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Chinese Journal of Integrative Medicine 2024年第3期30卷 213-221页

作者： ZHANG Yue XIAO Yan-wei MA Jing-xin WANG Ao-xue Department of Dermatology the Second Hospital of Dalian Medical UniversityDalianLiaoning Province116021China Department of Cell Biology Dalian Medical UniversityDalianLiaoning Province116044China

Objective:To investigate the effect and possible mechanism of hydroxysafflor yellow a(HSYA) on human immortalized keratinocyte cell proliferation and migration.Methods:HaCaT cells were treated with HSYA.Cell proliferation was detected by the cell counting kit-8 assay,and cell migration was measured using wound healing assay and Transwell migration assay.The mRNA and protein expression levels of heparin-binding epidermal growth factor(EGF)-like growth factor(HBEGF),EGF receptor(EGFR),phosphatidylinositol 3-kinase(PI3K),protein kinase B(AKT),mammalian target of rapamycin(mTOR),and hypoxia-inducible factor-1α(HIF-1α) were detected by quantitative real-time polymerase chain reaction(qRT-PCR) and Western blot,respectively.Circ_0084443-overexpressing HaCaT cells and empty plasmid HaCaT cells were constructed using the lentiviral stable transfection and treated with HSYA.The expression of circ_0084443 was detected by qRT-PCR.Results:HSYA(800 μmol/L) significantly promoted HaCaT cell proliferation and migration(P0.05).Conclusion:HSYA played an accelerative role in HaCaT cell proliferation and migration,which may be attributable to activating HBEGF/EGFR and PI3K/AKT signaling pathways,and had a particular inhibitory effect on the keratinocyte negative regulator circ_0084443.

关键词： hydroxysafflor yellow a circ_0084443 heparin-binding epidermal growth factor-like growth factor/epidermal growth factor receptor phosphatidylinositol 3-kinase/protein kinase B

hydroxysafflor yellow a induced ferroptosis of Osteosarcoma cancer cells by HIF-1α/HK2 and SLC7A11 pathway

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Oncology Research 2024年第5期32卷 899-910页

作者： YIWEN ZHU LIU YANG YING YU YING XIONG PING XIAO XIAO FU XIN LUO Department of Rehabilitation Medicine The Second Affiliated Hospital of Nanchang UniversityNanchang330006China Department of General Practice The Second Affiliated Hospital of Nanchang UniversityNanchang330006China

Osteosarcoma is a very serious primary bone cancer with a high death rate and a dismal prognosis.Since there is no permanent therapy for this condition,it is necessary to develop a cure.Therefore,this investigation was carried out to assess the impacts and biological functions of hydroxysafflor yellow a(HYSA)in osteosarcoma cell lines(MG63).In this investigational study,MG63 cells were utilized.Microarray experiments,quantitative polymerase chain reaction(qPCR),immunofluorescent staining,extracellular acidification rate(ECAR),oxygen consumption rate(OCR),glucose consumption,lactate production,and ATP levels,proliferation assay,5-Ethynyl-2′-deoxyuridine(EDU)staining,and Western blot were performed.In MG63 cells,HYSA lowered cell proliferation and metastasis rates,suppressed EDU cell number,and enhanced caspase-3/9 activity levels.HYSA reduced the Warburg effect and induced ferroptosis(FPT)in MG63 cells.Inhibiting ferroptosis diminished HYSA’s anti-cancer activities in MG63 cells.The stimulation of the HIF-1α/SLC7A11 pathway decreased HYSA’s anti-cancer activities in MG63 cells.HIF-1αis one target spot for HYSA in a model of osteosarcoma cancer(OC).HYSA altered HIF-1α’s thermophoretic activity;following binding with HYSA,HIF-1α’s melting point increased from~55°C to~60°C.HYSA significantly enhanced the thermal stability of exogenous WT HIF-1αwhile not affecting Mut HIF-1α,suggesting that ARG-311,GLY-312,GLN-347,and GLN-387 may be involved in the interaction between HIF-1αand HYSA.Conclusively,our study revealed that HYSA induced FPT and reduced the Warburg effect of OC through mitochondrial damage by HIF-1α/HK2/SLC7A11 pathway.HYSA is a possible therapeutic option for OC or other cancers.

