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Hepatoprotective effect of Geranium schiedeanum against ethanol toxicity during liver regeneration

World Journal of Gastroenterology 2015年第25期21卷 7718-7729页

作者： Eduardo Madrigal-Santillán Mirandeli Bautista juan a gayosso-de-lucio Yadira Reyes-Rosales Araceli Posadas-Mondragón ángel Morales-González Marvin A Soriano-Ursúa Jazmín García-Machorro Eduardo Madrigal-Bujaidar Iselaálvarez-González JoséA Morales-González Laboratorio de Medicina de Conservación Escuela Superior de MedicinaInstituto Politécnico NacionalPlan de San Luis y Díaz MirónMéxico DF 11340México área Académica de Farmacia ICSaUniversidad Autónoma del Estado de HidalgoPachuca de Sotoestado de HidalgoCP 42000México Escuela Superior de Cómputo Instituto Politécnico NacionalAv.Juan de Dios Bátiz s/n esquina Miguel Othón de MendizabalUnidad Profesional Adolfo López Mateos departamento de Fisiología Escuela Superior de MedicinaInstituto Politécnico NacionalPlan de San Luis y Díaz MirónColonia Casco de Santo TomasDel.Miguel HidalgoMéxico DF 11340México Laboratorio de Genética Escuela Nacional de Ciencias BiológicasInstituto Politécnico NacionalAv.Wilfrido MassieuUnidad A.López MateosZacatencoMéxico DF 07700México

AIM: To evaluate the effect of an extract of Geranium schiedeanum(Gs) as a hepatoprotective agent against ethanol(Et OH)-induced toxicity in rats. METHODS: Male Wistar rats weighing 200-230 g were subjected to a 70% partial hepatectomy(PH); they were then divided into three groups(groups 1-3). During the experiment, animals in group 1 drank only water. The other two groups(2-3) drank an aqueous solution of Et OH(40%, v/v). Additionally, rats in group 3 received a Gs extract daily at a dose of 300 mg/kg body weight intragastically. Subsequently, to identify markers of liver damage in serum, alanine aminotransferase, aspartate aminotransferase, albumin and bilirubin were measured by colorimetric methods. Glucose, triglyceride and cholesterol concentrations were also determined. In addition, oxidative damage was estimated by measuring lipid peroxidation [using thiobarbituric-acid reactive substances(TBARS)] in both plasma and the liver and by measuring the total concentration of antioxidants in serum and the total antioxidant capacity in the liver. In addition, a liver mass gain assessment, total DNA analysis and a morpho-histological analysis of the liver from animals in all three groups were performed and compared. Finally, the number of deaths observed in the three groups was ***: Administration of the Geranium shiedeanum extract significantly reduced the unfavorable effect of ethanol on liver regeneration(restitution liver mass: PHEt OH group 60.68% vs PH-Gs-Et OH group 69.22%). This finding was congruent with the reduced levels of hepatic enzymes and the sustained or increased levels of albumin and decreased bilirubin in serum. The extract also modified the metabolic processes that regulate glucose and lipid levels, as observed from the serum measurements. Lower antioxidant levels and the liver damage induced by Et OH administration appeared to be mitigated by the extract, as observed from the TBARs(PH-Et OH group 200.14 mmol/mg vs PH-Gs-Et OH group 5

关键词： Geranium schiedeanum Liver regeneration Ethanol Free radicals Nuclear factor erythroid-2-relatedfactor 2

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Hepatoprotective effect of silymarin

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World Journal of Hepatology 2014年第3期6卷 144-149页

作者： Nancy Vargas-Mendoza Eduardo Madrigal-Santillán ngel Morales-González Jaime Esquivel-Soto Cesar Esquivel-Chirino Manuel García-Luna y González-Rubio juan a gayosso-de-lucio José A Morales-González Institute of Health Sciences Autonomous University of Hidalgo State Laboratorio Medicina de Conservación Escuela Superior de MedicinaInstituto Politécnico Nacional Escuela Superior de Cómputo Instituto Politécnico NacionalAv.Juan de Dios Bátiz s/n esquina Miguel Othón de MendizabalUnidad Profesional Adolfo López Mateos Faculty of dentistry UNAM

The use of medicinal plants in treating illnesses has been reported since ancestral *** the case of hepatic diseases,several species such as Silybum marianum,Phyllanthus niruri,and Panus giganteus(Berk.)have been shown to ameliorate hepatic *** is a natural compound derived from the species Silybum marianum,which is commonly known as Milk *** plant contains at least seven flavoligands and the flavonoid *** hepatoprotective and antioxidant activity of silymarin is caused by its ability to inhibit the free radicals that are produced from the metabolism of toxic substances such as ethanol,acetaminophen,and carbon *** generation of free radicals is known to damage cellular membranes and cause *** enhances hepatic glutathione and may contribute to the antioxidant defense of the *** has also been shown that silymarin increases protein synthesis in hepatocytes by stimulating RNA polymerase I activity.A previous study on humans reported that silymarin treatment caused a slight increase in the survival of patients with cirrhotic alcoholism compared with untreated controls.

