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Baicalein causes alternation in dopamine metabolism in PC12 cells by inhibiting the expression of COMT and DAT

中国药理学通报 2015年第B11期31卷 201-202页

作者： HEGuo-rong LIXiao-xiu duguan-hua BeijingKeyLaboratoryofDrugTargerandScreeningResearch InstituteofMateriaMedicaChineseAcademyofMedicalSciencesandPekingUnionMedicalCollegeNo.1XianNongTanStreetBeijing100050

Aim Baicalein is the major flavonoid obtained from the Scutellaria root. Our previous studies have dem- onstrated that baicalein has a clear positive effect on recovery in an experimental model of Parkinsonism. The put- pose of this study was to investigate the role of baicalein in modulating dopamine （DA） metabolism in PC12 cells and to explore possible mechanisms of its actions. Methods The intracellular content and extracellular release of DA in both rotenone-treated and untreated PC12 cells were examined. Second, PC12 cells were first pretreated with baicalein （ 10 μmol · L^-1 ） for 10 rain, and then incubated with or without ionomycin （5 μmol · L^-1 ） for 10 rain to test whether short-term exposure to baicalein affected calcium-dependent or spontaneous DA release. Third, the intracellular and extracellular contents of DA and its related metabolites were examined. After treatment with baica- lein for 24 h, the The tyrosine hydroxylase （TH）, monoamine oxidase B （MAOB）, catechol-O-methyltransferase （COMT） and dopamine transporter （DAT） were detected by immunoblot analysis. Results The results showed that baicalein prevented rotenone-induced cytotoxicity and significantly increased the DA content in both rotenone- treated and untreated PC12 cells. Furthermore, it had no effect on ionomycin-induced or spontaneous DA release after short-term exposure but significantly increased DA content in a time- and dose-dependent manner after treat- ment for 6 h. Baicalein also significantly decreased the intracellular and extracellular homovanillic acid （HVA） content but increased the intracellular 3,4-dihydroxy phenylacetic acid （DOPAC） content. Finally, baicalein sig- nificantly decreased the expression of COMT and DAT, but it had no effect on the expression of TH and MAOB. Conclusion These data suggest that bacalein has the ability to increase DA content and modulate DA metabolism by inhibiting the expression of COMT and DAT. Our study provides evidence that baicalein may be

关键词： baicalein Parkinson' s disease PC12 cells rotenone dopamine metabolism

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Salvianolic acid A prevents MCAO/R-induced apoptosis through inhibiting PI3K/Akt/GSK3β-mediated signaling pathway

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中国药理学通报 2015年第B11期31卷 179-180页

作者： SONGJun-ke ZHANGWen ZHANGXue duguan-hua BeijingKeyLaboratoryofDrugTargetIndentificationandDrugScreening InstituteofMateriaMedicaChineseAcademyofMedicalSciences&PekingUnionMedicalCollegeBeijing100050

Aim Middle cerebral artery occlusion/reperfusion （MCAO/R） is a widely used animal model for cere- bral ischemia-reperfusion injury, which causes great harm to human health. Salvianolic acid A （SalA） from Dansh- en has been reported to possess various neuroprotection effects in lots of in vitro cell injury models. So in this study, the protection effects of SalA on MCAO/R injury were investigated and the protection mechanism was also dis- cussed. Methods MCAO for 1.5 h followed by 24 h of reperfusion induced severe brain injury. 10 mg · kg^-1 Sa- 1A was injected intravenously just after 1.5 h MCAO. The neurological deficit scores, infarct volume and cerebral edema were carried out after 24 h of reperfusion. Then the H＆E and Nissl staining methods were used to see wheth- er SalA could effectively ameliorated the pathological damages of brain. Then the Western blot assay was performed to study the possible signaling pathway stimulated by SalA. Results SalA （ 10 mg · kg^-1 ） could decrease the neurological deficit scores, infarct volume and cerebral edema of MCAO/R rats significantly （P 〈 0. 01, P 〈 0.05 and P 〈 0.01 ）. The brain pathological damages of MCAO/R rats could also be effectively ameliorated by the analy- sis of H＆E and Nissl staining results. Western blotting results showed that the upregulation of Caspase3 in MCAO/ R rat brain could be inhibited by SalA （P 〈 0.01）. With the administration of SalA, the Bcl-2 level in the brain was increased （ P 〈 0.01 ） and the Bax level was decreased （ P 〈 0.01 ） compared with model group. Furthermore, the phosphorylation levels of Akt, GSK3β and CREB decreased significantly in model group, while SalA treatment could significantly reverse the process （P 〈 0.01, P 〈 0.05 and P 〈 0. 05 ）. Conclusion These results indicated that SalA administration could protect rat brain against MCAO/R induced injury by ameliorating neurological deft-cits, decreasing the infarct volume and cerebral edema. And the anti-apoptosis effects of Sal

