzhen Third People's Hospital Department of Immunobiology Institute of Tissue Transplantation and ImmunologyJinan University School of Biomedical Sciences The University of Hong Kong Department of Cell Biology & Institute of Biomedicine Jinan University Australian Prostate Cancer Research Centre-Queensland and Institute of Health and Biomedical Innovation Queensland University of Technology Institute of Traditional Chinese Medicine and Natural Products College of PharmacyJinan University Biomedical Research Center of South China College of Life SciencesFujian Normal University JM Medical (Shenzhen) LLC GMH Institute of Central Nervous System Regeneration Jinan University

Whether and how garlic-derived S-allylmercaptocysteine(SAMC) inhibits hepatocellular carcinoma(HCC) is largely unknown. In the current study, the role of low-density lipoprotein receptor(lDlR)-related protein 6(lRP6) in HCC progression and the anti-HCC mechanism of SAMC was examined in clinical sample, cell model and xenograft/orthotopic mouse models. We demonstrated that SAMC inhibited cell proliferation and tumorigenesis, while induced apoptosis of human HCC cells without influencing normal hepatocytes. SAMC directly interacted with Wnt-pathway co-receptor lRP6 on the cell membrane. lRP6 was frequently over-expressed in the tumor tissue of human HCC patients(66.7% of 48 patients) and its overexpression only correlated with the over-expression of β-catenin, but not with age, gender, tumor size, stage and metastasis. Deficiency or over-expression of lRP6 in hepatoma cells could partly mimic or counteract the anti-tumor properties of SAMC, respectively. In vivo administration of SAMC significantly suppressed the growth of Huh-7 xenograft/orthotopic HCC tumor without causing undesirable side effects. In addition, stable down-regulation of lRP6 in Huh-7 facilitated the anti-HCC effects of SAMC. In conclusion, lRP6 can be a potential therapeutic target of HCC. SAMC is a promising specific anti-tumor agent for treating HCC subtypes with Wnt activation at the hepatoma cell surface.

关键词： S-allylmercaptocysteine HCC Wnt lRP6 Human Nude mice

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Hepatic COX1 loss leads to impaired autophagic flux and exacerbates nonalcoholic steatohepatitis

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药学学报:英文版 2023年第6期13卷 2628-2644页

作者： Qian Yu Chang li Qinghui Niu Jigang Wang Zhaodi Che Ke lei He Ren Boyi Ma Yixing Ren Pingping luo Zhuming Fan Huan Zhang Zhaohui liu george l.tipoe Jia Xiao Tumor Immunology and Cytotherapy of Medical Research Center and Center for GI Cancer Diagnosis and Treatmentthe Affiliated Hospital of Qingdao UniversityQingdao 266000China Bau Institute of Medical and Health Sciences Education and School of Biomedical Sciences LKS Faculty of Medicinethe University of Hong KongHong Kong 999077China School of Biomedical Sciences the Chinese University of Hong KongHong Kong 999077China Department of liver Center the Affiliated Hospital of Qingdao UniversityQingdao 266000China Department of Pathology the Affiliated Hospital of Qingdao UniversityQingdao 266000China Clinical Medicine Research Institute and Department of Metabolic and Bariatric Surgery the First Affiliated Hospital of Jinan UniversityGuangzhou 510632China Department of General Surgery and Institute of Hepato-Biliary-Pancreas and Intestinal DiseaseAffiliated Hospital of North Sichuan Medical CollegeNanchong 637000China Department of Applied Biology and Chemical Technology the Hong Kong Polytechnic UniversityHong Kong 999077China Research Center for Chinese Medicine Innovation the Hong Kong Polytechnic UniversityHong Kong 999077China

