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salvianolic acid a alleviates renal injury in systemic lupus erythematosus induced by pristane in BALB/c mice

Acta Pharmaceutica Sinica B 2017年第2期7卷 159-166页

作者： Yihuang Lin Yu Yan Huifang Zhang Yucai Chen Yangyang He Shoubao Wang Lianhua Fang Yang Lv Guanhua Du State Key Laboratory of Bioactive Substances and Functions of Natural Medicines Institute of Materia MedicaChinese Academy of Medical Sciences and Peking Union Medical College State Key Laboratory of Cardiovascular Disease Fuwai HospitalNational Center for Cardiovascular Diseases Beijing Key Laboratory of Drug Targets Identification and Drug Screening Institute of Materia MedicaChinese Academy of Medical Sciences and Peking Union Medical College Beijing Key Laboratory of Polymorphic Drugs Institute of Materia MedicaChinese Academy of Medical Sciences and Peking Union Medical College

The purpose of this study was to investigate the effects of salvianolic acid a(SAA) in systemic lupus erythematosus(SLE) induced by pristane in BALB/c mice.Lupus mice were established by confirming elevated levels of autoantibodies and IL-6 after intraperitoneal injection of pristane.Mice were then treated with daily oral doses of SAA for 5 months in parallel with mice treated with prednisone and aspirin as positive controls.The levels of autoantibodies were monitored at monthly intervals and nephritic symptoms observed by hematoxylin and eosin(H&E) and periodic acid-Schiff(PAS) staining.Western blot analysis of renal tissue was also employed.SAA treatment caused a significant reduction in the levels of anti-Sm autoantibodies and reduced renal histopathological changes and pathological effects.SAA treatment also significantly inhibited the phosphorylation of IKK,IκB and NFκB in renal tissues of lupus mice.In conclusion,the results suggest that SAA alleviates renal injury in pristane-induced SLE in BALB/c mice through inhibition of phosphorylation of IKK,IκB and NFκB.

关键词： salvianolic acid a SLE Renal injury Autoantibodies Pristane BALB/c mice NFκB

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salvianolic acid a ameliorates AGEs-induced glomerular endothelial dysfunction and protects against diabetic nephropathy

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中国药理学与毒理学杂志 2017年第10期31卷 1011-1012页

作者： Bi-yu HOU Yue-rong ZHAO Gui-fen QIANG Xi CHEN Xiu-ying YANG Li ZHANG Guan-hua DU Beijing Key Laboratory of Drug Target Identification and Drug Screening Institute of Materia MedicaChinese Academy of Medical Sciences & Peking Union Medical College School of Traditional Chinese Medicine Guangdong Pharmaceutical University

OBJECTIVE Diabetic nephropathy(DN)has been one of the most common complications of diabetes and the leading cause of end-stage renal disease.Glomerular hyperfiltrationis central in earlystage of DN and leads to the progression of renal architectonic and functional abnormalities.salvianolic acid a(SalA)has been proved to protect diabetic complications such as hepatic fibrosis and neuropathy.The present study was designed to investigate the effects of SalA on glomerular endothelial dysfunctionand diabetic nephropathy.METHODS Primary glomerular endothelial cells were subjected to assess permeability under injury of advanced glycation end-products(AGEs).AGEs-induced changes of Rho A/ROCK pathway and cytoskeleton rearrangement were assessed bywestern blotandimmunofluorescence.The beneficial effects of SalA on diabetic nephropathy were investigated in a rat model induced by high-fat and high-glucose diet combined with low dose of streptozocin(35 mg·kg^(-1),ip).Renal function and architectonic changes were evaluated by biochemical assay and PAS staining.RESULTS SalA 3μMameliorated AGEs-induced glomerular endothelial permeability(P<0.05)and suppressed rearrangement of cytoskeleton through inhibiting AGE-RAGE-Rho A/ROCK pathway.SalA1 mg·kg^(-1)markedly reduced endothelium loss(P<0.01)and glomerular hyperfiltration(P<0.05)in diabetic kidney.Subsequently,SalA 1 mg·kg^(-1) suppressed glomerular hypertrophy and mesangial matrix expansion,eventually reduced 24 h-urinary albumin and ameliorated renal function by decreasing blood urine nitrogen(BUN),serum creatinine(Scr)and serum n-acetyl-β-d-glucosaminidase(NAG).AGEs-RAGE-Nox4-induced oxidative stress was suppressed by the treatment of SalA 1 mg·kg^(-1).CONCLUSION SalA ameliorated AGEs-induced glomerular endothelial hyperpermeability,and effectively protected against early-stage diabetic nephropathy by reducing hyperfiltration and alleviating renal structural deterioration through inhibiting AGEs and its downstream pathway.Thus,SalA might be a promising therapeutic agent for th