关键词： Silybum marianum Hepatoprotector Lipoperoxidation Silymarin

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Inflammasome links traumatic brain injury, chronic traumatic encephalopathy, and Alzheimer's disease

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Neural Regeneration Research 2025年第6期20卷 1644-1664页

作者： Gabriela Seplovich Yazan Bouchi juan Pablo de Rivero Vaccari Jennifer C.Munoz Pareja Andrew Reisner Laura Blackwell Yehia Mechref Kevin K.Wang J.Adrian Tyndall Binu Tharakan Firas Kobeissy department of Surgery Morehouse School of MedicineAtlantaGAUSA department of Neurobiology Center for NeurotraumaMultiomics&Biomarkers(CNMB)Neuroscience InstituteMorehouse School of MedicineAtlantaGAUSA department of Neurological Surgery and the Miami Project to Cure Paralysis University of Miami Miller School of MedicineMiamiFLUSA Division of Pediatric Critical Care Department of PediatricsUniversity of Miami Miller School of MedicineMiamiFLUSA department of Pediatrics Emory UniversityAtlantaGAUSA department of Neurosurgery Children’s Healthcare of AtlantaAtlantaGAUSA department of Chemistry and Biochemistry Texas Tech UniversityLubbockTXUSA Morehouse School of Medicine AtlantaGAUSA

Traumatic brain injury, chronic traumatic encephalopathy, and Alzheimer's disease are three distinct neurological disorders that share common pathophysiological mechanisms involving neuroinflammation. One sequela of neuroinflammation includes the pathologic hyperphosphorylation of tau protein, an endogenous microtubule-associated protein that protects the integrity of neuronal cytoskeletons. Tau hyperphosphorylation results in protein misfolding and subsequent accumulation of tau tangles forming neurotoxic aggregates. These misfolded proteins are characteristic of traumatic brain injury, chronic traumatic encephalopathy, and Alzheimer's disease and can lead to downstream neuroinflammatory processes, including assembly and activation of the inflammasome complex. Inflammasomes refer to a family of multimeric protein units that, upon activation, release a cascade of signaling molecules resulting in caspase-induced cell death and inflammation mediated by the release of interleukin-1β cytokine. One specific inflammasome, the NOD-like receptor protein 3, has been proposed to be a key regulator of tau phosphorylation where it has been shown that prolonged NOD-like receptor protein 3 activation acts as a causal factor in pathological tau accumulation and spreading. This review begins by describing the epidemiology and pathophysiology of traumatic brain injury, chronic traumatic encephalopathy, and Alzheimer's disease. Next, we highlight neuroinflammation as an overriding theme and discuss the role of the NOD-like receptor protein 3 inflammasome in the formation of tau deposits and how such tauopathic entities spread throughout the brain. We then propose a novel framework linking traumatic brain injury, chronic traumatic encephalopathy, and Alzheimer's disease as inflammasomedependent pathologies that exist along a temporal continuum. Finally, we discuss potential therapeutic targets that may intercept this pathway and ultimately minimize long-term neurological decline.

关键词： Alzheimer's disease caspase-1 chronic traumatic encephalopathy inflammasomes neurodegeneration neuroinflammation NLRP1 NLRP3 pyroptosis tauopathy traumatic brain injury

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Pathogenesis and clinical management of arboviral diseases

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World Journal of Virology 2025年第1期14卷 9-50页

作者： Victoria Cenci Dietrich juan Marcos Caram Costa Marina Maria Gomes Leite Oliveira Carlos Eduardo Oliveira Aguiar Luis Guilherme de Oliveira Silva Marcel Silva Luz Fabian Fellipe Bueno Lemos Fabrício Freire de Melo Instituto Multidisciplinar em Saúde Universidade Federal da BahiaVitória da Conquista 45029-094BahiaBrazil

Arboviral diseases are viral infections transmitted to humans through the bites of arthropods,such as mosquitoes,often causing a variety of pathologies associated with high levels of morbidity and *** the past decades,these infections have proven to be a significant challenge to health systems worldwide,particularly following the considerable geographic expansion of the dengue virus(deNV)and its most recent outbreak in Latin America as well as the difficult-tocontrol outbreaks of yellow fever virus(YFV),chikungunya virus(CHIKV),and Zika virus(ZIKV),leaving behind a substantial portion of the population with complications related to these ***,the world is experiencing a period of intense globalization,which,combined with global warming,directly contributes to wider dissemination of arbovirus vectors across the ***,all continents remain on high alert for potential new ***,this review aims to provide a comprehensive understanding of the pathogenesis of the four main arboviruses today(deNV,ZIKV,YFV,and CHIKV)discussing their viral characteristics,immune responses,and mechanisms of viral evasion,as well as important clinical aspects for patient *** includes associated symptoms,laboratory tests,treatments,existing or developing vaccines and the main associated complications,thus integrating a broad historical,scientific and clinical approach.