关键词： hydroxysafflor yellow a Osteosarcoma HIF-1α FPT

hydroxysafflor yellow a protects against thioacetamide-induced liver fibrosis in rats via suppressing proinflammatory/fibrogenic mediators and promoting hepatic stellate cell senescence and apoptosis

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Asian Pacific Journal of Tropical Biomedicine 2023年第8期13卷 348-358页

作者： Sayed H.Seif el-Din Olfat A.Hammam Shahira M.Ezzat Samira Saleh Marwa M.Safar Walaa H.El-Maadawy Naglaa M.El-Lakkany Pharmacology Department Theodor Bilharz Research InstituteWarak El-HadarImbaba P.O.Box 30Giza 12411Egypt Pathology Department Theodor Bilharz Research InstituteWarak El-HadarImbaba P.O.Box 30Giza 12411Egypt Pharmacognosy Department Faculty of PharmacyCairo UniversityCairo 11562Egypt Pharmacognosy Department Faculty of PharmacyOctober University for Modern Sciences and ArtsGizaEgypt Pharmacology and Toxicology Department Faculty of PharmacyCairo UniversityCairo 11562Egypt Pharmacology and Biochemistry Department Faculty of PharmacyThe British University in EgyptCairoEgypt

Objective:To evaluate the effect of hydroxysafflor yellow a(HSYA)on thioacetamide-induced liver fibrosis.Methods:Thioacetamide was administered to rats intraperitoneally in doses of 200 mg/kg twice a week for 12 weeks.Thioacetamide-intoxicated rats were given silymarin(50 mg/kg)or HSYA(5 mg/kg)orally every day for 8 weeks.Liver enzymes,fibrosis markers,histological changes as well as immunohistochemistry of TNF-α,IL-6,p21,α-SMA,and caspase-3 were examined.The effect of HSYA on HSC-T6 activation/proliferation and apoptosis was also determined in vitro.Results:HSYA decreased liver enzymes,TNF-α,IL-6,and p21 expressions,hepatic PDGF-B,TIMP-1,TGF-β1,and hydroxyproline levels,as well as fibrosis score(S2 vs.S4)compared to the thioacetamide group.HSYA also downregulatedα-SMA while increasing caspase-3 expression.Surprisingly,at 500μg/mL,HSYA had only a slightly suppressive effect on HSC proliferation,with a 9.5%reduction.However,it significantly reduced TGF-β1,inhibitedα-SMA expression,induced caspase-3 expression,and promoted cell senescence.Conclusions:HSYA may be a potential therapeutic agent for delaying and reversing the progression of liver fibrosis.More research on HSYA at higher doses and for a longer period is warranted.

关键词： hydroxysafflor yellow a Thioacetamide Hepatic stellate cells Inflammatory markers Liver fibrosis p21 α-SMA Apoptosis

hydroxysafflor yellow a Attenuate LipopolysaccharideInduced Endothelium Inflammatory Injury

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Chinese Journal of Integrative Medicine 2016年第1期22卷 36-41页

作者：金鸣孙春燕臧宝霞 Department of Pharmacology Beijing Institute of Heart Lung and Blood Vessel DiseasesBeijing Anzhen HospitalCapital Medical University

