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Alkaloids, flavonoids, polyphenols might be responsible for potent antiarthritic effect of Solanum nigrum

Journal of Traditional Chinese Medicine 2019年第5期39卷 632-641页

作者： Alamgeer Shanila Akhter Ambreen Malik Uttra Umme Habiba Hasan laboratory of cardiovascular Research and integrative pharmacology College of Pharmacy University of Sargodha

OBJECTIVE: To evaluate in vitro and in vivo antiarthritic potential of Solanum nigrum (S. nigrum). METHODS: Aqueous methanolic (70∶30) extract of S. nigrum was prepared. The in vitro antiarthritic effect was evaluated in terms of its inhibition of protein denaturation and membrane stabilization. While, formaldehyde, complete Freund's adjuvant (CFA) and Collagen induced arthritis rat models were used to study in vivo antiarthritic activities of S. nigrum at dose level of 200, 400 and 800 mg/kg. RESULTS: The extract exhibited inhibition of protein denaturation and protected red blood cell by stabilizing the membranes in a concentration dependent manner, with maximum effect attained at 800 μg/mL. Moreover, there was a marked reduction in paw edema observed in extract treated animals, when compared to arthritic control animals in all in vivo models and 800 mg/kg dose got maximum reduction of paw edema. In CFA and collagen models, plant extract restored body weight, hematologic parameters, radiographic and histopathoOBJECTIVE: To evaluate in vitro and in vivo antiarthritic potential of Solanum nigrum (S. nigrum). METHODS: Aqueous methanolic (70∶30) extract of S. nigrum was prepared. The in vitro antiarthritic effect was evaluated in terms of its inhibition of protein denaturation and membrane stabilization. While, formaldehyde, complete Freund's adjuvant (CFA) and Collagen induced arthritis rat models were used to study in vivo antiarthritic activities of S. nigrum at dose level of 200, 400 and 800 mg/kg. RESULTS: The extract exhibited inhibition of protein denaturation and protected red blood cell by stabilizing the membranes in a concentration dependent manner, with maximum effect attained at 800 μg/mL. Moreover, there was a marked reduction in paw edema observed in extract treated animals, when compared to arthritic control animals in all in vivo models and 800 mg/kg dose got maximum reduction of paw edema. In CFA and collagen models, plant extract restored body weigh

关键词： Arthritis Solanum nigrum Protein denaturation Formaldehyde Freund's adjuvant Collagen

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Traditional medicines of plant origin used for the treatment of inflammatory disorders in Pakistan：A review

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Journal of Traditional Chinese Medicine 2018年第4期38卷 636-656页

作者： Alamgeer Ambreen Malik Uttra Haseeb Ahsan Umme Habiba Hasan Mueen Ahmad Chaudhary laboratory of cardiovascular Research and integrative pharmacology College of PharmacyUniversity of SarcjodhaSargodha 40100Pakistan

OBJECTIVE:To pool data on ethnobotanical medicine for the treatment of inflammatory disorders in ***:We reviewed 237 research publications based on data from the six provinces in Pakistan(Punjab = 85,Khyber Pakhtunkhwa = 65,Sindh =15,Balochistan = 8,Gilgit Baltistan = 22,Azad Jammu and Kashmir = 42) published until June 2015 in various *** was achieved using seven online databases:Science Direct,Google,Google Scholar,Pub Med,Wiley Online Library,SpringerLink,and *** were analyzed from different ***:People from Pakistan made use of 371 plant species belonging to 263 genera and 99 families for the treatment of inflammatory *** from the Asteraceae family were used most *** were the dominant growth *** were the plant parts used most *** were the main preparation *** plant species were used most frequently in thedwellers of most regions of Pakistan.A total of 111 plants were shown experimentally to have neither anti-arthritic nor anti-inflammatory activities,and148 plant species were ***-four species had commercial *** plant species were imported,and 25 plant species were exported,from ***:This review provides baseline data for plant species in Pakistan that have potential anti-inflammatory/anti-arthritic activities.

