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icariin attenuates vascular endothelial dysfunction by inhibiting inflammation through GPER/Sirt1/HMGB1 signaling pathway in type 1 diabetic rats

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Chinese Journal of Natural Medicines 2024年第4期22卷 293-306页

作者： YAO Wenhui TAO Rongpin WANG Kai DING Xuansheng School of Basic Medicine and Clinical Pharmacy China Pharmaceutical UniversityNanjing211198China

icariin, a flavonoid glycoside, is extracted from Epimedium. This study aimed to investigate the vascular protective effects of icariin in type 1 diabetic rats by inhibiting high-mobility group box 1 (HMGB1)-related inflammation and exploring its potential mechanisms. The impact of icariin on vascular dysfunction was assessed in streptozotocin (STZ)-induced diabetic rats through vascular reactivity studies. Western blotting and immunofluorescence assays were performed to measure the expressions of target proteins. The release of HMGB1 and pro-inflammation cytokines were measured by enzyme-linked immunosorbent assay (ELISA). The results revealed that icariin administration enhanced acetylcholine-induced vasodilation in the aortas of diabetic rats. It also notably reduced the release of pro-inflammatory cytokines, including interleukin-8 (IL-8), IL-6, IL-1β, and tumor necrosis factor-alpha (TNF-α) in diabetic rats and high glucose (HG)-induced human umbilical vein endothelial cells (HUVECs). The results also unveiled that the pro-inflammatory cytokines in the culture medium of HUVECs could be increased by rHMGB1. The increased release of HMGB1 and upregulated expressions of HMGB1-related inflammatory factors, including advanced glycation end products (RAGE), Toll-like receptor 4 (TLR4), and phosphorylated p65 (p-p65) in diabetic rats and HG-induced HUVECs, were remarkably suppressed by icariin. Notably, HMGB1 translocation from the nucleus to the cytoplasm in HUVECs under HG was inhibited by icariin. Meanwhile, icariin could activate G protein-coupled estrogen receptor (GPER) and sirt1. To explore the role of GPER and Sirt1 in the inhibitory effect of icariin on HMGB1 release and HMGB-induced inflammation, GPER inhibitor and Sirt1 inhibitor were used in this study. These inhibitors diminished the effects of icariin on HMGB1 release and HMGB1-induced inflammation. Specifically, the GPER inhibitor also negated the activation of Sirt1 by icariin. These findings suggest that icariin activates GPER and increases the exp

关键词： icariin Diabetes Inflammation Vascular endothelial dysfunction GPER HMGB1

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icariin accelerates bone regeneration by inducing osteogenesisangiogenesis coupling in rats with type 1 diabetes mellitus

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World Journal of Diabetes 2024年第4期15卷 769-782页

作者： Sheng Zheng Guan-Yu Hu Jun-Hua Li Jia Zheng Yi-Kai Li Department of Traditional Chinese Orthopedics and Traumatology Center for Orthopedic SurgeryThe Third Affiliated Hospital of Southern Medical UniversityGuangzhou 510630Guangdong ProvinceChina School of Traditional Chinese Medicine Southern Medical UniversityGuangzhou 510515Guangdong ProvinceChina Department of Endocrinology Peking University First HospitalBeijing 100034China

BACKGROUND icariin(ICA),a natural flavonoid compound monomer,has multiple pharmacological activities.However,its effect on bone defect in the context of type 1 diabetes mellitus(T1DM)has not yet been examined.AIM To explore the role and potential mechanism of ICA on bone defect in the context of T1DM.METHODS The effects of ICA on osteogenesis and angiogenesis were evaluated by alkaline phosphatase staining,alizarin red S staining,quantitative real-time polymerase chain reaction,Western blot,and immunofluorescence.Angiogenesis-related assays were conducted to investigate the relationship between osteogenesis and angiogenesis.A bone defect model was established in T1DM rats.The model rats were then treated with ICA or placebo and micron-scale computed tomography,histomorphometry,histology,and sequential fluorescent labeling were used to evaluate the effect of ICA on bone formation in the defect area.RESULTS ICA promoted bone marrow mesenchymal stem cell(BMSC)proliferation and osteogenic differentiation.The ICA treated-BMSCs showed higher expression levels of osteogenesis-related markers(alkaline phosphatase and osteocalcin)and angiogenesis-related markers(vascular endothelial growth factor A and platelet endothelial cell adhesion molecule 1)compared to the untreated group.ICA was also found to induce osteogenesis-angiogenesis coupling of BMSCs.In the bone defect model T1DM rats,ICA facilitated bone formation and CD31hiEMCNhi type H-positive capillary formation.Lastly,ICA effectively accelerated the rate of bone formation in the defect area.CONCLUSION ICA was able to accelerate bone regeneration in a T1DM rat model by inducing osteogenesis-angiogenesis coupling of BMSCs.

