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Reply to“Wnt/beta-catenin signaling inhibitors and nonalcoholic fatty liver disease:Potential therapeutic implications”

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Hepatobiliary & Pancreatic Diseases International 2023年第4期22卷 439-440页

The Author Reply:We sincerely appreciated the interest of Polyzos et al.,in our review article and sharing their improvised thoughts regarding the Wnt signaling modulators for the treatment of postmenopausal women with osteoporosis and nonalcoholic fatty liver disease(NAFLD).Several experimental studies have showed that the aberrant Wnt/β-catenin signaling promotes the development and/or progression of a variety of chronic liver diseases including NAFLD[1,2].Therefore,our review emphasized on the modulation of Wnt/β-catenin signaling and the role of its mediators in NAFLD progression.Given that NAFLD prevalence is constantly increas-ing,and that osteoporosis is associated with women over 50 years of age with NAFLD[3],there is an unmet need for an effective treatment.Sclerostin blocks the canonical Wnt signaling pathway of bone formation.Therefore,romosozumab,a humanized anti-sclerostin monoclonal antibody,was approved for the treatment of osteoporosis.Romosozumab binds to sclerostin,permitting the en-gagement of Wnt ligands with their co-receptors,resulting in an increase in bone formation and bone mineral density.

关键词： liver Wnt constantly

Mitochondria: A critical hub for hepatic stellate cells activation during chronic liver diseases

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Hepatobiliary & Pancreatic Diseases International 2021年第4期20卷 315-322页

作者： devaraj ezhilarasan Department of Pharmacology the Blue LabMolecular Medicine and Toxicology DivisionSaveetha Dental CollegeSaveetha Institute of Medical and Technical Sciences(SIMATS)Chennai 600077Tamil NaduIndia

Background: Upon liver injury, quiescent hepatic stellate cells(q HSCs), reside in the perisinusoidal space, phenotypically transdifferentiate into myofibroblast-like cells(MFBs). The q HSCs in the normal liver are less fibrogenic, migratory, and also have less proliferative potential. However, activated HSCs(a HSCs) are more fibrogenic and have a high migratory and proliferative MFBs phenotype. HSCs activation is a highly energetic process that needs abundant intracellular energy in the form of adenosine triphosphate(ATP) for the synthesis of extracellular matrix(ECM) in the injured liver to substantiate the injury. Data sources: The articles were collected through Pub Med and EMBASE using search terms "mitochondria and hepatic stellate cells", "mitochondria and HSCs", "mitochondria and hepatic fibrosis", "mitochondria and liver diseases", and "mitochondria and chronic liver disease", and relevant publications published before September 31, 2020 were included in this review. Results: Mitochondria homeostasis is affected during HSCs activation. Mitochondria in a HSCs are highly energetic and are in a high metabolically active state exhibiting increased activity such as glycolysis and respiration. a HSCs have high glycolytic enzymes expression and glycolytic activity induced by Hedgehog(Hh) signaling from injured hepatocytes. Increased glycolysis and aerobic glycolysis(Warburg effect) endproducts in a HSCs consequently activate the ECM-related gene expressions. Increased Hh signaling from injured hepatocytes downregulates peroxisome proliferator-activated receptor-γ expression and decreases lipogenesis in a HSCs. Glutaminolysis and tricarboxylic acid cycle liberate ATPs that fuel HSCs to proliferate and produce ECM during their activation. Conclusions: Available studies suggest that mitochondria functions can increase in parallel with HSCs activation. Therefore, mitochondrial modulators should be tested in an elaborate manner to control or prevent the HSCs activation during liver injury to subsequently regress hep

关键词： Hepatic stellate cells Glutaminolysis Glycolysis Hedgehog Myofibroblasts

Critical role of estrogen in the progression of chronic liver diseases

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Hepatobiliary & Pancreatic Diseases International 2020年第5期19卷 429-434页

作者： devaraj ezhilarasan Department of Pharmacology Biomedical Research Unit and Laboratory Animal CentreSaveetha Dental College and HospitalsSaveetha Institute of Medical and Technical SciencesChennai 600077Tamil NaduIndia