The mechanisms underlying autophagic defects in nonalcoholic steatohepatitis(NASH)remain largely *** aimed to elucidate the roles of hepatic cyclooxygenase 1(COX1)in autophagy and the pathogenesis of diet-induced steatohepatitis in *** nonalcoholic fatty liver disease(NAFlD)liver samples were used to examine the protein expression of COX1 and the level of ***1^(Δhepa)mice and their wildtype littermates were generated and fed with 3 different NASH *** found that hepatic COX1 expression was increased in patients with NASH and diet induced NASH mice models accompanied by impaired ***1 was required for basal autophagy in hepatocytes and liver specific COX1 deletion exacerbated steatohepatitis by inhibiting ***,COX1 directly interacted with WD repeat domain,phosphoinositide interacting 2(WIPI2),which was crucial for autophagosome ***-associated virus(AAV)-mediated rescue of WIPI2 reversed the impaired autophagic flux and improved NASH phenotypes in Cox1^(Δhepa)mice,indicating that COX1 deletion-mediated steatohepatitis was partially dependent on WIPI2-mediated *** conclusion,we demonstrated a novel role of COX1 in hepatic autophagy that protected against NASH by interacting with *** the COX1 WIPI2 axis may be a novel therapeutic strategy for NASH.

关键词： Autophagy Inflammation lipid metabolism Nonalcoholic fatty liver disease Cyclooxygenase 1 Phosphatidylinositol 3-phosphate WD repeat domain Phosphoinositide interacting 2 Autophagosome maturation

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S-Allylmercaptocysteine improves alcoholic liver disease partly through a direct modulation of insulin receptor signaling

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Acta Pharmaceutica Sinica B 2021年第3期11卷 668-679页

作者： Pingping luo Ming Zheng Rui Zhang Hong Zhang Yingxia liu Wei li Xiaoming Sun Qian Yu george ltipoe Jia Xiao Clinical Medicine Research Institute the First Affiliated Hospital of Jinan UniversityGuangzhou 510632China Department of Interventional Surgery the First Affiliated Hospital of Jinan UniversityGuangzhou 510632China State Key Discipline of Infectious Diseases Department of Infectious DiseasesShenzhen Third People’s HospitalShenzhen 518000China Faculty of Pharmaceutical Sciences Toho UniversityChiba 2748510Japan School of Integrative Pharmacy Institute of Integrative Pharmaceutical ResearchGuangdong Pharmaceutical UniversityGuangzhou 510000China School of Biomedical Sciences Li Ka Shing Faculty of Medicinethe University of Hong KongHong Kong 999077China

Alcoholic liver disease(AlD) causes insulin resistance, lipid metabolism dysfunction, and inflammation. We investigated the protective effects and direct regulating target of S-allylmercaptocysteine(SAMC) from aged garlic on liver cell injury. A chronic ethanol-fed AlD in vivo model(the NIAAA model) was used to test the protective functions of SAMC. It was observed that SAMC(300 mg/kg, by gavage method) effectively ameliorated AlD-induced body weight reduction, steatosis,insulin resistance, and inflammation without affecting the health status of the control mice, as demonstrated by histological, biochemical, and molecular biology assays. By using biophysical assays and molecular docking, we demonstrated that SAMC directly targeted insulin receptor(INSR) protein on the cell membrane and then restored downstream IRS-1/AKT/GSK3 b signaling. liver-specific knock-down in mice and siRNA-mediated knock-down in AMl-12 cells of Insr significantly impaired SAMC(250 mmol/l in cells)-mediated protection. Restoration of the IRS-1/AKT signaling partly recovered hepatic injury and further contributed to SAMC’s beneficial effects. Continuous administration of AKT agonist and recombinant IGF-1 in combination with SAMC showed hepato-protection in the mice ***-term(90-day) administration of SAMC had no obvious adverse effect on healthy mice. We conclude that SAMC is an effective and safe hepato-protective complimentary agent against AlD partly through the direct binding of INSR and partial regulation of the IRS-1/AKT/GSK3 b pathway.