关键词： Arboviruses Arbovirus infections dengue Zika virus Yellow fever Chikungunya virus Clinical diagnosis Pathogenesis Flavivirus Togaviridae infections

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Stiffness-tunable biomaterials provide a good extracellular matrix environment for axon growth and regeneration

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Neural Regeneration Research 2025年第5期20卷 1364-1376页

作者： Ronglin Han Lanxin Luo Caiyan Wei Yaru Qiao Jiming Xie Xianchao Pan juan Xing department of Pathophysiology School of Basic Medical SciencesSouthwest Medical UniversityLuzhouSichuan ProvinceChina department of Medicinal Chemistry School of PharmacySouthwest Medical UniversityLuzhouSichuan ProvinceChina

Neuronal growth, extension, branching, and formation of neural networks are markedly influenced by the extracellular matrix—a complex network composed of proteins and carbohydrates secreted by cells. In addition to providing physical support for cells, the extracellular matrix also conveys critical mechanical stiffness cues. During the development of the nervous system, extracellular matrix stiffness plays a central role in guiding neuronal growth, particularly in the context of axonal extension, which is crucial for the formation of neural networks. In neural tissue engineering, manipulation of biomaterial stiffness is a promising strategy to provide a permissive environment for the repair and regeneration of injured nervous tissue. Recent research has fine-tuned synthetic biomaterials to fabricate scaffolds that closely replicate the stiffness profiles observed in the nervous system. In this review, we highlight the molecular mechanisms by which extracellular matrix stiffness regulates axonal growth and regeneration. We highlight the progress made in the development of stiffness-tunable biomaterials to emulate in vivo extracellular matrix environments, with an emphasis on their application in neural repair and regeneration, along with a discussion of the current limitations and future prospects. The exploration and optimization of the stiffness-tunable biomaterials has the potential to markedly advance the development of neural tissue engineering.

关键词： alginate axon growth biomaterials extracellular matrix neural repair neurons neuroregeneration polyacrylamide polydimethylsiloxane stiffness

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Anti-amyloid antibodies in Alzheimer’s disease: what did clinical trials teach us?

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Neural Regeneration Research 2025年第4期20卷 1092-1093页

作者： Danko Jeremic Lydia Jiménez-Díaz juan D.Navarro-López NeuroPhysiology&Behavior Lab University of Castilla-La ManchaBiomedical Research Center(CRIB)School of Medicine of Ciudad RealCiudad RealSpain

Although many causes of Alzheimer’s disease(AD)may exist,both the original amyloid cascade and tau hypotheses posit that abnormal misfolding and accumulation of amyloid-β(Aβ)and tau protein is the central event causing the ***,that conclusion could be only partly true,and there is conflicting evidence about the role of both proteins in AD,being able to precede and influence one *** researchers argue that these proteins are mere executors rather than primary causes of ***,there have been continuing refinements of both hypotheses,with alternative explanations proposed.Aβand tau proteins may be independently involved in specific neurotoxic pathways;yet there may be other crucial processes going on in early ***,accumulating evidence suggests that Aβand tau act synergistically,rather than additively in disease onset(Jeremic et al.,2021,2023a).

关键词： amyloid Alzheimer additive

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Sora文生视频大模型对学术期刊出版的机遇、挑战及应对

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新疆师范大学学报（哲学社会科学版） 2025年第2期46卷 79-88页

作者：刘娟新疆师范大学期刊社新疆乌鲁木齐830017

随着Sora文生视频大模型的迅猛发展,学术期刊出版正在经历深刻的变革与重塑。Sora技术的多模态特征与智能化能力,一方面促进学术信息的动态整合与开放获取,推动传统出版模式向协同创新与知识共享的新范式转型;另一方面,赋予著作权归属... 详细信息

随着Sora文生视频大模型的迅猛发展,学术期刊出版正在经历深刻的变革与重塑。Sora技术的多模态特征与智能化能力,一方面促进学术信息的动态整合与开放获取,推动传统出版模式向协同创新与知识共享的新范式转型;另一方面,赋予著作权归属和著作权风险治理等新的价值意蕴。面对Sora文生视频大模型对学术期刊出版带来的机遇和挑战,学术期刊应构建跨学科协作网络、重塑基于价值的学术评价标准、创新人才培养机制,强化全球学术出版治理。文本通过系统分析大语言模型、文生视频大模型驱动下的新兴学术生态,旨在为学术界提供理论视角和实践样态,实现知识生产的原创性与伦理性,推动学术出版在新技术环境中的学术治理现代化及可持续高质量发展。

