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Oridonin induces apoptosis of HeLa cells via altering expression of Bcl-2/Bax and activating caspase-3/ICAD pathway

Acta Pharmacologica Sinica 2004年第5期25卷 149-156页

作者： Shin-ichi TASHIRO,Satoshi ONODERA,Takashi IKEJIMA department of Clinical and biomedical sciences Showa College of pharmaceutical sciences Tokyo 194-8543 Japan department of Clinical and biomedical sciences Showa College of pharmaceutical sciences Tokyo 194-8543 Japan China-Japan Research Institute of Medical and pharmaceutical sciences Shenyang pharmaceutical University Shenyang 110016 China prof

AIM: To study the mechanisms by which oridonin inhibited HeLa cell growth in vitro. METHODS: Viability oforidonin-induced HeLa cells was measured by MTT assay. Apoptotic cells with condensed nuclei were visualizedby phase contrast microscopy. Nucleosomal DNA fragmentation was assayed by agarose gel *** activity was assayed using fluorometric protease assay. ICAD, Bcl-2, and Bax proteins expression weredetected by Western blot analysis. RESULTS: Oridonin induced oligonucleosomal fragmentation of DNA andincreased caspase-3 activity, on the other hand, reduced the expression of inhibitor of caspase-3-activated DNase(ICAD), a caspase-3 substrate, at 12 h in HeLa cells. Oridonin-induced DNA fragmentation, caspase-3 activationand down-regulation of ICAD expression were effectively inhibited by a caspase-3 inhibitor, z-DEVD-fmk (z-Asp-Glu-Val-Asp-fmk). However, pretreatment with an inhibitor of poly (ADP-ribose) polymerase (PARP), 3, 4-dihydro-5-[4-(1-piperidinyl)butoxy]-1(2H)-isoquinolinone (DPQ), did not suppress oridonin-induced HeLa cell death. Inaddition, oridonin-induced apoptosis was associated with an increase in the expression of the apoptosis inducerBax, and a significant reduction in expression of the apoptosis suppressor Bcl-2 in mitochondria. CONCLUSION:Oridonin induces HeLa cells apoptosis by altering balance of Bcl-2 and Bax protein expression and activation ofcaspase-3/ICAD pathway.

关键词： oridonin HeLa cells apoptosis caspase 3 caspases bcl-2 genes bax genes Western blotting

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Systematical identification of regulatory GPCRs by single-cell trajectory inference reveals the role of ADGRD1 and GPR39 in adipogenesis

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Science China Life sciences 2025年

作者： Chuan Ye Xuemei Wang Jun Lin Chenyang Wu Yuhua Gao Chenghao Guo Yunxi Liao Ziyan Rao Shaodong Huang Weixuan Chen Ying Huang Jinpeng Sun Dongyu Zhao Changtao Jiang Center of Basic Medical Research Institute of Medical Innovation and ResearchPeking University Third Hospital department of Physiology and Pathophysiology School of Basic Medical SciencesPeking University department of biomedical Informatics School of Basic Medical SciencesPeking University State Key Laboratory of Vascular Homeostasis and Remodeling Peking University Center for Obesity and Metabolic Disease Research School of Basic Medical SciencesPeking University State Key Laboratory of Female Fertility Promotion Center for Reproductive MedicineDepartment of Obstetrics and GynecologyPeking University Third Hospital National Clinical Research Center for Obstetrics and Gynecology Peking University Third Hospital department of Endocrinology and Metabolism Peking University Third Hospital Key Laboratory Experimental Teratology of the Ministry of Education Department of Biochemistry and Molecular BiologySchool of Basic Medical SciencesCheeloo College of MedicineShandong University department of Immunology School of Basic Medical SciencesPeking University