Background:Estrogens regulate sexual function and also have a significant role in various pathophysiological processes.Estrogens have a non-reproductive role as the modulators of the immune system,growth,neuronal function,and metabolism.Estrogen receptors are expressed in the liver and their impaired expression and function are implicated with obesity and liver associated metabolic dysfunctions.The purpose of the current review is to discuss the disparity role of estrogens on several forms of liver diseases.Data sources:A comprehensive search in PubMed and EMBASE was conducted using the keywords“estrogens and liver diseases”,“estradiol and liver diseases”,“hormones and liver diseases”,“endocrine function in liver diseases”,and“female hormones in liver diseases”.Relevant papers published before September 30,2019 were included.Results:The present review confirms the imperative role of estrogen in various forms of chronic liver diseases.Estrogens play a key role in maintaining homeostasis and make the liver less susceptible to several forms of chronic liver diseases in healthy premenopausal individuals.In contrast,clinical studies also showed increased estrogen levels with chronic liver diseases.Conclusions:Several studies reported the protective role of estrogens in chronic liver diseases and this has been widely accepted and confirmed in experimental studies using ovariectomized rat models.However,in a few clinical studies,increased estrogen levels are also implicated in chronic liver diseases.Therefore,further studies are warranted at molecular level to explore the role of estrogen in various forms of chronic liver diseases.

关键词： Estrogen Hepatic fibrosis Chronic liver diseases Hepatic stellate cells

Silibinin alleviates N-nitrosodimethylamine-induced glutathione dysregulation and hepatotoxicity in rats

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Chinese Journal of Natural Medicines 2016年第1期14卷 40-47页

作者： devaraj ezhilarasan Slvanesan Karthikeyan Food and Hepatotoxicology Laboratory Department of Pharmacology and Environmental Toxicology University of MadrasTaramani Chennai 600113 India

The present study was designed to evaluate the hepatoprotective and antioxidant potentials of silibinin(SBN)against N-nitrosodimethylamine(DMN)-induced toxic insults in the rat liver.The liver damage was induced in Wistar albino rats by repeated administration of DMN(10 mg·kg-1 b.w.,i.p.)on 3 consecutive days per week for 3 weeks.SBN(100 mg·kg-1 b.w.,p.o.)was given daily to the DMN treated rats for two weeks.The marker enzymes of liver toxicity and second-line enzymic and non-enzymic antioxidants were evaluated in serum and liver tissues before and after SBN treatment.Histopathology of the liver was evaluated by H & E staining.The DMN treatment produced a progressive increase in all the serum marker enzymes(AST,ALT,ALP,LDH,and γ-GT),peaking on Day 21.This treatment produced highly significant decreases in all the second-line antioxidant parameters(GSH,GST,GR,GPx,and vitamins C and E).The SBN treatment significantly reversed the DMN-induced damages,towards normalcy.Histopathological studies confirmed the development of liver toxicity in DMN-treated rats,which was reversed by SBN treatment in corroboration with the aforementioned biochemical results,indicating the hepatoprotective and antioxidant properties of SBN.In conclusion,the DMN-induced degenerative changes in the liver were alleviated by SBN treatment and this protective ability may be attributed to its antioxidant,free radical scavenging,and membrane stabilizing properties.

关键词： Dimethylnitrosamine Silibinin Oxidative stress Hepatotoxicity Glutathione dysregulation

Hepatic fibrosis： It is time to go with hepatic stellate cell-specifictherapeutic targets

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Hepatobiliary & Pancreatic Diseases International 2018年第3期17卷 192-197页

作者： devaraj ezhilarasan Etienne Sokal Mustapha Najimi Biomedical Research Unit and Laboratory Animal Centre Saveetha Dental College and HospitalsSaveetha Institute of Medical and Technical SciencesChennai 600 077Tamil NaduIndia Institut de Recherche Expérimentale et Clinique(IREC) Laboratory of Pediatric Hepatology and Cell TherapyUniversité Catholique de LouvainBrussels 1200Belgium

Hepatic fibrosis is a pathological lesion, characterized by the progressive accumulation of extracellularmatrix （ECM） in the perisinusoidal space and it is a major problem in chronic liver diseases. Phenotypicactivation of hepatic stellate cells （HSC） plays a central role in the progression of hepatic fibrosis. Retardation of proliferation and clearance of activated HSCs from the injured liver is an appropriate therapeuticstrategy for the resolution and treatment of hepatic fibrosis. Clearance of activated HSCs from the injuredliver by autophagy inhibitors, proapoptotic agents and senescence inducers with the high affinity towardthe activated HSCs may be the novel therapeutic strategy for the treatment of hepatic fibrosis in the nearfuture.