关键词： salvianolic acid a diabetic nephropathy glomerular hyperfiltration

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salvianolic acid a attenuates vascular remodeling in a pulmonary arterial hypertension rat model

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中国药理学与毒理学杂志 2016年第10期30卷 1011-1012页

作者： CHEN Yu-cai YUAN Tian-yi ZHANG Hui-fang FANG Lian-hua DU Guan-hua Beijing Key Laboratory of Drug Targets Identification and Drug Screening Institute of Materia Medica Chinese Academy of Medical Sciences and Peking Union Medical College

OBJECTIVE The current therapeutic approaches have a limited effect on the dysregulated pulmonary vascular remodeling,which is characteristic of pulmonary arterial hypertension(PAH).In this study we exam-ined whether salvianolic acid a(SAA)extracted from the traditional Chinese medicine′Dan Shen′attenuated vascular remodeling in a PAH rat model,and elucidated the underlying mechanisms.METHODS PAH was induced in rats by injecting a single dose of monocrotaline(MCT 60 mg·kg-1,sc).The rats were orally treated with either SAA(0.3,1,3 mg·kg-1·d-1)or a positive control bosentan(30 mg·kg-1·d-1)for 4 weeks.Echocardiography and hemodynamic measurements were performed on d 28.Then the hearts and lungs were harvested,the organ indices and pulmonary artery wall thickness were calculated,and biochemical and histochemical analysis were conducted.The levels of apoptotic and signaling proteins in the lungs were measured using immunoblotting.RESULTS Treatment with SAA or bosentan effectively ameliorated MCTinduced pulmonary artery remodeling,pulmonary hemodynamic abnormalities and the subsequent increases of right ventricular systolic pressure(RVSP).Furthermore,the treatments significantly attenuated MCT-induced hypertrophic damage of myocardium,parenchymal injury and collagen deposition in the lungs.Moreover,the treatments attenuated MCT-induced apoptosis and fibrosis in the lungs.The treatments partially restored MCT-induced reductions of bone morphogenetic protein typeⅡreceptor(BMPRⅡ)and phosphorylated Smad1/5 in the lungs.CONCLUSION SAA ameliorates the pulmonary arterial remodeling in MCT-induced PAH rats most likely via activating the BMPRⅡ-Smad pathway and inhibiting apoptosis.Thus,SAA may have therapeutic potential for the patients at high risk of PAH.

关键词： salvianolic acid a pulmonary artery hypertension apoptosis BMPR Ⅱ Smad vascular remolding

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Preparation and Certification of a New salvianolic acid a Reference Material for Food and Drug Research

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Natural Products and Bioprospecting 2020年第2期10卷 67-75页

作者： Dezhi Yang Bin Su Yancai Bi Li Zhang Baoxi Zhang Junke Song Yang Lu Guanhua Du Beijing City Key Laboratory of Polymorphic Drugs Center of Pharmaceutical PolymorphsInstitute of Materia MedicaChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100050People’s Republic of China Soteria Pharmaceutical Co. Ltd.Laiwu 271100People’s Republic of China Beijing City Key Laboratory of Drug Target and Screening Research National Center for Pharmaceutical ScreeningInstitute of Materia MedicaChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100050People’s Republic of China

salvianolic acid a(Sal A),a water-soluble ingredient in Danshen,has various biological activities.Sal A and its impurities have similar physical and chemical properties,as well as strong reducibility;therefore,they are difficult to prepare and purify.In this study,high-purity Sal A was obtained by purification of sephadex chromatography and preparative chromatography.Furthermore,HPLC-DAD tandem ECD and HPLC-DAD tandem MS methods were used for non-volatile organic impurity analysis,ICP-MS method was used for non-volatile inorganic impurities and mass balance method and quantitative nuclear magnetic resonance were employed to certify the product.The structures of Sal A and its relative impurities were validated by nuclear magnetic resonance spectroscopy and mass spectrometry,and their contents were quantified as well.Following the principles of ISO Guides 34:2009 and 35:2005,a Sal A reference material was certified,covering homogeneity studies,stability studies,characterization,and uncertainty estimations.