关键词： Alcoholic liver disease S-Allylmercaptocysteine Insulin receptor Insulin resistance IRS-1 AKT GSK3b Safety

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环氧合酶1是化学肝损伤的重要保护因子

环氧合酶1是化学肝损伤的重要保护因子

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第十六届中国科协年会——分13感染、免疫和疫苗论坛

作者：肖佳邢飞跃 george l.tipoe 暨南大学生命科学技术学院免疫生物学系香港大学李嘉诚医学院解剖学系

环氧合酶-1(COX-1)是COX家族中组成性表达的成员。为探讨COX-1在急性肝损伤中的作用和机制,通过注射四氯化碳(CCl4)诱导野生型或COX-1敲除小鼠的急性肝损伤,研究各种损伤表征的变化。结果表明,完全或部分敲除COX-1基因、使用药物抑制CO... 详细信息

环氧合酶-1(COX-1)是COX家族中组成性表达的成员。为探讨COX-1在急性肝损伤中的作用和机制,通过注射四氯化碳(CCl4)诱导野生型或COX-1敲除小鼠的急性肝损伤,研究各种损伤表征的变化。结果表明,完全或部分敲除COX-1基因、使用药物抑制COX-1酶活性均可恶化四氯化碳造成的急性肝损伤,主要表现在:(1)恶化的肝脏组织学和血清中转氨酶的变化;(2)通过CYP2E1介导的氧化压力的恶化;(3)升高的肝脏炎症反应;(4)恶化的肝脏凋亡反应。研究表明,肝脏中COX-1的基本表达水平对于肝脏抵御化学急性损伤非常重要。

关键词：细胞生物学环氧合酶四氯化碳前列腺素急性肝损伤

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Feeding behavior and hormoligosis associated with imidacloprid resistance in Asian citrus psyllid,Diaphorina citri

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Insect Science 2024年第4期31卷 1211-1221页

作者： Xue Dong Chen Justin george lauren M.Diepenbrock Hunter Gossett Guoping liu Jawwad A.Qureshi lukasz l.Stelinski Entomology and Nematology Department University of FloridaCitrus Research and Education CenterLake AlfredFloridaUSA Southern Insect Management Research Unit USDA-ARSStonevilleMississippiUSA Entomology and Nematology Department University of FloridaSouthwest Florida Research and Education CenterImmokaleeFloridaUSA

Imidacloprid is a neonicotinoid insecticide used for managing the Asian citrus psyllid,Diaphorina citri Kuwayama,which serves as vector of phytopathogens causing citrus ***,development of resistance to neonicotinoids among populations of *** has coincided with occasional control failures in the *** objectives of this research were to(1)survey current levels of imidacloprid resistance in Florida citrus;(2)compare feeding behavior between imidacloprid-resistant and susceptible *** using electrical penetration graph recordings,and(3)investigate the possible amplification of insecticide hormoligosis associated with *** surveys confirmed that the susceptibility of *** populations to imidacloprid has decreased in commercial Florida citrus groves compared with a laboratory-susceptible *** 12 generations of selection,resistance to imidacloprid increased by 438 fold compared with the susceptible ***-susceptible *** feeding on citrus exhibited significantly more bouts associated with intercellular pathway(C),phloem penetration(D),phloem salivation(E1),and nonprobing(Np)activities than imidacloprid-resistant ***,there were no differences observed in the frequency or duration of phloem ingestion or xylem feeding between susceptible and resistant *** was no statistical difference in fecundity between resistant and susceptible ***,the fecundity of imidacloprid-susceptible female *** treated with a sublethal concentration of imidacloprid(lC_(25))increased significantly compared with controls,while such hormoligosis was less pronounced among imidacloprid-resistant *** results suggest that imidacloprid-resistant psyllids may cease feeding sooner than susceptible counterparts following sublethal exposure to this insecticide,indicative of a behavioral resistance mechanism.

关键词： artificial selection electrical penetration graph feeding behavior hormoligosis insecticide resistance sublethal exposure

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Disparate outcomes in Hispanic patients with metabolic dysfunctionassociated steatotic liver disease/steatohepatitis and type 2 diabetes: large cohort study

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World Journal of Diabetes 2024年第5期15卷 886-897页

作者： Joseph Matthew Gosnell george Golovko Esteban Arroyave Akshata Moghe Michael l Kueht Omar AbdulSaldarriaga Kevin H McKinney Heather l Stevenson Monique R Ferguson Department of Pathology University of Texas Medical BranchGalvestonTX 77555United States Department of Pharmacology&Toxicology University of Texas Medical BranchGalvestonTX 77555United States Department of Medicine University of Texas Health Science Center at HoustonHoustonTX 77030United States Department of Surgery University of Texas Medical BranchGalvestonTX 77555United States Center for Tropical Diseases Department of Internal MedicineUniversity of Texas Medical BranchGalvestonTX 77555United States Department of Internal Medicine University of Texas Medical BranchGalvestonTX 77555United States