关键词： Hepatic stellate cells Apoptosis Autophagy Senescence Extracellular matrix

Improved Integrated Deep Model for Pap-Smear Cell Analysis

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Journal of Systems Science and Information 2024年第1期12卷 113-124页

作者： Somasundaram devaraj Nirmala MADIAN Gnanasaravanan SUBRAMANIAM Rithaniya CHELLAMUTHU Muralitharan KRISHANAN School of Electronics Engineering Vellore Institute of TechnologyVellore 632014India Department of Biomedical Engineering Dr.N.G.P Institute of TechnologyCoimbatore 641045India Karunya Institute of Technology and Sciences Coimbatore 641114India Department of Computer Science Institute of Mathematical ScienceSungkyunkwan UniversitySuwon 16419South Korea

Cervical cancer is the fourth most common malignancy to strike a woman globally.If discovered early enough,it can be effectively treated.Although there is a chance of error owing to human error,the Pap smear is a good tool for first screening for cervical cancer.It also takes a lot of time and effort to complete.The aim of this study was to reduce the possibility of error by automating the process of classifying cervical cancer using Pap smear images.For the purpose of this study,dual convolution neural networks with LSTM were employed to classify images due to deep learning approaches inspire distinct features and powerful classifiers for many computer vision applications.The proposed deep learning model based on convolution neural networks(CNN)with the long short-term memory(LSTM)network is to learn features which give better recognition accuracy.The overall model is known as Smear-net.In which‘smear’indicates‘pap-smear cancer cells’and‘net’refers to neural network.The parameters such as,Accuracy,Precision,Recall,Accuracy,Sensitivity,and Specificity are used to validate the models.The proposed method provides the improved accuracy of 99.57 percentage for classification of the pap-smear cells.The proposed approaches demonstrate the effectiveness of our contributions by testing and comparing with the state-of-the-art techniques.

关键词： pap-smear deep learning convolution neural network smear-net

Silibinin induces hepatic stellate cell cycle arrest via enhancing p53/p27 and inhibiting Akt downstream signaling protein expression

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Hepatobiliary & Pancreatic Diseases International 2017年第1期16卷 80-87页

作者： devaraj ezhilarasan Jonathan Evraerts Brice Sid Pedro Buc Calderon Sivanesan Karthikeyan Etienne Sokal Mustapha Najimi institut de recherche expérimentale et clinique (irec) laboratory of pediatric hepatology and cell therapyuniversité catholique de louvain 1200 Brussels Belgium louvain drug research institute toxicology and cancer biology research group pmnt unituniversité catholique de louvain 1200 Brussels Belgium facultad de ciencias de la salud universidad arturo prat Iquique Chil department of pharmacology and environmental toxicology food and hepatotoxicology laboratory dr. alm post graduate institute of basic medical sciences university of madrastaramani campus Chennai-600 l13 India

BACKGROUND： Proliferation of hepatic stellate cells （HSCs） plays a pivotal role in the progression of liver fibrosis conse- quent to chronic liver injury. Silibinin, a flavonoid compound, has been shown to possess anti-fibrogenic effects in animal models of liver fibrosis. This was attributed to an inhibition of cell proliferation of activated HSCs. The present study was to gain insight into the molecular pathways involved in silibinin anti-fibrogenic effect. METHODS： The study was conducted on LX-2 human stellate cells treated with three concentrations of silibinin （10, 50 and 100 μmol/L） for 24 and 96 hours. At the end of the treatment cell viability and proliferation were evaluated. Protein expression of p27, p21, p53, Akt and phosphorylated-Akt was evaluated by Western blotting analysis and Ki-67 protein expression was by immunocytochemistry. Sirtuin activity was evaluated by chemiluminescence based assay. RESULTS： Silibinin inhibits LX-2 cell proliferation in doseand time-dependent manner; we showed that silibinin upregulated the protein expressions of p27 and p53. Such regulation was correlated to an inhibition of both downstream Akt and phosphorylated-Akt protein signaling and Ki-67 protein expression. Sirtuin activity also was correlated to silibinin- inhibited proliferation of LX-2 cells. CONCLUSION： The anti-proliferative effect of silibinin on LX-2 human steUate cells is via the inhibition of the expres- sions of various cell cycle targets including p27, Akt and sir- tuin signaling.