关键词： Sora 学术期刊出版技术伦理学术伦理学术生态系统

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Navigating medial patellotibial ligament reconstruction:Clinical perspectives and surgical strategies

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World Journal of Clinical Cases 2025年第1期13卷 6-10页

作者： juan Pablo Zicaro Ignacio Garcia-Mansilla Division of Knee Hospital Italiano de Buenos AiresBuenos Aires 1109Argentina

The surgical approach for patellar instability usually refers to reconstruction of the medial patellofemoral ligament associated with an osteotomy of the tibial tuberosity or a trochleoplasty when *** medial patellotibial ligament and the medial patellomeniscal ligament are secondary stabilizers of the *** this,both the medial patellotibial and patellofemoral ligaments aid in patellar rotation and tilt when the knee is flexed beyond 45°.The medial patellotibial ligament plays a particularly important role in the final stages of stretching in extension and between 40 degrees to 90 degrees of *** clinical relevance and surgical indications for medial patellotibial ligament reconstruction associated with medial patellofemoral ligament reconstruction are still *** editorial explores the surgical indications and clinical results for medial patellotibial ligament reconstruction to improve readers’understanding of this technique,especially because reported clinical outcomes have remained sparse.

关键词： Medial patellotibial ligament Patellar instability Reconstruction Surgical

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Reassessing the AMPK-MTORC1 balance in autophagy in the central nervous system

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Neural Regeneration Research 2025年第11期20卷 3209-3210页

作者： Marta García-juan Mario Villa Irene Benito-Cuesta Lara Ordónez-Gutiérrez Francisco Wandosell Centro de Biología Molecular“Severo Ochoa”(CSIC-UAM) Nicolas Cabrera 1Universidad Autónoma de MadridMadridSpain Fisiología Animal Departamento de BiologíaFacultad de CienciasUniversidad Autónoma de MadridMadridSpain department of Clinical Neuroscience CMM Karolinska Universitetssjukhuset SolnaStockholmSweden departamento de Bioquímica y Biología Molecular Universidad Complutense de MadridMadridSpain Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas(CIBERNED) MadridSpain

Autophagy is a cellular degradation and recycling system,indispensable for cellular and organ development,homeostasis,and *** cellular process is evolutionarily highly conserved to quality control of many proteins and dysfunctional organelles,which finally recycle components as amino *** process is effective during normal physiology as part of anabolism and plays an additional important role during starvation(Dikic and Elazar,2018).Different types of autophagy have been chara cterized based on their dynamic,mechanism of action,target substrates,and protein *** of them are macroautophagy(hereafter called"autophagy"),microa utophagy,and chape rone-media ted autophagy(Fleming et al.,2022).

关键词： homeostasis system hereafter

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Salsolinol as an RNA m~6A methylation inducer mediates dopaminergic neuronal death by regulating YAP1 and autophagy

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Neural Regeneration Research 2025年第3期20卷 887-899页

作者： Jianan Wang Yuanyuan Ran Zihan Li Tianyuan Zhao Fangfang Zhang juan Wang Zongjian Liu Xuechai Chen Beijing International Science and Technology Cooperation Base for Antiviral Drugs College of Chemistry and LifeBeijing University of TechnologyBeijingChina department of Rehabilitation Beijing Rehabilitation HospitalCapital Medical UniversityBeijingChina

Salsolinol(1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline,Sal)is a catechol isoquinoline that causes neurotoxicity and shares structural similarity with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine,an environmental toxin that causes Parkinson's ***,the mechanism by which Sal mediates dopaminergic neuronal death remains *** this study,we found that Sal significantly enhanced the global level of N~6-methyladenosine(m~6A)RNA methylation in PC12 cells,mainly by inducing the downregulation of the expression of m~6A demethylases fat mass and obesity-associated protein(FTO)and alk B homolog 5(ALKBH5).RNA sequencing analysis showed that Sal downregulated the Hippo signaling *** m~6A reader YTH domain-containing family protein 2(YTHDF2)promoted the degradation of m~6A-containing Yes-associated protein 1(YAP1)mRNA,which is a downstream key effector in the Hippo signaling ***,downregulation of YAP1 promoted autophagy,indicating that the mutual regulation between YAP1 and autophagy can lead to *** findings reveal the role of Sal on m~6A RNA methylation and suggest that Sal may act as an RNA methylation inducer mediating dopaminergic neuronal death through YAP1 and *** results provide greater insights into the neurotoxic effects of catechol isoquinolines compared with other studies and may be a reference for assessing the involvement of RNA methylation in the pathogenesis of Parkinson's disease.

关键词： ALKBH5 autophagy FTO Hippo pathway m~6A Parkinson's disease RNA methylation salsolinol YAP1 YTHDF2

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