关键词： Certified reference material salvianolic acid a Mass balance method qNMR High resolution mass spectrum

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Blocking Effect of salvianolic acid a on Calcium Channels in Isolated Rat Ventricular Myocytes

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Chinese Journal of Integrative Medicine 2012年第5期18卷 366-370页

作者：王宝刘建勋孟红旭林成仁 The Laboratory Research Center Xiyuan HospitalChina Academy of Chinese Medical Sciences

Objective： To study the effect of salvianolic acid a （SAA） on L-type calcium current （I-CaL） in isolated ventdcular myocytes of Sprague-Dawley rats. Methods： SPA powder was dissolved in normal Tyrode＇s solution to reach the concentrations of 1, 10, 100, and 1000 μmol/L. The traditional whole-cell patch-clamp recording technique was employed to evaluate the effects of SAA on I-CaL in single ventricular myocytes which were prepared by Langendorff perfusion apparatus from Sprague-Dawley rats. Results： SPA （1, 10, 100, and 1000 μmol/L） inhibited I-CaL peak value by 16.23%± 1.3% （n=6, P〈0.05）, 22.9% ± 3.6% （n=6, P〈0.05）, 53.4% ± 3.0% （n=8, P〈0.01）, and 62.26% ± 2.9% （n=8, P〈0.01）, respectively. SAA reversibly inhibited I-CaL in a dose-dependent manner and with a half-blocking concentration （IC50） of 38.3 μmol/L. SAA at 100 μmol/L elevated the I-V curve obviously, and shifted the half-active voltage （V0.5） from （-15.78± 0.86） mV to （-11.24 ± 0.77） mV （n=6, P〈0.05） and the slope （K） from 5.33 ±0.74 to 4.35±0.74 （n=6, P〉0.05）. However, it did not alter the shapes of I-V curve, steady-state inactivation curve, or recovery from inactivation curve. Conclusions： SAA inhibited I-CaL in a dose-dependent manner. It shifted the steady-state activation curve to a more positive voltage, which indicated that the drug affected the activated state of calcium channels, and suggested that the Ca2. antagonistic effect of SPA be beneficial in the treatment of myocardial ischemia reperfusion injury.

关键词： salvianolic acid a ventricuiar myocytes patch-clamp technique L-type calcium channels

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salvianolic acid a attenuates isoproterenol-induced myocardial infarction in mice through PI3K/Akt signal pathway

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中国药理学与毒理学杂志 2016年第10期30卷 1005-1006页

作者： FANG Lian-hua NIU Zi-ran CHEN Yu-cai YUAN Tian-yi LI Li WANG Shou-bao WANG Yue-hua LYU Yang DU Guan-hua Beijing Key Laboratory of Drug Targets Identification and Drug Screening Institute of Materia MedicaChinese Academy of Medical Sciences and Peking Union Medical College Beijing Key Laboratory of Polymorphic Drugs Institute of Materia MedicaChinese Academy of Medical Sciences and Peking Union Medical College

OBJECTIVE To investigate the protective effect of salvianolic acid a(Sal A)on isoproterenol-induced myocardial infarction in mice and its possible mechanisms.METHODS The mice were subcutaneously injected with isopropranol(ISO 8 mg·kg-1)to induce myocardial infarction and evaluated the myocardial protective effect of Sal A from mortality rate,electrocardiogram(ECG),heart function,myocardial infarction index,serum myocardial enzymes and explored its possible mechanisms from inflammatory,antioxidant and cells apoptosis.RESULTS Sal A can dose-dependently enhanced the heart function of myocardial infarction mice,reduced the heart index,inhibited the myocardial enzyme leakage,showed obvious myocardial protection effects.ELISA results showed that Sal A can reduce the expression of myocardial inflammatory cytokines such as IL-6,TNF-α.Western blotting confirmed that Sal A can increase the expression of anti-apoptotic proteins Bcl-2,reduce the expression of apoptosis protein Bax,and raise the phosphorylation level of PI3K and Akt.CONCLUSION Sal A have displayed significant protective effect against isoproterenol-induced myocardial infarction and its mechanism may be related to increasing of PI3K/Akt signal pathway and inhibition of cell apoptosis and inflammatory reaction.