关键词： silibinin hepatic stellate cells in vitro cell cycle arrest proliferation

Plant derived antioxidants and antifibrotic drugs:past,present and future

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Journal of Coastal Life Medicine 2014年第9期2卷 738-745页

作者： devaraj ezhilarasan Etienne Sokal Sivanesan Karthikeyan Mustapha Najimi Institut de Recherche Expérimentale et Clinique Laboratory of Pediatric Hepatology and Cell TherapyUniversitéCatholique de LouvainBrusselsBelgium Department of Pharmacology and Environmental Toxicology Food and Hepatotoxicology LaboratoryDr.ALM Post Graduate Institute of Basic Medical SciencesUniversity of MadrasChennaiIndia

Hepatic fibrosis occurs as a wound-healing process after several forms of chronic hepatic injury.Activation and proliferation of hepatic stellate cells play pivotal role in the pathogenesis of hepatic fibrosis.Many researchers,from the therapeutic perspective,have focused their attention on searching for novel agents with inhibitory effects on hepatic stellate cells proliferation and activation to prevent hepatic fibrogenesis and a number of plant derived antioxidants have been tested as anti-fibrogenic agents,they generally suppress proliferation and collagen synthesis.Plants remain an imperative source of novel drugs,novel drug leads and new chemical entities.The plant based drug discovery resulted primarily in the development of antioxidant,anti-cancer and other anti-infectious agents and continues to contribute to the new leads in clinical trials.This review summarizes some of those most important plant derived anti-fibrotic drugs and their beneficial effects on experimentally induced hepatic fibrosis in vitro and in vivo.The plant derived antioxidant compounds described herein are curcumin,silymarin,silibinin,baicalein,resveratrol,salvianolic acids,tetrandine,quercetin and berberine.Studies from ours and as demonstrated by pervious workers much information has been accumulated over the past two decades through in vivo and in vitro.In light of those studies,it has been confirmed that plants derived antioxidants,particularly flavanoids,show a significant influence to block hepatic fibrosis regardless of any etiology.This review outlines recent progress in the use of plant derived drugs against experimentally induced liver fibrosis by in vitro and in vivo studies and summarizes the possible mechanisms anti-fibrotic effects of these compounds.

关键词： Curcumin Hepatic stellate cells Hepatic fibrosis Antioxidant Silibinin

Early Detection Glaucoma and Stargardt’s Disease Using Deep Learning Techniques

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Intelligent Automation & Soft Computing 2023年第5期36卷 1283-1299页

作者： Somasundaram devaraj Senthil Kumar Arunachalam Department of Electronics and Communication Engineering Sri Shakthi Institute of Engineering and TechnologyCoimabatore641062TamilnaduIndia

Retinal fundus images are used to discover many diseases.Several Machine learning algorithms are designed to identify the Glaucoma disease.But the accuracy and time consumption performance were not improved.To address this problem Max Pool Convolution Neural Kuan Filtered Tobit Regres-sive Segmentation based Radial Basis Image Classiﬁer(MPCNKFTRS-RBIC)Model is used for detecting the Glaucoma and Stargardt’s disease by early period using higher accuracy and minimal time.In MPCNKFTRS-RBIC Model,the ret-inal fundus image is considered as an input which is preprocessed in hidden layer 1 using weighted adaptive Kuanﬁlter.Then,preprocessed retinal fundus is given for hidden layer 2 for extracting the features like color,intensity,texture with higher accuracy.After extracting these features,the Tobit Regressive Segmenta-tion process is performed by hidden layer 3 for partitioning preprocessed image within more segments by analyzing the pixel with the extracted features of the fundus image.Then,the segmented image was given to output layer.The radial basis function analyzes the testing image region of a particular class as well as training image region with higher accuracy and minimum time consumption.Simulation is performed with retinal fundus image dataset with various perfor-mance metrics namely peak signal-to-noise ratio,accuracy and time,error rate concerning several retina fundus image and image size.

关键词： Glaucoma detection max pool convolution neural network kuanﬁlter radial basis function