关键词： icariin Osteogenesis-angiogenesis coupling Type 1 diabetes mellitus Bone defect Bone regeneration

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icariin ameliorates viral myocarditis by inhibiting TLR4-mediated ferroptosis

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Asian Pacific Journal of Tropical Biomedicine 2024年第3期14卷 106-114,I0002-I0005页

作者： Wei Luo Yi Lu Jun-Hua Deng Peng Liu Yan Huang Wan-Xi Liu Chun-Li Huang Laboratory of the Atherosclerosis and Ischemic Cardiovascular Diseases Department of CardiologyAffiliated Hospital of Youjiang Medical University for NationalitiesYoujiang Medical University for NationalitiesBaiseGuangxi 533000China Department of Critical Care Medicine Affiliated Hospital of Youjiang Medical University for NationalitiesBaiseGuangxi 533000China Department of Respiratory and Critical Care Medicine Affiliated Hospital of Youjiang Medical University for NationalitiesBaiseGuangxi 533000China Postgraduate School of Youjiang Medical University for Nationalities BaiseGuangxi 533000China Department of Neonatology Affiliated Hospital of Youjiang Medical University for NationalitiesBaiseGuangxi 533000China Department of Nephrology People’s Hospital of PubeiQinzhouGuangxi 535300China Urban Community Health Service Center of Youjiang District BaiseGuangxi 533000China

Objective:To explore the mechanism by which icariin alleviates viral myocarditis.Methods:CVB3-induced cardiomyocytes were used as an in vitro model of viral myocarditis to assess the effects of icariin treatment on cell viability,inflammation,and apoptosis.Moreover,the effects of icariin on ferroptosis and TLR4 signaling were assessed.After AC16 cells were transfected with TLR4 overexpression plasmids,the role of TLR4 in mediating the regulatory effect of icariin in viral myocarditis was investigated.Results:icariin significantly elevated cell viability and reduced inflammatory factors TNF-α,IL-1β,IL-6,and IL-18.Flow cytometry revealed that icariin decreased apoptosis rate,and the protein expression of Bax and cleaved caspase 3 and 9 in CVB3-induced cardiomyocytes.Additionally,it suppressed ferroptosis including lipid peroxidation and ferrous ion,as well as the TLR4 signaling.However,TLR4 overexpression abrogated the modulatory effects of icariin.Conclusions:icariin mitigates CVB3-induced myocardial injury by inhibiting TLR4-mediated ferroptosis.Further animal study is needed to verify its efficacy.

关键词： Viral myocarditis CVB3 TLR4 Ferroptosis icariin

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icariin plus curcumol enhances autophagy through the mTOR pathway and promotes cathepsin B-mediated pyroptosis of prostate cancer cells

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Asian Pacific Journal of Tropical Biomedicine 2024年第2期14卷 55-64页

作者： Xu-Yun Wang Wen-Jing Xu Bo-Nan Li Tian-Song Sun Wen Sheng Department of Andrology Beijing Hospital of Traditional Chinese MedicineCapital Medical UniversityBeijing100010China Department of Dermatology The First Affiliated Hospital of Hunan University of Chinese MedicineChangsha410021China School of Integrated Chinese and Western Medicine Hunan University of Chinese MedicineChangsha410208China Andrology Laboratory Hunan University of Chinese MedicineChangsha410208China School of Rehabilitation Medicine and Health Care Hunan University of MedicineHuaihua418000China School of Traditional Chinese Medicine Hunan University of MedicineHuaihua418000China