BACKGROUND Metabolic dysfunction-associated steatotic liver disease(MASlD)and metabolic dysfunction-associated steatohepatitis(MASH)are a growing health burden across a significant portion of the global patient ***,these conditions seem to have disparate rates and outcomes between different ethnic *** combination of MASlD/MASH and type 2 diabetes increases the risk of hepatocellular carcinoma(HCC),and Hispanic patients experience the greatest burden,particularly those in South *** To compare outcomes between Hispanic and non-Hispanic patients in the United States,while further focusing on the Hispanic population within Southeast Texas to determine whether the documented disparity in outcomes is a function of geographical circumstance or if there is a more widespread reason that all clinicians must account for in prognostic *** This cohort analysis was conducted with data obtained from TriNetX,llC(“TriNetX”),a global federated health research network that provides access to deidentified medical records from healthcare organizations *** cohort networks were used:University of Texas Medical Branch(UTMB)hospital and the United States national database collective to determine whether disparities were related to geographic regions,like Southeast *** This study findings revealed Hispanics/latinos have a statistically significant higher occurrence of HCC,type 2 diabetes mellitus,and liver fibrosis/cirrhosis in both the United States and the UTMB Hispanic/latino *** mortality in Hispanics/latinos was lower within the United States group and not statistically elevated in the UTMB *** This would appear to support that Hispanic patients in Southeast Texas are not uniquely affected compared to the national Hispanic population.

关键词： Metabolic dysfunction-associated steatotic liver disease Metabolic dysfunction-associated steatohepatitis Hispanic Diabetes mellitus TriNetX Non-alcoholic fatty liver disease Non-alcoholic steatohepatitis Steatotic liver disease Hepatocellular carcinoma

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Beneficial mechanisms of aerobic exercise on hepatic lipid metabolism in non-alcoholic fatty liver disease

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Hepatobiliary & Pancreatic Diseases International 2015年第2期14卷 139-144页

作者： Rui Guo Emily C liong Kwok Fai So Man-lung Fung george l.tipoe Departments of Anatomy li Ka Shing Faculty of Medicine The University of Hong Kong Physiology Li Ka Shing Faculty of MedicineThe University of Hong Kong

BACKGROUND：Non-alcoholic fatty liver disease（NAFlD）refers to any fatty liver disease that is not due to excessive use of *** probably results from abnormal hepatic lipid metabolism and insulin *** exercise is shown to improve *** review aimed to evaluate the molecular mechanisms involved in the beneficial effects of aerobic exercise on *** SOURCE：We searched articles in English on the role of aerobic exercise in NAFlD therapy in Pub ***： The mechanisms of chronic aerobic exercise in regulating the outcome of NAFlD include：（i） reducing in- trahepatic fat content by down-regulating sterol regulatory element-binding protein-lc and up-regulating peroxisome proliferator-activated receptor y expression levels; （ii） decreas- ing hepatic oxidative stress through modulating the reactive oxygen species, and enhancing antioxidant enzymes such as catalase and glutathione peroxidase; （iii） ameliorating hepatic inflammation via the inhibition of pro-inflammatory media- tors such as tumor necrosis factor-alpha and interleukin-1 beta; （iv） attenuating mitochondrial dependent apoptosis by reducing cytochrome C released from the mitochondria to the cytosol; and （v） inducing hepato-protective autophagy. CONClUSION： Aerobic exercise, via different mechanisms, significantly decreases the fat content of the liver and improves the outcomes of patients with NAFlD.