关键词： apoptosis PI3K/Akt GSK3β cerebral blotting brain Caspase3 protect

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Metabolism and regulation of FNDC 5 in skeletal muscle

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中国药理学通报 2015年第B11期31卷 13-14页

作者： YANGXiu-ying MargaretCL TSEHUXiang ChiBunChan duguan-hua BeijingKeyLaboratoryofDrugTargetandScreeningResearch InstituteofMateriaMedicaChineseAcademyofMedicalSciences&PekingUnionMedicalCollegeBeijing UniversityofOklahomaHealthSciencesCenter OklahomaCityOK73104USA

Purpose： Fibronectin type III domain-containing protein 5 （FNDC5）, also known as irisin, is a myokine secreted from muscle in response to exercise and improves obesity and glucose homeostasis. However, the molecular mecha- nisms that regulate FNDC5 expression and the functional significance of FNDC5 in skeletal muscle remain un- known. In this study, we explored the possible pathways that induce FNDC5 expression and delineated its metabol- ic effects on skeletal muscle. Methods： C2C12 myotubes were treated with various concentrations of Sp-cAMP, forskolin, and ionomycin respectively for various durations. FNDC5 and related metabolic genes＇ expressions were measured by quantitative real-time polymerase chain reaction （qRT-PCR）. Cyclic AMP responsive element-binding protein （CREB） phosphorylation was measured by Western blot. Oxidative phosphorylation was quantified by oxy- gen consumption rate （OCR） measurement using XF-96 analyzer （Seahorse Bioscience）. The statistical signifi- cance was calculated by one-way analysis of variance （ANOVA）. Data were considered significant when P 〈 0.05. Results： We found that cAMP and forskolin dose and time dependently increased FNDC5 expression in C2C12 myotubes. A synergistic effect of forskolin and ionomycin on FNDC5 expression was also found. CREB phosphoryl- ation was elevated in myotubes simultaneously upon these treatments. C2C12 myotubes over expressing CREB dis- plays increased FNDC5 expression as well, suggesting CREB was a regulator of FNDC5 expression. Functionally, irisin treatment enhanced mitochondrial biogenesis of C2C12 myotubes through increasing peroxisome proliferator- activated receptor gamma coactivator-1α （PGC-1α）, nuclear respiratory factor 1 （NRF1） and mitochondrial tran-scription factor A （TFAM） expressions, leading to increase myotube mitochondrial respirations and ATP produc- tion. Conclusions Our observation indicates that irisin is a metabolic modulator of skeletal muscle, whose expres- sion is controll

关键词： FNDC5 skeletal muscle cAMP metabolism intracellular pathway mitochondria

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Ginkgolide K protects cardiomyocytes against ER stress through stimulating ER-associated degradation （ERAD） and autophagy

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中国药理学通报 2015年第B11期31卷 181-182页

作者： WANGShou-bao WANGZhen-zhong FANQi-ru duguan-hua WANGXin XIAOWei FacultyofLifeSciences TheUniversityofManchesterManchesterM139NTUK