关键词： Inflammation Anti-inflammatoryagents Anti-arthritic Ethnobotanical Market Review

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Vascular endothelial growth factor:a double-edged sword in the development of white matter lesions

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Neural Regeneration Research 2025年第1期20卷 191-192页

作者： Narek Manukjan Daniel Fulton Zubair Ahmed WMatthijs Blankesteijn Sébastien Foulquier Department of pharmacology and Toxicology Maastricht UniversityMaastrichtThe Netherlands CARIM-School for cardiovascular Diseases Maastricht UniversityMaastrichtThe Netherlands Neuroscience and Ophthalmology Institute of Inflammation and AgeingUniversity of BirminghamEdgbastonBirminghamUK Centre for Trauma Sciences Research University of BirminghamEdgbastonBirminghamUK MHeNs-School for Mental Health and Neuroscience Maastricht UniversityMaastrichtThe Netherlands Department of Neurology Maastricht University Medical CenterMaastrichtThe Netherlands

As the population ages,the burden of age-related diseases becomes ***,over 55 million people suffer from dementia worldwide,with Alzheimer’s disease being the most common ***,it is becoming clearer that underlying vascular pathology such as cerebral small vessel disease(cSVD)may be a more detrimental cause for dementia(Cuadrado-Godia et al.,2018).It is estimated that 10%-30%of the elderly population and 35%-90%of all dementia patients exhibit signs of *** term cSVD refers to pathology affecting the small vessels of the brain,which can lead to lacunar cerebral infarcts,enlarged perivascular spaces,and cortical hemorrhages(Cuadrado-Godia et al.,2018).CSVD is often associated with cognitive decline,gait problems,and dementia(Cuadrado-Godia et al.,2018).

关键词： pathology becoming white

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Protective effects of iptakalim,a novel ATP-sensitive potassium channel opener,on global cerebral ischemia-evoked insult in gerbils

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Acta Pharmacologica Sinica 2006年第6期27卷 665-672页

作者： Hua CHEN~(2,4)Yong YANG~(2,4)Hong-hong YAO~2 Xing-chun TANG~2 Jian-hua DING~2 Hai WANG~3 Gang HU~(2,5)2 laboratory of Neuropharmacology,Department of Anatomy,Histology and pharmacology,Nanjing Medical University,Nanjing 210029,China 3 Department of cardiovascular pharmacology,Beijing Institute of pharmacology and Toxicology,Beijing 100850,China Department of Anatomy Laboratory of Neuropharmacology Histology and Pharmacology Nanjing Medical University Nanjing China Department of cardiovascular pharmacology Beijing Institute of Pharmacology and Toxicology Beijing China

Aim:To investigate the protective role of iptakalim,a novel ATP sensitive potas-sium channel opener,on global cerebral ischemia-evoked insult in gerbils andglutamate-induced PC 12 cell ***:Global cerebral ischemia was in-duced by occluding the bilateral common carotid arteries in gerbils for 5 *** field maze and T-maze were employed to investigate the experimental thera-peutic value of iptakalim on ischemic brain insult（n=8）.The pyramidal cells in thehippocampal CA1 regions were counted to assess the protective effects *** released from the gerbil hippocampus and PC12 cells weredetermined by *** calcium was measured by Fluo-3 AM with ABio-Rad Radiance 2100TM confocal system in conjunction with a Nikon *** glutamate uptake measurements were determined by liq-uid scintillation ***:Iptakalim（0.5-4.0 mg/kg per day,ip）couldreduce the high locomotor activity evoked by ischemia and improve global cere-bral ischemia-induced working memory *** studies revealedthat iptakalim could increase the survival neuron in the hippocampus CA1 zone ina dose-dependent ***,iptakalim could reverse ischemia-evokedincreases of glutamate in the hippocampus of *** an in vitro study,iptakalimprotected PC12 cells against glutamate-induced excitotoxicity,reduced the[Ca2+]iincreases,and enhanced the glutamate uptake activity of primary ***:Iptakalim plays a key role in preventing global cerebralischemia-evoked insults in gerbils and glutamate-induced PC12 cell injury by *** might be a promising novel candidate for the preventionand/or treatment of stroke.

关键词： ATP-sensitive potassium channel opener iptakalim global cerebral ischemia neuroprotection excitotoxicity

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Minocycline protects against myocardial ischemia/reperfusion injury in rats by upregulating MCPIP1 to inhibit NF-κB activation

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Acta Pharmacologica Sinica 2019年第8期40卷 1019-1028页

作者： Quan Yi Fang-hui Tan Jia-an Tan Xiu-hui Chen Qing Xiao Ying-hua Liu Gui-ping Zhang Jian-dong Luo Department of pharmacology School of Pharmaceutical SciencesGuangzhou Medical University Guangzhou Institute of cardiovascular Disease Guangzhou Key Laboratory of Cardiovascular Disease Second Affiliated Hospital Guangzhou Medical University