关键词： salvianolic acid a isoproterenol myocardial infarction apoptosis inflammation signaling pathway

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salvianolic acid a alleviates renal injury in systemic lupus erythematosus induced by pristane in BALB/c mice

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中国药理学与毒理学杂志 2016年第10期30卷 1039-1040页

作者： LIN Yi-huang YAN Yu ZHANG Hui-fang CHEN Yu-cai HE Yang-yang WANG Shou-bao FANG Lian-hua LYU Yang DU Guan-hua Beijing Key Laboratory of Drug Targets Identification and Drug Screening Institute of Materia MedicaChinese Academy of Medical Sciences and Peking Union Medical College State Key Laboratory of Cardiovascular Disease Fuwai Hospital National Center for Cardiovascular Diseases Beijing Key Laboratory of Polymorphic Drugs Institute of Materia MedicaChinese Academy of Medical Sciences and Peking Union Medical College

OBJECTIVE To investigate the effects of salvianolic acid a(SAA)in systemic lupus erythematosus(SLE)induced by pristane in BALB/c mice,this study was performed.METHODS Lupus mice were established by confirming elevated levels of autoantibodies and IL-6 after intraperitoneal injection of pristane.Micewere then treated with daily oral doses of SAA for 5months in parallel with mice treated with prednisone and aspirin as positive controls.The levels of autoantibodies were monitored at monthly intervals and nephritic symptoms observed by hematoxylin and eosin(H&E)and periodic acid-Schiff(PAS)staining.Western blot analysis of renal tissue was also employed.RESULTS SAA treatment caused a significant reduction in the levels of anti-Sm autoantibodies and reduced renal histopathological changes and pathological effects.SAA treatment also significantly inhibited the phosphorylation of IKK,IκB and NFκB in renal tissues of lupus mice.CONCLUSION The results suggest that SAA alleviates renal injury in pristane-induced SLE in BALB/c mice through inhibition of phosphorylation of IKK,IκB and NFκB.

关键词： salvianolic acid a systemic lupus erythematosus renal injury autoantibodies pristane NF-κB

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salvianolic acid a reduces endothelial-mesenchymal transition of HPAECs

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中国药理学与毒理学杂志 2019年第9期33卷 683-683页

作者： FANG Lian-hua YUAN Tian-yi CHEN Yu-cai LYU Yang DU Guan-hua Beijing Key Laboratory of Drug Targets Identification and Drug Screening 2.Beijing Key Laboratory of Polymorphic DrugsInstitute of Materia MedicaChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100050China

OBJECTIVE salvianolic acid a(SAA),a polyphenols acid,is a bioactive ingredient from a traditional Chinese medicine named Danshen(Salvia Miltiorrhiza Bunge).According to previous studies,it was shown to possess various effects such as anti-oxidative stress,anti-diabetic complications and anti-pulmonary hypertension.This study is aimed to investigate the effect of SAA on pulmonary arterial endothelial-mesenchymal transition(endoMT)induced by hypoxia and the underlying mechanisms.METHODS Primary cultured human pulmonary arterial endothelial cells(HPAECs)were exposed to 1%O2 for 48 h with or without SAA treatment.RESULTS SAA treatment improved the morphology of HPAECs and inhibited the cytoskeleton remodeling and reduced migration distances.It was observed that the produc⁃tion of ROS in cells was significantly reduced by the treatment of SAA.Meanwhile,SAA alleviated the loss of CD31 and slightly inhibited the expression ofα-SMA.The mechanisms study shows that SAA treatment increased the phosphoryla⁃tion levels of Smad1/5,but inhibited that of Smad2/3.Furthermore,SAA attenuated the phosphorylation levels of ERK and Cofilin,which were enhanced by hypoxia.CONCLUSION SAA treatment can protect HPAECs from endoMT induced by hypoxia,which may perform via the downstream effectors of BMPRs or TGFβR including Smads,ERK and ROCK/cofilin pathways.