Objective:To examine the effect of icariin plus curcumol on prostate cancer cells PC3 and elucidate the underlying mechanisms.Methods:We employed the Cell Counting Kit 8 assay and colony formation assay to assess cell viability and proliferation.Autophagy expression was analyzed using monodansylcadaverine staining.Immunofluorescence and Western blot analyses were used to evaluate protein expressions related to autophagy,pyroptosis,and the mTOR pathway.Cellular damage was examined using the lactate dehydrogenase assay.Moreover,cathepsin B and NLRP3 were detected by co-immunoprecipitation.Results:icariin plus curcumol led to a decrease in PC3 cell proliferation and an enhancement of autophagy.The levels of LC3-Ⅱ/LC3-Ⅰand beclin-1 were increased,while the levels of p62 and mTOR were decreased after treatment with icariin plus curcumol.These changes were reversed upon overexpression of mTOR.Furthermore,3-methyladenine resulted in a decrease in inflammatory cytokines,pyroptosis-related protein levels,and lactate dehydrogenase concentration,compared to the icariin plus curcumol group.Inhibiting cathepsin B reversed the regulatory effects of icariin plus curcumol.Conclusions:icariin plus curcumol demonstrates great potential as a therapeutic agent for castration-resistant prostate cancer by enhancing autophagy via the mTOR pathway and promoting pyroptosis mediated by cathepsin B.These findings provide valuable insights into the molecular mechanisms underlying the therapeutic potential of icariin and curcumol for prostate cancer treatment.

关键词： icariin Curcumol Autophagy mTOR Cathepsin B Pyroptosis Prostate cancer

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icariin ameliorates memory deficits through regulating brain insulin signaling and glucose transporters in 3×Tg-AD mice

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Neural Regeneration Research 2023年第1期18卷 183-188页

作者： Fei Yan Ju Liu Mei-Xiang Chen Ying Zhang Sheng-Jiao Wei Hai Jin Jing Nie Xiao-Long Fu Jing-Shan Shi Shao-Yu Zhou Feng Jin Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnomedicine of Ministry of Education Zunyi Medical UniversityZunyiGuizhou ProvinceChina Institute of Digestive Diseases Affiliated Hospital of Zunyi Medical UniversityZunyiGuizhou ProvinceChina

icariin,a major prenylated flavonoid found in Epimedium spp.,is a bioactive constituent of Herba Epimedii and has been shown to exert neuroprotective effects in experimental models of Alzheimer’s disease.In this study,we investigated the neuroprotective mechanism of icariin in an APP/PS1/Tau triple-transgenic mouse model of Alzheimer’s disease.We performed behavioral tests,pathological examination,and western blot assay,and found that memory deficits of the model mice were obviously improved,neuronal and synaptic damage in the cerebral cortex was substantially mitigated,and amyloid-βaccumulation and tau hyperphosphorylation were considerably reduced after 5 months of intragastric administration of icariin at a dose of 60 mg/kg body weight per day.Furthermore,deficits of proteins in the insulin signaling pathway and their phosphorylation levels were significantly reversed,including the insulin receptor,insulin receptor substrate 1,phosphatidylinositol-3-kinase,protein kinase B,and glycogen synthase kinase 3β,and the levels of glucose transporter 1 and 3 were markedly increased.These findings suggest that icariin can improve learning and memory impairments in the mouse model of Alzheimer’s disease by regulating brain insulin signaling and glucose transporters,which lays the foundation for potential clinical application of icariin in the prevention and treatment of Alzheimer’s disease.