关键词： non-alcoholic fatty liver disease chronic aerobic exercise oxidative stress inflammation apoptosis autophagy

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Therapeutic approaches to non-alcoholic fatty liver disease: past achievements and future challenges

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Hepatobiliary & Pancreatic Diseases International 2013年第2期12卷 125-135页

作者： Jia Xiao Rui Guo Man lung Fung Emily C liong george l.tipoe Departments of Anatomy Li Ka Shing Faculty of Medicine The University of Hong Kong Gene and Cell Engineering Research Center Shenzhen Institute of Advanced Technology Chinese Academy of Sciences Departments of Physiology Li Ka Shing Faculty of Medicine The University of Hong Kong Research Centre of Heart Brain Hormone and Healthy Aging CentreLi Ka Shing Faculty of Medicine The University of Hong Kong

BACKGROUND: Non-alcoholic fatty liver disease (NAFlD) is a leading cause of chronic liver injury and mortality in Western countries and China. However, as to date, there is no direct and effective therapy for this disease. The aim of this review is to analyze the key progress and challenges of main current therapeutic approaches in NAFlD. DATA SOURCE: We carried out a PubMed search of English-language articles relevant to NAFlD therapy. RESUlTS: There are two major therapeutic strategies for NAFlD treatment: (1) lifestyle interventions (including weight reduction, dietary modification and physical exercise) and (2) pharmaceutical therapies. lifestyle interventions, particularly chronic and moderate intensity exercise, are the most effective and recognized clinical therapies for NAFlD. For pharmaceutical therapies, although their effects and mechanisms have been extensively investigated in laboratory studies, they still need further tests and investigations in clinical human trials. CONClUSION: Future advancement of NAFlD therapy should focus on the mechanistic studies on cell based and animal models and human clinical trials of exercise, as well as the combination of lifestyle intervention and pharmaceutical therapy specifically targeting main signaling pathways related to lipid metabolism, oxidative stress and inflammation.

关键词： non-alcoholic fatty liver disease therapy pharmaceuticals exercise

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Polyethylene glycol has immunoprotective effects on sciatic allografts, but behavioral recovery and graft tolerance require neurorrhaphy and axonal fusion

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Neural Regeneration Research 2025年第4期20卷 1192-1206页

作者： Tyler A.Smith liwen Zhou Cameron l.Ghergherehchi Michelle Mikesh Cathy Z.Yang Haley O.Tucker JuliAnne Allgood Jared S.Bushman george D.Bittner Department of Molecular Biosciences University of Texas at AustinAustinTXUSA Department of Neuroscience University of Texas at AustinAustinTXUSA Division of Pharmaceutical Sciences University of WyomingLaramieWYUSA

Behavioral recovery using(viable)peripheral nerve allografts to repair ablation-type(segmental-loss)peripheral nerve injuries is delayed or poor due to slow and inaccurate axonal ***,such peripheral nerve allografts undergo immunological rejection by the host immune *** contrast,peripheral nerve injuries repaired by polyethylene glycol fusion of peripheral nerve allografts exhibit excellent behavioral recovery within weeks,reduced immune responses,and many axons do not undergo Wallerian *** relative contribution of neurorrhaphy and polyethylene glycol-fusion of axons versus the effects of polyethylene glycol per se was unknown prior to this *** hypothesized that polyethylene glycol might have some immune-protective effects,but polyethylene glycol-fusion was necessary to prevent Wallerian degeneration and functional/behavioral *** examined how polyethylene glycol solutions per se affect functional and behavioral recovery and peripheral nerve allograft morphological and immunological responses in the absence of polyethylene glycol-induced axonal ***-type sciatic nerve injuries in outbred Sprague–Dawley rats were repaired according to a modified protocol using the same solutions as polyethylene glycol-fused peripheral nerve allografts,but peripheral nerve allografts were loose-sutured(loose-sutured polyethylene glycol)with an intentional gap of 1–2 mm to prevent fusion by polyethylene glycol of peripheral nerve allograft axons with host *** to negative control peripheral nerve allografts not treated by polyethylene glycol and in contrast to polyethylene glycol-fused peripheral nerve allografts,animals with loose-sutured polyethylene glycol peripheral nerve allografts exhibited Wallerian degeneration for all axons and myelin degeneration by 7 days postoperatively and did not recover sciatic-mediated behavioral functions by 42 days *** morphological signs of rejection,such as col

关键词： allograft rejection axotomy macrophage myelin nerve repair polyethylene glycol(PEG) sciatic nerve T cell transplantation Wallerian degeneration

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