关键词： salvianolic acid a endothelial-mesenchymal transition HPAEC hypoxia Smads pathway

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salvianolic acid a protects myocardial ischemia/reperfusion injury via reducing platelet activation and inflammation

Salvianolic acid A protects myocardial ischemia/reperfusion ...

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2015年浙江省心电生理与起搏学术年会

作者： Yuan xiaolin Zhu ni Zhao xuyong Xiang yijia Ye shiyong Zhong Peng Zeng chunlai Department of cardiology the fifth affiliated hospital of Wenzhou medical University

Objective To investigate the protective effect of salvianolic acid a(SAA) on myocardial ischemia / reperfusion injury.Methods Male SD rats were subjected ischemia for 45 minutes by ligation of coronary artery to establish acute myocardial ischemia/reperfusion models.SAA(10mg/kg) or tirofiban(60ug/kg) was given by jugular vein injection 10 min before reperfusion.After reperfusion for 3 hours,the level of platelet aggregation was measured using an aggregometer and the content of nitric oxide(NO) was detected by ultraviolet spectrop hotometer.Serum levels of p-selectin,cardiac troponin T(cTnT),creatine kinase isoenzyme MB(CK-MB),inflammatory cytokine interleukin-1β(IL-1β),and tumor necrosis factor-α(TNF-α) were measured at 3 hours and 24 hours after reperfusion.Histopathological analysis of ischemic myocardial morphology was determined on hematoxylin-eosin and the area of infracted area was evaluated by evans blue and triphenyltetra zolium chloride staining.Result:Treatment of SAA increased survival rate following myocardial Ischemia/Reperfusion,relieved myocardial cell damage and inflammation,decreased myocardial infarct size,inhibited platelet aggregation,reduced the serum levels of p-Selectin,TNF-α,IL-1β,cTnT and CK-MB,enhanced nitric oxide concentration of myocardial tissue.Conclusions:SAA has protective effects on myocardial ischemia / reperfusion injury by means of antiplatelet and anti-inflammation

关键词： salvianolic acid a myocardial ischemia reperfusion infraction area platelet aggregation rate inflammation

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salvianolic acid a attenuates on the endothelial-mesenchymal transition of HPAECs

Salvianolic acid A attenuates on the endothelial-mesenchymal...

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第九届中国药理学会补益药药理专业委员会学术研讨会

作者： FANG Lian-hua YUAN Tian-yi CHEN Yu-cai LYU Yang DU Guan-hua Beijing Key Laboratory of Drug Targets Identification and Drug Screening Beijing Key Laboratory of Polymorphic Drugs Institute of Materia MedicaChinese Academy of Medical Sciences and Peking Union Medical College

Objective:salvianolic acid a(SAA),a polyphenols acid,is a bioactive ingredient from a traditional Chinese medicine named Dan shen(Salvia Miltiorrhiza Bunge).According to previous studies,it was shown to possess various effects such as anti-oxidative stress,anti-diabetic complications and anti-pulmonary hypertension.This study is aimed to investigate the effect of S AA on pulmonary arterial endothelial-mesenchymal transition(endoMT) induced by hypoxia and the underlying mechanisms.Method:Primary cultured human pulmonary arterial endothelial cells(HPAECs) were exposed to 1%O for 48 hours with or without SAA treatment.Results:SAA treatment improved the morphology of HPAECs and inhibited the cytoskeleton remodeling and reduced migration distances.It was observed that the production of ROS in cells was significantly reduced by the treatment of SAA.Meanwhile,SAA alleviated the loss of CD31 and slightly inhibited the expression of α-SMA.The mechanisms study shows that SAA treatment increased the phosphorylation levels of Smad1/5,but inhibited that of Smad2/3.Furthermore,SAA attenuated the phosphorylation levels of ERK and Cofilin,which were enhanced by hypoxia.Conclusions:According to these results,our study indicated that SAA treatment can protect HPAECs from endoMT induced by hypoxia,which may perform via the downstream effectors of BMPRs or TGFβR including Smads,ERK and ROCK/cofilin pathways.

关键词： salvianolic acid a Endothelial-mesenchymal transition HPAEC Hypoxia Smads pathway

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