关键词： Alzheimer’s disease amyloid-beta brain insulin signaling glucose transporter glucose uptake icariin memory neurodegenerative disease tau hyperphosphorylation triple-transgenic Alzheimer’s disease mice

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Exploration of the mechanism by which icariin modulates hippocampal neurogenesis in a rat model of depression

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Neural Regeneration Research 2022年第3期17卷 632-642页

作者： Ning-Xi Zeng Hui-Zhen Li Han-Zhang Wang Kai-Ge Liu Xia-Yu Gong Wu-Long Luo Can Yan Li-Li Wu Research Center for Basic Integrative Medicine Guangzhou University of Chinese MedicineGuangzhouGuangdong ProvinceChina

icariin(ICA) has a significant capacity to protect against depression and hippocampal injury,but it cannot effectively cross the bloodbrain barrier and accumulate in the brain.Therefore,the mechanism by which ICA protects against hippocampal injury in depression remains unclear.In this study,we performed proteomics analysis of cerebrospinal fluid to investigate the mechanism by which ICA prevents dysfunctional hippocampal neurogenesis in depression.A rat model of depression was established through exposure to chronic unpredictable mild stress for 6 weeks,after which 120 mg/kg ICA was administered subcutaneously every day.The results showed that ICA alleviated depressive symptoms,learning and memory dysfunction,dysfunctional neurogenesis,and neuronal loss in the dentate gyrus of rats with depression.Neural stem cells from rat embryonic hippocampi were cultured in media containing 20% cerebrospinal fluid from each group of rats and then treated with 100 μM corticosterone.The addition of cerebrospinal fluid from rats treated with ICA largely prevented the corticosterone-mediated inhibition of neuronal proliferation and differentiation.Fifty-two differentially expressed proteins regulated by chronic unpredictable mild stress and ICA were identified through proteomics analysis of cerebrospinal fluid.These proteins were mainly involved in the ribosome,PI3 K-Akt signaling,and interleukin-17 signaling pathways.Parallel reaction monitoring mass spectrometry showed that Rps4 x,Rps12,Rps14,Rps19,Hsp90 b1,and Hsp90 aa1 were up-regulated by chronic unpredictable mild stress and down-regulated by ICA.In contrast,Htr A1 was down-regulated by chronic unpredictable mild stress and up-regulated by ICA.These findings suggest that ICA can prevent depression and dysfunctional hippocampal neurogenesis through regulating the expression of certain proteins found in the cerebrospinal fluid.The study was approved by the Experimental Animal Ethics Committee of Guangzhou University of Chinese Medicine of China in March 2017.

关键词： cerebrospinal fluid chronic unpredictable mild stress depression dysfunctional hippocampal neurogenesis hippocampus icariin proteomics ribosome pathway

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Potential role of microRNA-503 in icariin-mediated prevention of high glucose-induced endoplasmic reticulum stress

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World Journal of Diabetes 2023年第8期14卷 1234-1248页

作者： Bao-Lin Su Liang-Liang Wang Liang-You Zhang Shu Zhang Qiang Li Gang-Yi Chen Department of Nephrology The First Affiliated Hospital of Guangzhou University of Traditional Chinese MedicineGuangzhou 510405Guangdong ProvinceChina

BACKGROUND Dysregulated microRNA(miRNA)is crucial in the progression of diabetic nephropathy(DN).AIM To investigate the potential molecular mechanism of icariin(ICA)in regulating endoplasmic reticulum(ER)stress-mediated apoptosis in high glucose(HG)-induced primary rat kidney cells(PRKs),with emphasis on the role of miR-503 and sirtuin 4(SIRT4)in this process.METHODS Single intraperitoneal injection of streptozotocin(65 mg/kg)in Sprague-Dawley rats induce DN in the in vivo hyperglycemic model.Glucose-treated PRKs were used as an in vitro HG model.An immunofluorescence assay identified isolated PRKs.Cell Counting Kit-8 and flow cytometry analyzed the effect of ICA treatment on cell viability and apoptosis,respectively.Real-time quantitative polymerase chain reaction and western blot analyzed the levels of ER stressrelated proteins.Dual luciferase analysis of miR-503 binding to downstream SIRT4 was performed.RESULTS ICA treatment alleviated the upregulated miR-503 expression in vivo(DN)and in vitro(HG).Mechanistically,ICA reduced HG-induced miR-503 overexpression,thereby counteracting its function in downregulating SIRT4 levels.ICA regulated the miR-503/SIRT4 axis and subsequent ER stress to alleviate HG-induced PRKs injury.CONCLUSION ICA reduced HG-mediated inhibition of cell viability,promotion of apoptosis,and ER stress in PRKs.These effects involved regulation of the miR-503/SIRT4 axis.These findings indicate the potential of ICA to treat DN,and implicate miR-503 as a viable target for therapeutic interventions in DN.