Aim Endoplasmic reticulum （ER） stress is increasingly recognized as an important contributor to the pathophysiology of many diseases, and therapeutic interventions that target ER stress response emerge as new thera- peutic modalities to treat cardiovascular diseases driven by prolonged ER stress. Ginkgolides K （GK） is a diterpene lactone constituent isolated from the leaves of Ginkgo biloba and has been found to possess potent neuroprotective properties. This study is aimed to investigate the cytoprotective effect of GK in cultured cardiomyocytes subjected to ER stress injury. Neonatal rat cardiomyocytes （NRCMs） were treated with ER stress inducer tunicamycin to mimic the ER stress injury. We demonstrated that GK pre-treatment mitigated ER stress-induced apoptosis in tunicamycin treated NRCMs. We observed that the activation of ER-associated degradation （ERAD） and autophagy were in- volved in the ER stress inhibition exerted by GK. These beneficial effects of GK were nearly abolished by the addi- tion of specific short interfering RNA （siRNA） for IRElα and XBP-1. Therefore, we conclude that GK might be a promising therapeutic agent for ER stress-mediated cardiovascular diseases, and ER-associated degradation （ERAD） and autophagy play a vital role in GK mediated cytoprotection.

关键词： Ginkgolide K ER stress Neonatal rat cardiomyocytes (NRCMs) ER-associated degradation (ERAD) Autophagy

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The vasorelaxant effect of pinocembrin on the rat basilar artery and its potential mechanisms

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中国药理学通报 2015年第B11期31卷 158-159页

作者： LILi WUXiao-ping NIUZi-ran ZHOURui MAYin-zhong duguan-hua BeijingKeyLaboratoryofDrugTargetsIdentificationandDrugScreening InsituteofMateriaMedicaChineseAcademyofMedicalSciences&PekingUnionMedicalCollegeBeijing100050

Aim To evaluate the vasorelaxant effects of the flavonone pinocembrin in isolated rat basilar artery rings and to investigate its possible mechanisms. Methods The isotonic contractions of the basilar artery rings from SD rats were recorded. Results Pinocembrin exerted vasorelaxation in a close-dependent manner in KCL （60 mmol · L^-1 ） or 5-HT （ 1 μmol · L^- 1）-induced sustained contraction and partial loss of the vasorelaxation in endothelium- denuded rings. Pretreatment with pinocembrin （30 or 50 μmol · L^-1 ） attenuated contractile responses to KC1 （ 10 - 60 mmol · L^-1 ） and 5-HT （0. 001 - 10 μmol · L^-1 ）. The pinocembrin -induced vasorelaxation was significant- ly reduced by the nitric oxide synthase inhibitor Nco-nitro-L-arginine methyl ester （L-NAME, 100 μmol · L^-1） , the guanylate cyclase inhibitor ODQ （5 μmol · L^-1） and the cyclooxygenase inhibitor indomethacin （5 μmol · L^-l）. The voltage-dependent K＋ channel blocker 4-aminopyridine （100 μmol · L^-1）, the ATP-sensitive K ＋ channel blocker glibenclamide （10μmol · L^-1） and Ca2＋-activated K ＋ channel blocker tetraethylammonium （1 retool· L^-1） remarkably attenuated pinocembrin-induced relaxations. Pinocembrin also inhibited contraction in- duced by increasing external calcium in Ca2＋-free medium plus 60 mmol · L^-1 KC1. Conclusion These results demonstrate that pinocembrin has a vasorelaxant effect on isolated rat basilar artery rings and may exert its action through an endothelium-dependent pathway, involving NO-cGMP, and also through an endothelium-independent 2＋ pathway, opening K ＋ channels and blockade of Ca channels.