Adipogenesis is the healthy expansion of white adipose tissue (WAT),serving as a compensatory response to maintain metabolic homeostasis in the presence of excess energy in the ***,the identification of novel regulatory molecules in adipogenesis,specifically membrane receptors such as G protein-coupled receptors (GPCRs),holds significant clinical *** receptors can serve as viable targets for pharmaceuticals,offering potential for restoring metabolic homeostasis in individuals with *** utilized trajectory inference methods to analyze three distinct single-nucleus sequencing (sNuc-seq) datasets of adipose tissue and systematically identified GPCRs with the potential to regulate *** verification in primary adipose progenitor cells (APCs) of mice,we discovered that ADGRD1 promoted the differentiation of APCs,while GPR39 inhibits this *** the obese mouse model induced by a high-fat diet(HFD),both gain-of-function and loss-of-function studies validated that ADGRD1 promoted adipogenesis,thereby improving metabolic homeostasis,while GPR39 inhibited adipogenesis,leading to metabolic ***,through the analysis of 2,400 ChIP-seq data and 1,204 bulk RNA-seq data,we found that the transcription factors (TFs) MEF2D and TCF12 regulated the expression of ADGRD1and GPR39,*** study revealed the regulatory role of GPCRs in adipogenesis,providing novel targets for clinical intervention of metabolic dysfunction in obese patients.

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Tranylcypromine upregulates Sestrin 2 expression to ameliorate NLRP3-related noise-induced hearing loss

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Neural Regeneration Research 2025年第5期20卷 1483-1494页

作者： Xihang Chen Zhifeng Chen Menghua Li Weiwei Guo Shuolong Yuan Liangwei Xu Chang Lin Xi Shi Wei Chen Shiming Yang Senior department of Otolaryngology Head and Neck Surgery Chinese PLA General HospitalChinese PLA Medical SchoolBeijingChina State Key Laboratory of Hearing and Balance Science BeijingChina National Clinical Research Center for Otolaryngologic Diseases BeijingChina Key Laboratory of Hearing Science Ministry of EducationBeijingChina Beijing Key Laboratory of Hearing Impairment Prevention and Treatment BeijingChina department of Otorhinolaryngology Head and Neck Surgery The First Affiliated Hospital of Fujian Medical UniversityFuzhouFujian ProvinceChina department of Otolaryngology Head and Neck Surgery The 940th Hospital of Joint Logistics Support Force of Chinese PLALanzhouGansu ProvinceChina Key Laboratory of Tropical Biological Resources of Ministry of Education School of Pharmaceutical SciencesHainan UniversityHaikouHainan ProvinceChina Academician Workstation of Hainan University School of Pharmaceutical SciencesYazhou BaySanyaHainan ProvinceChina

Noise-induced hearing loss is the primary non-genetic factor contributing to auditory ***,there are currently no effective pharmacological interventions for patients with noise-induced hearing ***,we present evidence suggesting that the lysine-specific demethylase 1 inhibitor–tranylcypromine is an otoprotective agent that could be used to treat noise-induced hearing loss,and elucidate its underlying regulatory *** established a mouse model of permanent threshold shift hearing loss by exposing the mice to white broadband noise at a sound pressure level of 120 d B for 4 *** found that tranylcypromine treatment led to the upregulation of Sestrin2(SESN2)and activation of the autophagy markers light chain 3B and lysosome-associated membrane glycoprotein 1 in the cochleae of mice treated with *** noise exposure group treated with tranylcypromine showed significantly lower average auditory brainstem response hearing thresholds at click,4,8,and 16 k Hz frequencies compared with the noise exposure group treated with *** findings indicate that tranylcypromine treatment resulted in increased SESN2,light chain 3B,and lysosome-associated membrane glycoprotein 1 expression after noise exposure,leading to a reduction in levels of 4-hydroxynonenal and cleaved caspase-3,thereby reducing noise-induced hair cell ***,immunoblot analysis demonstrated that treatment with tranylcypromine upregulated SESN2 expression via the autophagy *** treatment also reduced the production of NOD-like receptor family pyrin domaincontaining 3(NLRP3)*** conclusion,our results showed that tranylcypromine treatment ameliorated cochlear inflammation by promoting the expression of SESN2,which induced autophagy,thereby restricting NLRP3-related inflammasome signaling,alleviating cochlear hair cell loss,and protecting hearing *** findings suggest that inhibiting lysine-specific demethylase 1 is a

关键词： 4-hydroxynonenal apoptosis autophagy cleaved caspase-3 inflammation NOD-like receptor family pyrin domain-containing 3(NLRP3) noise-induced hearing loss oxidative stress Sestrin2 tranylcypromine

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Olfactory receptors in neural regeneration in the central nervous system