关键词： icariin MicroRNA-503 Sirtuin 4 Endoplasmic reticulum stress Diabetic nephropathy Kidney damage

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icariin protects vascular endothelial cells from oxidative stress through inhibiting endoplasmic reticulum stress

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Journal of Integrative Medicine 2019年第3期17卷 205-212页

作者： Fang-yuan Wang Jian Jia Huan-huan Song Cheng-ming Jia Chang-bo Chen Jing Ma Department of Traditional Chinese Medicine Army Medical Center in Traditional Chinese MedicineXijing HospitalForth Military Medical University

Objective: To investigate the protective effect and underlying mechanism(s) of icariin(ICA) in preventing hydrogen peroxide(H_2O_2)-induced vascular endothelial cell injury via endoplasmic reticulum stress(ERS).Methods: To study the effects of ICA on H_2O_2-induced damage, we used the cell counting kit-8 assay to detect cell viability and the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay to determine cell adhesion and apoptosis, respectively. Spectrophotometry and enzyme-linked immunosorbent assay were used to measure the expression levels of superoxide dismutase(SOD) and glutathione peroxidase(GSH-Px). Subsequently, glucose-regulated protein 78(GRP78), activating transcription factor-4(ATF4) and eukaryotic initiation factor-2 a(eIF2 a) were detected using Western blotting.Results: In human umbilical vein endothelial cells, different concentrations of ICA exhibited multiple effects, including reduced H_2O_2 damage, improved cell viability and adhesion, reduced cell apoptosis and increased SOD and GSH-Px activity. Among the ICA concentrations used, only the H_2O_2+ 100 lmol/L ICA group had significant differences compared to the H_2O_2 group. ERS activators H_2O_2 and DL-dithiothreitol(DTT) significantly increased GRP78, ATF4 and eIF2 a expressions, decreased cell activity and reduced SOD and GSH-Px activity. In contrast, the H_2O_2+ 100 lmol/L ICA and H_2O_2+ 100 lmol/L ICA + DTT groups had significant inhibitory effects on the expressions of GRP78,ATF4 and eIF2 a proteins, showing enhanced cell viability and SOD and GSH-Px activity.Conclusion: The results showed the dose-dependent effects of ICA against H_2O_2-induced injury in vascular endothelial cells. The inhibition of GRP78, ATF4 and eIF2 a protein expressions in the ERS, and the subsequent alleviation of oxidative stress damage, might be the molecular mechanism.

关键词： icariin Endoplasmic reticulum stress Human umbilical vein endothelial cells Oxidative stress

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icariin Protects SH-SY5Y Cells from Formaldehyde-Induced Injury through Suppression of Tau Phosphorylation

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Chinese Journal of Integrative Medicine 2016年第6期22卷 430-437页

作者：宋宜祥苗君叶强敏赫荣乔王学美黎巍威 Integrated Laboratory of Chinese and Western Medicine Peking University First Hospital State Key Laboratory of Brain and Cognitive Science Institute of Biophysics Chinese Academy of Sciences