Minocycline is a tetracycline antibiotic and has been shown to play a protective role in cerebral and myocardial ischemia/reperfusion(I/R).However,the underlying mechanism remains ***,we investigated whether monocyte chemotactic protein-induced protein-1(MCPIP1),a negative regulator of inflammation,was involved in the minocycline-induced cardioprotection in myocardial I/R in vivo and in vitro *** ischemia was induced in rats by left anterior descending coronary artery occlusion for 1 h and followed by 48 h *** was administered prior to ischemia(45 mg/kg,ip,BID,for 1 d)and over the course of reperfusion(22.5 mg/kg,ip,BID,for 2 d).Cardiac function and infarct sizes were *** of minocycline significantly decreased the infarct size,alleviated myocardial cell damage,elevated left ventricle ejection fraction,and left ventricle fractional shortening following I/R injury along with significantly decreased pro-inflammatory cytokine IL-1β and monocyte chemoattractant protein-1(MCP-1)levels in heart tissue.H9c2 cardiomyocytes were subjected to oxygen glucose deprivation(OGD)followed by reoxygenation(OGD/R).Pretreatment with minocycline(1-50μmol/L)dosedependently increased the cell viability and inhibited OGD/R-induced expression of MCP-1 and ***,minocycline dose-dependently inhibited nuclear translocation of NF-κB p65 in H9c2 cells subjected to OGD/*** both the in vivo and in vitro models,minocycline significantly increased MCPIP1 protein expression;knockdown of MCPIP1 with siRNA in H9c2 cells abolished all the protective effects of minocycline against OGD/R-induced *** results demonstrate that minocycline alleviates myocardial/R injury via upregulating MCPIP1,then subsequently inhibiting NF-κB activation and pro-inflammatory cytokine secretion.

关键词： myocardial ischemia and reperfusion H9c2 cardiomyocytes oxygen glucose deprivation minocycline cytokine NF-κB monocyte chemotactic protein-induced protein-1

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m^(6)A reader YTHDF1 promotes cardiac fibrosis by enhancing AXL translation

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Frontiers of Medicine 2024年第3期18卷 499-515页

作者： Han Wu Weitao Jiang Ping Pang Wei Si Xue Kong Xinyue Zhang Yuting Xiong Chunlei Wang Feng Zhang Jinglun Song Yang Yang Linghua Zeng Kuiwu Liu Yingqiong Jia Zhuo Wang Jiaming Ju Hongtao Diao Yu Bian Baofeng Yang Department of pharmacology(National Key laboratory of Frigid Zone cardiovascular Diseases the State-Province Key Laboratories of Biomedicine-Pharmaceutics of ChinaKey Laboratory of Cardiovascular ResearchMinistry of Education)College of PharmacyHarbin Medical UniversityHarbin150081China

Cardiac fibrosis caused by ventricular remodeling and dysfunction such as post-myocardial infarction(MI)can lead to heart *** N6-methyladenosine(m^(6)A)methylation has been shown to play a pivotal role in the occurrence and development of many *** investigating the biological function of the m^(6)A reader YTHDF1 in cardiac fibrosis,adeno-associated virus 9 was used to knock down or overexpress the YTHDF1 gene in mouse hearts,and MI surgery in vivo and transforming growth factor-β(TGF-β)-activated cardiac fibroblasts in vitro were performed to establish fibrosis *** results demonstrated that silencing YTHDF1 in mouse hearts can significantly restore impaired cardiac function and attenuate myocardial fibrosis,whereas YTHDF1 overexpression could further enhance cardiac dysfunction and aggravate the occurrence of ventricular pathological remodeling and fibrotic ***,zinc finger BED-type containing 6 mediated the transcriptional function of the YTHDF1 gene ***1 augmented AXL translation and activated the TGF-β-Smad2/3 signaling pathway,thereby aggravating the occurrence and development of cardiac dysfunction and myocardial ***,our data indicated that YTHDF1 was involved in activation,proliferation,and migration to participate in cardiac fibrosis in *** results revealed that YTHDF1 could serve as a potential therapeutic target for myocardial fibrosis.