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Neural Regeneration Research 2025年第9期20卷 2480-2494页

作者： Rafael Franco Claudia Garrigós Toni Capó Joan Serrano-Marín Rafael Rivas-Santisteban Jaume Lillo Molecular Neurobiology Laboratory Department of Biochemistry and Molecular BiomedicineFacultat de BiologiaUniversitat de BarcelonaBarcelonaSpain CiberNed Network Center for biomedical Research in Neurodegenerative Diseases Spanish National Health Institute Carlos ⅢMadridSpain School of Chemistry Universitat de BarcelonaBarcelonaSpain department of Biochemistry and Physiology School of Pharmacy and Food SciencesUniversitat de BarcelonaBarcelonaSpain Laboratory of Computational Medicine Biostatistics UnitFaculty of MedicineAutonomous University of BarcelonaCampus BellaterraBarcelonaSpain

Olfactory receptors are crucial for detecting odors and play a vital role in our sense of smell,influencing behaviors from food choices to emotional *** receptors also contribute to our perception of flavor and have potential applications in medical diagnostics and environmental *** ability of the olfactory system to regenerate its sensory neurons provides a unique model to study neural regeneration,a phenomenon largely absent in the central nervous *** gained from how olfactory neurons continuously replace themselves and reestablish functional connections can provide strategies to promote similar regenerative processes in the central nervous system,where damage often results in permanent *** the molecular and cellular mechanisms underpinning olfactory neuron regeneration could pave the way for developing therapeutic approaches to treat spinal co rd injuries and neurodegenerative diseases like Alzheimer's *** ctory receptors are found in almost any cell of eve ry orga n/tissue of the mammalian *** ectopic expression provides insights into the chemical structures that can activate olfactory *** addition to odors,olfactory receptors in ectopic expression may respond to endogenous compounds and molecules produced by mucosal colonizing *** analysis of the function of olfactory receptors in ectopic expression provides valuable information on the signaling pathway engaged upon receptor activation and the receptor's role in proliferation and cell differentiation *** review explo res the ectopic expression of olfa ctory receptors and the role they may play in neural regeneration within the central nervous system,with particular attention to compounds that can activate these receptors to initiate regenerative *** suggests that olfactory receptors could serve as potential therapeutic targets for enhancing neural repair and recovery following central nervous syste

关键词： adenosine receptors adrenergic receptors ectopic expression G proteincoupled receptors glia neurons

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Insights from an academic endeavor into central nervous system drug discovery

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Neural Regeneration Research 2025年第6期20卷 1717-1718页

作者： Lieve van Veggel An M.Voets Tim Vanmierlo Rudy Schreiber BIOMED biomedical Research Institute Faculty of Medicine and Life SciencesHasselt UniversityHasseltBelgium department of Psychiatry and Neuropsychology Division of Translational NeuroscienceEuropean Graduate School of NeuroscienceSchool for Mental Health and NeuroscienceMaastricht UniversityMaastrichtThe Netherlands Section of Psychopharmacology Neuropsychology and PsychopharmacologyFaculty of Psychology and NeuroscienceMaastricht UniversityMaastrichtThe Netherlands University MS Center(UMSC) Hasselt-PeltBelgium

Historically,"big pharma"did most central nervous system drug discovery R&D ***,in modern times their"management reductionism"resulted in disappointing pipelines and pharma resided to(late)development,regulatory approval,and marketing(Thong,2015).This had significant consequences for financing and executing research,resulting in a larger role for funding by governments and patient-organizations and a shift of research to academia(Mazzucato,2013).

关键词： academic approval consequences

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Antioxidant and lipoxygenase inhibitory properties of a novel flavonoid from Pistacia chinensis Bunge and its molecular docking analysis

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Traditional Medicine Research 2025年第2期10卷 30-36页