Objective： To investigate the neuroprotective effects of icariin on formaldehyde （FA）-treated human neuroblastoma SH-SY5Y cells and the possible mechanisms involved. Methods： SH-SY5Y cells were divided into FA treatment group, FA treatment group with icariin, and the control group. Cell viability, apoptosis, and morphological changes were determined by cell counting kit-8 （CCK 8）, flow cytometry, and confocal microscopy, respectively. The phosphorylation of Tau protein was examined by western blotting. Results： FA showed a half lethal dose （LD50） of 0.3 mmol/L in SH-SY5Y cells under the experimental conditions. icariin （1-10 μ mol/L） prevented FA-induced cell death in SH-SY5Y cells in a dose-dependent manner, with the optimal effect observed at 5 μmol/L. After FA treatment, the absorbance in FA group was 1.31±0.05, while in the group of icariin （5μmol/L） was 1.63±0.05. Examination of cell morphology by confocal microscopy demonstrated that 5 μmol/L icariin significantly attenuated FA-induced cell injury （P〈0.05）. Additionally, icariin inhibited FA-induced cell apoptosis in SH-SY5Y cells. Results from western blotting showed that icariin suppressed FA-induced phosphorylation at Thr 181 and Ser 396 of Tau protein, while having no effect on the expression of the total Tau protein level. Furthermore, FA activated Tau kinase glycogen synthase kinase 3 beta （GSK-3β） by enhancement of Y216 phosphorylation, but icariin reduced Y216 phosphorylation and increased Ser 9 phosphorylation. Conclusion： icariin protects SH-SY5Y cells from FA-induced injury possibly through the inhibition of GSK-3β -mediated Tau phosphoryiation.

关键词： icariin formaldehyde Tau phosphorylation glycogen synthase kinase 3 beta neuroprotection

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icariin promotes expression of PGC-1α,PPARα,and NRF-1 during cardiomyocyte differentiation of murine embryonic stem cells in vitro

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Acta Pharmacologica Sinica 2007年第10期28卷 1541-1549页

作者： Ling DING,Xing-guang LIANG,Dan-yan ZHU,Yi-jia LOU~2Institute of Pharmacology and Toxicology and Biochemical Pharmaceutics,College of Pharmaceutical Sciences,Zhejiang University,Hangzhou 310058,China Institute of Pharmacology and Toxicology and Biochemical Pharmaceutics College of Pharmaceutical Sciences Zhejiang University Hangzhou China

Aim:To investigate the effect of icariin on the expression of peroxisome proliferator-activated receptor γ coactivator-1 alpha (PGC-1 α),peroxisome proliferator-activated receptor alpha (PPARα),and nuclear respiratory factor 1 (NRF-1) oncardiomyocyte differentiation of murine embryonic stem (ES) cells in vitro.Methods:The cardiomyocytes derived from murine ES cells were verified byimmunocytochemistry using confocal laser scanning microscopy.Cardiac-specific sarcomeric proteins (ie α-actinin,troponin T) were evaluated when em-bryoid bodies (EB) were treated with icariin or retinoid acid.The expression ofPGC-1α,PPARα,and NRF-1 were analyzed using both semiquantitative RT-PCRand Western blotting in cardiomyocyte differentiation.The phosphorylation ofthe p38 mitogen-activated protein kinase (MAPK) was studied in the differentia-tion process,and its specific inhibitor SB203580 was employed to confirm thefunction of the p38 MAPK on icariin-induced cardiac differentiation.Results:The application of icariin significantly induced the cardiomyocyte differentiationof EB as indicated by the promoted expression of α-actinin and troponin T.Theexpression of PGC-1α,PPARα,and NRF-1 increased coincidently in early differ-entiation and the increase was dose-dependently upregulated by icariin treatment.The phosphorylation of the p38 MAPK peaked on d 6 and decreased after d 8,andthe activation was further enhanced and prolonged when the EB were subjectedto icariin,which was concurrent with the elevation of PGC-1α,PPARα,and NRF-1.Moreover,the inhibition of the p38 MAPK pathway by SB203580 efficientlyabolished icariin-stimulated cardiomyocyte differentiation and resulted in the cap-ture of the upregulation of PGC-1α,PPARα,and NRF-1.Conclusion:Takentogether,icariin promoted the expression of PGC-1α,PPARα,and NRF-1 duringcardiomyocyte differentiation of murine ES cells in vitro and the effect was partlyresponsible for the activation of the p38 MAPK.

关键词： icariin PGC-lα PPARα NRF-1 mitochondrial cardiomyocytes embryonic stem cells differentiation

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