关键词： pinocembrin basilar artery vasorelaxation calcium nitric oxide

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Combination Therapy of Actinomycin D and Cisplatin Achieved Stronger Cytotoxicity via Increasing PUMA Expression on KB Cells

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中国药理学通报 2015年第B11期31卷 239-239页

作者： WANGLin XUhuan-li YANGSheng-qian duguan-hua Beijingkeylaboratoryofdrugtargetsresearchandnewdrugscreening theInstituteofMateriaMedicaPekingUnionMedicalCollege100055Chian DepartmentofPharmacology SchoolofBasicMedicinetheCapitalUniversityofMedicalSciences

Aim To study the synergistic effect and mechanism of actinomycin D to the anti-cancer activity of cispl- atin on KB cells. Methods Cytotoxicity of actinomycin D on KB cells was evaluated by MTT and LDH Assay. Apoptosis was detected by Flow cytometry （FCM）. Expression of p53, PUMA, Bax, Bcl-2 and Bcl-xl was detected by WB （Western blot） or IF （immunofluorescence staining）. The translocation of PUMA, Bax, Bcl-2 and Bcl-xl was detected by confocal microscope. PUMA knockdown was achieved by PUMA siRNA. Results Actinomycin D synergistically enhanced the cytotoxicity of cisplatin on KB cells. Time-dependent increasing of PUMA and p53 in- duced by actinomycin D was accompanied by the translocation of PUMA and Bax/Bcl-xl in KB cells. Knockdown of PUMA effectively blocked the synergistic effect of actinomycin D to cisplatin. Conclusion Actinomycin D effi- ciently enhanced the anti-cancer activity of cisplatin on KB cells. Up-regulation of PUMA by actinomycin D is like- ly responsible for the observed synergistic effect between the two drugs. Combination of actinomycin D and cisplatin may lead to an effective cancer treatment strategy.

关键词： Actinomycin D cisplatin anti-cancer activity PUMA

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Baicalein ameliorates LPS-induced acute lung injury in mice through Inhibition of inflammatory responses

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中国药理学通报 2015年第B11期31卷 140-140页

作者： YANGSHENG-qian YUZi-ru YUANTian-yi WANGLin YANgHai-guang duguan-hua BeijingKeyLaboratoryofDrugTargetsIndetificationandDrugScrdding

Aim To study the effects of baicalein （BC）, a phenolic flavonoid extracted mainly from Scutellaria ba- icalensis Georgi, on lipopolysaccharide （LPS）-induced acute lung injury （ALI） in mice and the molecular mecha- nisms underlying. Methods Mice were administrated intranasally with LPS （20 mg · kg^-1/body weight） to estab- lish the ALI model. Then the mice were treated twice with BC （50,100 and 200 mg · kg^-1, p. o. ） 0. 5 hour and 12 hours after LPS stimulation, following another 12 hours, the lungs were collected for histological study. Results LPS caused marked inflammatory cell infiltration and myeloperoxidase activation in lungs, accompanied by significantly in- creased lung W/D ratio, from 7.97±0. 60 in normal group to 12. 49 ± 1.49 in the model. 77.88% reduction in the lung W/D ratio was observed in 200 mg· kg^-1 dose of baicalein. The myeloperoxidase activity was reduced to 40. 14% in mice treated with 200 mg · kg^-1. The number of total cells, neutrophils, and macrophages in BALF de- creased with increasing concentration of baicalein. Inflammatory cytokines level in serum declined significantly while insignificant changes of the same in BALF was observed in mice treated with 50,100 and 200 mg · kg^-1 doses of ba- icalein. Furthermore, LPS induced markedly the expression of inflammasomes and other inflammation-related genes in lung tissue. Treatment of LPS-exposed mice with BC significantly reduced the expression levels of these genes and al- leviated the pathological changes in lungs. Moreover, 1 μmol · L^-1 and 10 μmol · L^-1 BC inhibited remarkably the nuclear translocation of NF-kappaB p65 in Raw264.7 cells. Conclusion Baicalein alleviates LPS-induced acute lung injury in mice by suppressing NF-KB-mediated inflammatory responses and downregulation of inflammasomes.

关键词： acute lung injury baicalein NF-kappa B inflammasomes myeloperoxidase

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