Objective： This study observed attenuating effect of hydroxysafflor yellow a （HSYA）, an effective ingredient of aqueous extract of Carthamus tinctorius L, on lipopolysaccharide （LPS）-induced endothelium inflammatory injury. Methods： Eahy926 human endothelium cell （EC） line was used; thiazolyl blue tetrazolium bromide （MTT） test was assayed to observe the viability of EC; Luciferase reporter gene assay was applied to measure nuclear factor- κB （NF- κ B） p65 subunit nuclear binding activity in EC; Western blot technology was used to monitor mitogen activated protein kinase （MAPKs） and NF- κ B activation. Reverse transcription polymerase chain reaction （RT-PCR） method was applied to observe intercellular cell adhesion molecule-1 （ICAM-1） and E-selectin mRNA level; EC surface ICAM-1 expression was measured with flow cytometry and leukocyte adhesion to EC was assayed with Rose Bengal spectrophotometry technology. Results： HSYA protected EC viability against LPS-induced injury （P〈0.05）. LPS-induced NF- κ B p65 subunit DNA binding （P〈0.01） and nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor α （I κ B α） phosphorylation was inhibited by HSYA. HSYA attenuated LPS triggered ICAM-1 and E-selectin mRNA levels elevation and phosphorylation of p38 MAPK or c-Jun N-terminal kinase MAPK. HSYA also inhibited LPS-induced cell surface ICAM-1 protein expression （P〈0.01） and leukocyte adhesion to EC （P〈0.05）. Conclusion： HSYA is effective to protect LPS-induced high expression of endothelium adhesive molecule and inflammatory signal transduction.

关键词： hydroxysafflor yellow a lipopolysaccharide endothelium cell inflammation adhesive molecule

hydroxysafflor yellow a improves learning and memory in a rat model of vascular dementia by increasing VEGF and NR1 in the hippocampus

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Neuroscience Bulletin 2014年第3期30卷 417-424页

作者： Nan Zhang Mengya Xing Yiyi Wang Hao Liang Zhuo Yang Fudong Shi Yan Cheng Department of Neurology Tianjin Medical University General Hospital Tianjin Neurological Institute Key Laboratory of Post-traumatic Neuro-repair and Regeneration in the Central Nervous System Ministry of Education Tianjin Key Laboratory of Injuries Variations and Regeneration of the Nervous System Tianjin Haihe Hospital Nankai University

hydroxysafflor yellow a （HSYA） has angiogenesis- regulating and neuro-protective effects, but its effects on vascular dementia （VaD） are unknown. In this study, 30 adult Sprague-Dawley rats were. randomly allocated to five groups： normal, sham-operation, VaD alone （bilateral carotid artery occlusion）, VaD plus saline （control）, and VaD plus HSYA. One week after operation, the HSYA group received one daily tail-vein injection of 0.6 mg/100 g HSYA for two weeks. Five weeks after operation, the spatial memory of all five groups was evaluated by the water maze task, and synaptic plasticity in the hippocampus was assessed by the long-term potentiation （LTP） method. Vascular endothelial growth factor （VEGF） and N-methyi-D- aspartic acid receptor 1 （NR1） expression in the hippocampus was detected via Western blot. We found that, compared with the group with VaD alone, the group with HSYA had a reduced escape latency in the water maze （P 〈0.05）, and the LTP at CA3- CA1 synapses in the hippocampus was enhanced （P 〈0.05）. Western blot in the late-phase VaD group showed slight up-regulation of VEGF and down- regulation of NR1 in the hippocampus, while HSYA significantly up-regulated both VEGF and NRI. These results suggested that HSYA promotes angiogenesis and increases synaptic plasticity, thus improving spatial learning and memory in the rat model of VaD.

关键词： vascular dementia hydroxysafflor yellow a long-term potentiation NMDA receptor vascular endothelial growth factor

Protective effect of hydroxysafflor yellow a on MSCs against senescence induced by D-galactose

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Chinese Herbal Medicines 2023年第1期15卷 86-93页

作者： Xiaoqing Song Jinying Wang Yu Zhang Xinqian Du Qibing Qian Basic Medical College of Hebei North University Zhangjiakou 075000China