关键词： cardiac fibrosis YTHDF1 AXL ZBED6 heart failure

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LncRNA CCRR maintains Ca^(2+)homeostasis against myocardial infarction through the FTO-SERCA2a pathway

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Science China(Life Sciences) 2024年第8期67卷 1601-1619页

作者： Hua Yang Lina Xuan Shengjie Wang Huishan Luo Xiaomeng Duan Jianjun Guo Shijia Cui Jieru Xin Junwei Hao Xiufang Li Jun Chen Feihan Sun Xiaolin Hu Siyun Li Ying Zhang Lei Jiao Baofeng Yang Lihua Sun Department of pharmacology Harbin Medical University(State Key Laboratory of Frigid Zone Cardiovascular Diseasethe State-Province Key Laboratories of Biomedicine-Pharmaceutics of ChinaKey Laboratory of Cardiovascular ResearchMinistry of EducationJoint International Research Laboratory of Cardiovascular Medicine ResearchMinistry of EducationChina)College of PharmacyHarbin Medical UniversityHarbin 150081China

Cardiac conduction regulatory RNA(CCRR)has been documented as an antiarrhythmic lncRNA in our earlier *** study aimed to evaluate the effects of CCRR on SERCA2a and the associated Ca^(2+)homeostasis in myocardial infarction(MI).Overexpression of CCRR via AAV9-mediated delivery not only partially reversed ischemia-induced contractile dysfunction but also alleviated abnormal Ca^(2+)homeostasis and reduced the heightened methylation level of SERCA2a following *** effects were also observed in CCRR overexpressing transgenic mice.A conserved sequence domain of CCRR mimicked the protective function observed with the full ***,silencing CCRR in healthy mice led to intracellular Ca^(2+)overloading of *** increased SERCA2a protein stability by upregulating FTO *** direct interaction between CCRR and FTO protein was characterized by RNA-binding protein immunoprecipitation(RIP)analysis and RNA pulldown *** of NFATc3 was identified as an upstream mechanism responsible for CCRR downregulation in *** study demonstrates that CCRR is a protective lncRNA that acts by maintaining the function of FTO,thereby reducing the m^(6)A RNA methylation level of SERCA2a,ultimately preserving calcium homeostasis for myocardial contractile function in ***,CCRR may be considered a promising therapeutic strategy with a beneficial role in cardiac pathology.

关键词： CCRR calcium homeostasis FTO myocardial infarction SERCA2a

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DMH1(4-[6-(4-isopropoxyphenyl)pyrazolo[1,5-a]pyrimidin-3-yl]quinoline) inhibits chemotherapeutic drug-induced autophagy

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Acta Pharmaceutica Sinica B 2015年第4期5卷 330-336页

作者： Yue Sheng Bo Sun Xin Xie Na Li Deli Dong The State-Province Key Laboratories of Biomedicine-Pharmaceutics of China Key Laboratory of Cardiovascular Research Ministry of Education Department of PharmacologyHarbin Medical University

Our previous work found that DMH1(4-[6-(4-isopropoxyphenyl)pyrazolo [1,5-a]pyrimidin-3-yl]quinoline) was a novel autophagy inhibitor. Here, we aimed to investigate the effects of DMH1 on chemotherapeutic drug-induced autophagy as well as the efficacy of chemotherapeutic drugs in different cancer cells. We found that DMH1 inhibited tamoxifen- and cispcis-diaminedichloroplatinum(II)(CDDP)-induced autophagy responses in MCF-7 and HeLa cells, and potentiated the anti-tumor activity of tamoxifen and CDDP for both cells. DMH1 inhibited 5-fluorouracil(5-FU)-induced autophagy responses in MCF-7 and HeLa cells, but did not affect the anti-tumor activity of 5-FU for these two cell lines. DMH1 itself did not induce cell death in MCF-7 and HeLa cells, but inhibited the proliferation of these cells. In conclusion, DMH1 inhibits chemotherapeutic drug-induced autophagy response and the enhancement of efficacy of chemotherapeutic drugs by DMH1 is dependent on the cell sensitivity to drugs.

关键词： Autophagy Tamoxifen 5-Fluorouracil Cancer cells

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Nanomedicine-based treatment:An emerging therapeutical strategy for pulmonary hypertension

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Nano Research 2023年第5期16卷 7007-7029页

作者： Shuya Wang Qiaohui Chen Tianjiao Zhao Kelong Ai Changping Hu Department of pharmacology Xiangya School of Pharmaceutical SciencesCentral South UniversityChangsha 410078China Hunan Provincial Key laboratory of cardiovascular Research Changsha 410078China

Pulmonary hypertension(PH)can cause breathing difficulty,a rapid decline of exercise capacity,heart failure,eventually death of the *** latest epidemiological study demonstrates that PH has a much higher incidence than previously *** is still a highly fatal disease due to the many disadvantages of the current drugs,such as short half-life,lack of targeting,potent side *** PH pathological features offer great opportunities for nanomedicines for ***,emerging nanomedicines demonstrated great advantages in the therapeutic effect of PH by enhancing the accumulation of drugs in PH lesion,optimizing drug efficacy,minimizing drug side ***,this promising field of cross-cutting research is far from being widely explored due to the huge professional *** solve this problem,we provide a comprehensive review for the latest progresses of nanomedicines in the treatment of ***,we systematical summarized the PH pathological features and the current clinical drug treatment of *** advantages of nanomedicines are also deeply discussed in the treatment of ***,we focused on the research progresses of nanomedicines in PH through three aspects:advanced nano-drug delivery system for traditional drugs and new target drugs,gene therapy-based nanomedicines,other nanomedicines for the treatment of ***,we also discussed the prospects and challenges for the clinical application of nanomedicines in PH,provided directions for the research and development of nanomedicines for PH treatment in the future.