作者： Abdur Rauf Zuneera Akram Naveed Muhammad Najla AlMasoud Taghrid Saad Alomar Saima Naz Abdul Wadood Chandni Hayat Marcello Iriti department of Chemistry University of SwabiAmbar 23561Pakistan department of Pharmacology Faculty of Pharmaceutical SciencesBaqai Medical UniversityKarachi 74600Pakistan department of Pharmacy Abdul Wali Khan University MardanMardan 23200Pakistan department of Chemistry College of SciencePrincess Nourah bint Abdulrahman UniversityRiyadh 11671Saudi Arabia department of Biotechnology BKUC-Bacha Khan University CharsaddaCharsadda 24620Pakistan department of Biochemistry Abdul Wali Khan University MardanMardan 23200Pakistan department of biomedical Surgical and Dental SciencesUniversity of MilanMilan 20129Italy National Interuniversity Consortium of Materials Science and Technology(INSTM) Firenze 50121Italy

Background:Pistacia chinensis Bunge has been traditionally used to manage various conditions,including asthma,pain,inflammation,hepatoprotection,and *** study was conducted to investigate the antioxidant and anti-lipoxygenase(LOX)properties of the isolated compound 2-(3,4-dihydroxyphenyl)-5,7-dihydroxy-4H-chromen-4-one from Pistacia ***:LOX assay and antioxidant activity using 2,2-diphenyl-1-picrylhydrazyl(DPPH)assay were *** docking studies were conducted using a molecular operating ***:The LOX assay revealed significant inhibitory effects at 0.2µM concentration,with an IC50 value of 37.80µ*** antioxidant effect demonstrated dose-dependency across 5 to 100µg/mL concentrations,reaching 93.09%at 100µg/mL,comparable to ascorbic acid’s 95.43%*** docking studies highlighted strong interactions with the lipoxygenase enzyme,presenting an excellent docking score of-10.98 kcal/***:These findings provide valuable insights into Pistacia chinensis’chemical components and biological effects,reinforcing its traditional medicinal applications.

关键词： Pistacia chinensis Bunge antioxidant DPPH assay antilipoxygenase docking analysis

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Basement membrane and blood-brain barrier

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Stroke & Vascular Neurology 2019年第2期4卷 78-82页

作者： Lingling Xu Abhijit Nirwane Yao Yao department of pharmaceutical and biomedical sciences University of GeorgiaAthensGeorgiaUSA

The blood-brain barrier (BBB) is a highly complex and dynamic structure, mainly composed of brain microvascular endothelial cells, pericytes, astrocytes and the basement membrane (BM). The vast majority of BBB research focuses on its cellular constituents. Its non- cellular component, the BM, on the other hand, is largely understudied due to its intrinsic complexity and the lack of research tools. In this review, we focus on the role of the BM in BBB integrity. We first briefly introduce the biochemical composition and structure of the BM. Next, the biological functions of major components of the BM in BBB formation and maintenance are discussed. Our goal is to provide a concise overview on how the BM contributes to BBB integrity.

关键词： barrier blood basement

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Pseudolaric acid B induces apoptosis,senescence,and mitotic arrest in human breast cancer MCF-7

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Acta Pharmacologica Sinica 2007年第12期28卷 1975-1983页

作者： Shin-ichi TASHIRO Satoshi ONODERA Takashi IKEJIMA department of Clinical and biomedical sciences Showa Pharmaceutical University Tokyo 194-8543Japan China-Japan Research Institute of Medical pharmaceutical sciences Shenyang Pharmaceutical UniversityShenyang 110016China

Aim:The aim of the present study was to investigate the inhibitory effect ofpseudolaric acid B （PAB） on human breast cancer MCF-7 ***:3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide analysis,morphologicalchanges,acridine orange staining,and agarose gel electrophoresis were appliedto detect *** percentage of apoptotic and necrotic cells was calcu-lated by the lactate dehydrogenase activity-based cytotoxicity assay;senescenceassociated （SA）-β-galactosidase activity was detected to evaluate senescence;flow cytometric analysis of propidium iodide staining was carried out to investi-gate the distribution of cell cycle,and the protein expression was examined byWestern blot ***:During apoptosis,the half maximal inhibitoryconcentration IC50was 3.4 and 1.35 μmol/L at 36 and 48 h after PAB treatment,*** MCF-7 cells exposed to PAB showed typical characteristics ofapoptosis,including the morphological changes and DNA ***-7 cells treated with 4 μmol/L PAB for 36 h underwent apoptosis,but *** apoptosis induced by PAB was independent of the death *** senescent cells became larger and flatter,and the SA-β-galactosi-dase staining was *** induced obvious mitotic arrest and it precededapoptosis and *** expressions of p21 and p53 was upregulated withPAB treatment,and cyclin B 1 was upregulated and transported from the cyto-plasm to nuclei,and sustained stable ***:PAB induced mitoticarrest in the MCF-7 cells and inhibited proliferation through apoptosis *** apoptosis was independent of the death receptor pathway.