Objective: To examine the protective effects of hydroxysafflor yellow a(HSYA) against the senescence of mesenchymal stem cells(MSCs) induced by D-galactose(D-gal) in vitro, and investigate the potential mechanism involved.Methods: Grouping experiment, Normal control(NC) group: conventional culture with complete medium;Senescence group: MSCs were cultured for 48 h with complete medium containing 10 g/L D-gal;HSYA group: on the basis of senescence induction, HSYA with the suitable concentration was used to protect MSCs. The key experimental indices associated with oxidative stress, inflammatory response, cell senescence, proliferation and apoptosis were measured through chemical colorimetry, β-galactosidase staining, Ed U incorporation and flow cytometry, respectively. The relative quantity(RQ) of proteins related closely to cell proliferation, apoptosis, and NF-κB signaling were measured by Western blotting.Results: As compared with Senescence group, treatment with HSYA(120 mg/L) effectively ameliorated the adverse situation of MSCs. Oxidation stress and inflammation along with D-Gal induction was dramatically alleviated in MSCs;The β-Gal-positive staining indicated that MSC senescence was significantly mitigated;The proliferative capability of MSCs was significantly increased by up-regulating PCNA and inhibiting p16 expression;The anti-apoptotic effect on MSCs was exerted by down-regulating the RQ of cleaved Caspase-3 and Bax;The activity of NF-κB signaling in MSCs was notably suppressed through inhibiting phosphorylation of IKKβ and p65.Conclusion: HSYA(120 mg/L) significantly delayed the D-Gal-induced senescence process in MSCs through attenuating inflammatory reaction and oxidative stress, and suppressing the activity of NF-κB signaling.

关键词： cell senescenc hydroxysafflor yellow a mesenchymal stem cells

Protective Effect of hydroxysafflor yellow a on Bleomycin-Induced Pulmonary Inflammation and Fibrosis in Rats

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Chinese Journal of Integrative Medicine 2018年第1期24卷 32-39页

作者： JIN Ming WANG Lin WU Yan ZANG Bao-xia TAN Li Department of Pharmacology Beijing Institute of Heart Lung and Blood Vessel Diseases Beijing Anzhen HospitalCapital Medical University

Objective： To observe the effect of hydroxysafflor yellow a （HSYA）, an active ingredient of a traditional Chinese herbal medicine Carthamus tinctorius L., on lung inflammation and pulmonary fibrosis induced by bleomycin （BLM） in rats. Methods： Animals were divided into 6 groups including normal group, model group, three HSYA groups and dexamethasone （DXM） group. Three doses of HSYA （35.6, 53.3, and 80.0 mg？kg–1？day–1） were intraperitoneally （i.p.） injected in rats for 3 weeks after BLM administration and DXM was used as the positive control （n=8 or 12）. Arterial blood gas was assayed and morphological changes were observed. Lung mRNA expressions of tumor necrosis factor （TNF）-α, interleukin （IL）-1β, IL-6 and some cytokines in lung tissue were detected by real-time polymerase chain reaction. Nuclear factor-κB p65 or α-smooth muscle actin （α-SMA） protein distribution in rat lung tissue was observed by immunohistochemistry. Results： On the 7th day after BLM administration, lung tissue showed serious inflammation. Treatment with HSYA or DXM ameliorated lung inflammation. After treatment with HSYA or DXM, oxygen partial pressure （PaO2） increased （HSYA 80.0 mg？kg–1, P〈0.01） and CO2 partial pressure （PaCO2） decreased （HSYA 53.3, 80.0 mg？kg–1, P〈0.05）. Moreover, the mRNA expression of TNF-α, IL-1β, and IL-6; and the number of NF-κB p65 positive cells was lower in HSYA 53.3 and 80.0 mg？kg–1 groups than those in the model group （all P〈0.05）. Twenty-one days after BLM administration, HSYA or DXM treatment ameliorated fibrosis, increased PaO2 （HSYA 53.3, 80.0 mg？kg–1, P〈0.01）, and decreased PaCO2 （53.3 and 80.0 mg？kg–1, P〈0.05）. Further, the mRNA expression of TGF-β1, α-SMA, and collagen Ⅰ as well as the number of α-SMA positive cells increased in the model group and HSYA can attenuate these changes （53.3, 80.0 mg？kg–1, P〈0.05）. Hematoxylin and eosin and Masson＇s trichrome staining indicated that the fibrosis and collagen deposition were ameliorated in HSYA groups （53.3, 80.0 mg？kg–1, P〈0.05）. Conclusion： HSYA could alleviat

关键词： hydroxysafflor yellow a pulmonary fibrosis pulmonary inflammation nuclear factor- K B p65,α-smooth muscle actin Chinese medicine

Effect and Safety of hydroxysafflor yellow a for Injection in Patients with Acute Ischemic Stroke of Blood Stasis Syndrome: A Phase Ⅱ , Multicenter, Randomized, Double-Blind, Multiple-Dose, Active-Controlled Clinical Trial