关键词： pulmonary hypertension nanomedicines enhanced penetration and retention effects polymer liposome

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Effect of arotinolol on right ventricular function in patients with dilated cardiomyopathy

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Journal of Geriatric Cardiology 2007年第3期4卷 170-173页

作者： Hong Yang Li Xu Yongkang Tao Zhimin Xu Xiuqing Du Naqiang Lu Kefei Dou Jinglin Zhao Xianqi Yuan Yanfen Zhao Rongfang Shi Chaomei Fan Key laboratory of Clinical Trials Research in cardiovascular Drugs Ministry of HealthClinical Pharmacology CenterCardiovascular Institute and Fuwai Hospital CAMS and PUMCBeijing 100037China Key Laboratory of Clinical Trials Research in Cardiovascular DrugsMinistry of HealthClinical Pharmacology CenterCardiovascular Institute and Fuwai Hospital CAMS and PUMCBeijing 100037China Key Laboratory of Clinical Trials Research in Cardiovascular DrugsMinistry of HealthClinical Pharmacology CenterCardiovascular Institute and Fuwai Hospital CAMS and PUMCBeijing 100037China Key Laboratory of Clinical Trials Research in Cardiovascular DrugsMinistry of HealthClinical Pharmacology CenterCardiovascular Institute and Fuwai Hospital CAMS and PUMCBeijing 100037China Beijing Nuclear Industry Hospital Beijing 100042China. Beijing Nuclear Industry Hospital Beijing 100042China. Key Laboratory of Clinical Trials Research in Cardiovascular DrugsMinistry of HealthClinical Pharmacology CenterCardiovascular Institute and Fuwai Hospital CAMS and PUMCBeijing 100037China Key Laboratory of Clinical Trials Research in Cardiovascular DrugsMinistry of HealthClinical Pharmacology CenterCardiovascular Institute and Fuwai Hospital CAMS and PUMCBeijing 100037China Key Laboratory of Clinical Trials Research in Cardiovascular DrugsMinistry of HealthClinical Pharmacology CenterCardiovascular Institute and Fuwai Hospital CAMS and PUMCBeijing 100037China Key Laboratory of Clinical Trials Research in Cardiovascular DrugsMinistry of HealthClinical Pharmacology CenterCardiovascular Institute and Fuwai Hospital CAMS and PUMCBeijing 100037China Key Laboratory of Clinical Trials Research in Cardiovascular DrugsMinistry of HealthClinical Pharmacology CenterCardiovascular Institute and Fuwai Hospital CAMS and PUMCBeijing 100037China Key Laboratory of Clinical Trials Research in Cardiovascular DrugsMinistry of HealthClinical Pharmacology CenterCardiovascular Institute and Fuwai Hospital CAMS and PUMCBeijing 100037Ch

Objective Dilated cardiomyopathy(DCM) is generally considered to be accompanied by both left and right ventricular dysfunction,but most studies only analyze the left ventricular function. In this study,we evaluated the effect of arotinolol on right ventricular function in patients with DCM. Methods Right ventricular ejection fraction(RVEF) and right ventricular diameter(RVD) were measured by two-dimensional echocardiography(2-DE) in 33 DCM patients;RVEF measured by first-pass radionuclide angiography(FPRA) was compared with that by 2-DE. Results The treatment with arotinolol for one year resulted in a reduction in the right ventricular diameter(baseline,23.0 ± 8.3 mm vs after one-year treatment,20.7 ± 5.4 mm;P=0.004 ) and an associated increase in ejection fraction(baseline,36.9 ± 10.3% vs after one-year treatment,45.8 ± 9.6%;P < 0.001 ) ;there is a high correlation between the 2-DE method and radionuclide ventriculographic method. The correlation coefficient is 0.933(P<0.001) . Conclusion Arotinolol therapy could not only improve left ventricular function,but also improve right ventricular function in DCM patients.

关键词： dilated cardiomyopathy arotinolol right ventricular function

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