关键词： apoptosis senescence mitotic arrest human breast cancer MCF-7 pseudolaric acid B

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Involvement of mitochondria and caspase pathways in N-demethyl-clarithromycin-induced apoptosis in human cervical cancer HeLa cell

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Acta Pharmacologica Sinica 2006年第12期27卷 1622-1629页

作者： Takashi IKEJIMA Shin-ichi TASHIRO Satoshi ONODERA China-Japan Research Institute of Medical pharmaceutical sciences Shenyang Pharmaceutical UniversityShenyang 110016China department of Clinical and biomedical sciences Showa Pharmaceutical UniversityTokyo 194-8543Japan

Aim:To study the mechanisms by which N-demethyl-clarithromycin(NDC)induces human cervical cancer HeLa cell apoptosis in ***:The viabilityof N-demethyl-clarithromycin-induced HeLa cells was measured by MTT *** cells with condensed nuclei were visualized by phase *** DNA fragmentation was assayed by agarose *** of mitochondrial transmembrane potential wasanalyzed by a FACScan ***-3,poly-(ADP-ribose)polymerase(PARP),caspase-activated DNase(ICAD),Bcl-2,Bax,p53,and SIRT1 proteinexpression and the release of cytochrome c were detected by Western blot ***:N-demethyl-clarithromycin,an anti-inflammatory substance,inhibitedHeLa cell growth in a dose-and time-dependent manner.N-demethyl-clarithro-mycin induced HeLa cell death through the apoptotic *** pan-caspaseinhibitor(z-VAD-fmk),caspase-3 inhibitor(z-DEVD-fmk)and the caspase-9 inhibi-tor(z-LEHD-fmk)partially enhanced cell viability induced by N-demethyl-clarithromycin,but the caspase-8 inhibitor(z-IETD-fmk)had almost no ***-3 was activated then followed by the degradation of caspase-3 substrates,the inhibitor of ICAD and PARE Simultaneously,mitochondrial transmembranepotential was markedly reduced and the release of cytochrome c in the cytosolwas increased.N-demethyl-clarithromycin upregulated the expression ratio ofmitochondrial Bax/Bcl-2,and significantly increased the expression of the *** also downregulated anti-apoptotic protein SIRT1 ***:N-demethyl-clarithromycin induced apoptosis in HeLa cells via themitochondrial pathway.

关键词： N-demethyl-clarithromycin HeLa cells caspase mitochondria

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Evodiamine induces tumor cell death through different pathways: apoptosis and necrosis

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Acta Pharmacologica Sinica 2004年第1期 85-91页

作者： Shin-ichi TASHIRO,Satoshi ONODERA,Takashi IKEJIMA department of Clinical and biomedical sciences Showa pharmaceutical University Tokyo 194-8543 Japan department of Clinical and biomedical sciences Showa pharmaceutical University Tokyo 194-8543 Japan China-Japan Research Institute of Medical and pharmaceutical sciences department of Clinical and biomedical sciences Showa pharmaceutical University Tokyo 194-8543 Japan

AIM: To study the different death pathways in human cervical cancer HeLa and melanoma A375-S2 cells Initiated by evodiamine. METHODS: Viability of evodiamine-induced HeLa and A375-S2 cells was measured by MTT assay. Apoptotic cells with condensed or fragmented nuclei were visualized by Hoechst 33258 staining. Nucleoso mal DNA fragmentation was assayed by agarose gel electrophoresis. Proportion of cell death through apoptotic and necrotic pathways was determined by LDH activity-based cytotoxicity assays. Cell cycle distribution was observed by flow cytometry. RESULTS: Evodiamine induced HeLa and A375-S2 cell death dose- and time-dependently. Caspase-3 and -8 were activated in apoptosis induced by evodiamine 15μmol/L. However, over 24- h

关键词： evodiamine apoptosis necrosis caspases MAP kinase signaling system

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