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Chinese Journal of Integrative Medicine 2020年第6期26卷 420-427页

作者： HU Ming-zhe ZHOU Zi-yi ZHOU Zhong-yu LU Hui GAO Min LIU Long-min SONG Hai-qing LIN An-ji WU Qing-ming ZHOU Hong-fei LI Lei WANG Xia CAI Ye-feng The Second Clinical College of Guangzhou University of Chinese Medicine Guangzhou(510006)China Department of Neurology The Second Affiliated Hospital of Guangzhou University of Chinese MedicineGuangzhou(510120)China Department of Acupuncture and Moxibustion Hubei Provincial Hospital of Traditional Chinese MedicineWuhan(430061)China Department of Neurology Ruikang Hospital Affiliated to Guangxi University of Chinese MedicineNanning(530011)China Department of Neurology Guangdong Second Traditional Chinese Medicine HospitalGuangzhou(510095)China Department of Traditional Chinese Medicine Putuo HospitalShanghai University of Traditional Chinese MedicineShanghai(200062)China Department of Neurology Xuanwu HospitalCapital Medical UniversityBeijing(100053)China Department of Traditional Chinese Medicine Xiamen Hospital of Traditional Chinese MedicineXiamen(361001)China Departm ent of Acupuncture and Moxibustion The Second Affiliated Hospital of Hunan University of Traditional Chinese MedicineChangsha(410005)China Departm ent of Neurology The Affiliated Hospital of Liaoning University of Traditional Chinese MedicineShenyang(110032)China School of Public Health Tongji Medical CollegeHuazhong University of Science and TechnologyW uhan(430030)China Youcare Pharm aceutical Group Dingcheng Branch Beijing(100176)China

Objective:To assess the effect and safety of hydroxysafflor yellow a for Injection(HSYAI)in treating patients with acute ischemic stroke(AIS)and blood stasis syndrome(BSS).Methods:A multicenter,randomized,double-blind,multiple-dose,active-controlled phaseⅡtrial was conducted at 9 centers in China from July 2013 to September 2015.Patients with moderate or severe AIS and BSS were randomly assigned to low-,medium-,high-dose HSYAI groups(25,50 and 70 mg/d HSYAI by intravenous infusion,respectively),and a control group(Dengzhan Xixin Injection(灯盏细辛注射液,DZXXI)30 mL/d by intravenous infusion),for 14 consecutive days.The primary outcome was the Modified Rankin Scale(mRS)score 1 at days 90 after treatment.The secondary outcomes included the National Institute of Health Stroke Scale(NIHSS)score 1,Barthel Index(BI)score 95,and BSS score reduced 30%from baseline at days 14,30,60,and 90 after treatment.The safety outcomes included any adverse events during 90 days after treatment.Results:Of the 266 patients included in the effectiveness analysis,66,67,65 and 68 cases were in the low-,medium-,and high-dose HSYAI and control groups,respectively.The proportions of patients in the medium-and high-dose HSYAI groups with mRS score 1 at days 90 after treatment were significantly larger than the control group(P0.05).Conclusions:HSYAI was safe and well-tolerated at all doses for treating AIS patients with BSS.The medium(50 mg/d)or high dose(75 mg/d)might be the optimal dose for a phaseⅢtrial.

关键词： hydroxysafflor yellow a acute ischemic stroke randomized controlled trial blood stasis syndrome Chinese medicine

hydroxysafflor yellow a (HSYA) protects hippocampal neurons from excitotoxic death through inhibition of synaptic NMDA receptors

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Hydroxysafflor yellow A (HSYA) protects hippocampal neurons ...

The safflower MBW complex regulates HYSA accumulation through degradation by the E3 ligase CtBB1

中国生理学会第24届全国会员代表大会暨生理学学术大会

作者：王兴涛高速于洋杨柳孙晖马春蕾滨州医学院生理学教研室神经科学研究所山东省"脑中风重点实验室"

hydroxysafflor yellow a(HSYA)was reported to be neuroprotective both in middle cerebral artery occlusion(MCAO)animal model and in cultured cortical neurons.However,the underlying mechanism remains unclear.It has been known that mass glutamate release and over stimulation of N-methyl-d-aspartate(NMDA)type glutamate receptors are the main cause of neuronaldeath inbrain ischemia.With patch-clamp recordings of mouse hippocampal slices,primary hippocampal cultures,Ca2+imaging,and Western blot approaches,we found that HSYA effectively inhibited NMDA rreceptor-mediated excitatory postsynaptic currents(NMDAR EPSCs)which had a half maximum inhibition of0μM.HSYA was also suppressed presynaptic glutamate transmitter release.Moreover,HSYA suppressed NMDAR-mediated oxygen-glucose-deprivation(OGD)evoked long-term potentiation(LTP)which resemble the reperfusion damage in brain ischemia.In cell viability assay,HSYA attenuated NMDA induced apoptotic and necrotic cell death rate.The attenuation effect was HSYA concentration dependent.Ca2+imaging experiments also exihibited that NMDA-evoked inctracellular Ca2+concentration([Ca2+]i)increase was distinctly reduced or even abolished by containing different concentration of HSYA in extracellular solution.In western blot assay,we found that the intracellular apoptotic signaling molecule,cleaved-caspase3,expression was also suppressed by HSYA.Furthermore,HSYA protected CA1pyramidal cells of hippocampus against NMDA receptor-mediated membrane depolarization currents in OGD condition.All together,our data for the first time give the direct evidences that HSYA inhibits NMDAR-mediated synaptic transmission in hippocampal slices and intracellular Ca2+increase evoked by NMDA in hippocampal cultures,exerting the neuronal protection effect in the condition of high concentration of extracellular NMDA or glutamate,such as in brain ischemia.Our data indicate that HSYA has a strong neuronal protection effect on NMDAR-mediated excitotoxic death and might be the promising medicine in the treatment of

关键词： NMDA receptor neuron excitotoxicity hydroxysafflor yellow a Patch-clamp recordings Ca2+ imaging

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Journal of Integrative Plant Biology 2023年第5期65卷 1277-1296页

作者： Yingqi Hong Yanxi Lv Jianyi Zhang Naveed Ahmad Xiaokun Li Na Yao Xiuming Liu Haiyan Li College of Life Sciences Engineering Research Center of the Chinese Ministry of Education for Bioreactor and Pharmaceutical DevelopmentJilinAgriculturalUniversityChangchun130118China Collegeof Tropical Crops Hainan UniversityHaikou 570100China Joint Center for Single Cell Biology School of Agriculture and BiologyShanghajiaotong UniversityShanghai 200240China Institute of Life Sciences Wenzhou Medical UniversityWenzhou 325000China Biomedical Collaborative Innovation Center of Zhejiang Province Wenzhou Medical UniversityWenzhou 325000China

The regulatory mechanism of the MBW(MYB-bHLH-WD40) complex in safflower(Carthamus tinctorius) remains unclear. In the present study,we show that the separate overexpression of the genes CtbHLH41, CtMYB63, and CtWD40-6 in Arabidopsis thaliana increased anthocyanin and procyanidin contents in the transgenic plants and partially rescued the trichome reduction phenotype of the corresponding bhlh41, myb63,and wd40-6 single mutants. Overexpression of CtbHLH41, CtMYB63, or CtWD40-6 in safflower significantly increased the content of the natural pigment hydroxysafflor yellow a(HYSA)and negatively regulated safflower petal size.Yeast-two-hybrid, functional, and genetic assays demonstrated that the safflower E3 ligase CtBB1(BIG BROTHER 1) can ubiquitinate CtbHLH41,marking it for degradation through the 26S proteasome and negatively regulating flavonoid accumulation. CtMYB63/CtWD40-6 enhanced the transcriptional activity of CtbHLH41 on the CtDFR(dihydroflavonol 4-reductase) promoter.We propose that the MBW-CtBB1 regulatory module may play an important role in coordinating HYSA accumulation with other response mechanisms.

关键词： CtBB1 hydroxysafflor yellow a MBW safflower ubiquitination