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[ ABSTRACT] AIM:To investigate the effect of Jia-jian-yi-yin decoction on endothelium-dysfunction in ovariecto-mized rats.METHODS:The ovariectomized rats were treated with Jia-jian-yi-yin decoction or turbid liquid of estradiol va-lerate for 8 weeks.The vascular ring tension was measured.Scanning electron microscopy and Western blotting were ap-plied to assess the function of endothelium-dependent dilation, aortic endothelial morphology and the expression of endothe-lial lipase.The pathologic sections were prepared to observe the effect of Jia-jian-yi-yin decoction on the uterus.RE-SULTS:In ovariectomized rats, the decrease in endothelium-dependent relaxation to acetylcholine ( ACh) was reversed to normal level, the endothelial morphology returned to normal without lipid accumulation and the endothelial lipase expression was decreased by Jia-jian-yi-yin decoction.Furthermore, no obvious change of the wet weight of uterine between the ovari-ectomized rats with or without Jia-jian-yi-yin decoction treatment was observed.CONCLUSION:Jia-jian-yi-yin decoction may have protective effects on endothelium-dependent vasodilation and aortic endothelial morphology in estrogen-deficient animals.
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This paper elaborates on the importance and necessity of implementing information technology in medical education,the application of information technology in the whole process of medical education,the conceptual construction of medical students' life-long education,the construction of practical teaching resources and the cultivation of information capacity both in teachers and students,etc.In the meantime,this paper introduces the basic framework of medical network and remote education center of Sun Yat-sen University under construction.
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[Objective] The aim of the present study was to investigate the role of membrane estrogen receptor (mER) mediated pathway in the proliferation and apoptosis of endothelial progenitor cells (EPCs). [Methods] Bone marrow (BM)-derived EPCs were cultured. The cells were divided into different groups, plus or not plus estrogen receptor blocker (ICI 182,780), PI3K inhibitors (LY294002), and NOS inhibitor (L-NAME) to show the effect of E_2-BSA on EPCs. The proliferation of EPCs was determined by MTT and nitric oxide (NO) release was measured by chromatometry. Apoptotic cell death was determined using the Hochest 33258 staining. The expression of phosphorylated eNOS (p-eNOS) were detected by Western blot. [Results] E_2-BSA could increase EPCs proliferation, and this effect was inhibited by estrogen receptor blocker ICI 182,780, thus indicated that mER-initiated membrane signaling pathways were involved in the action of estrogen on EPCs. E_2-BSA increased nitric oxide production and inhibited apoptosis induced by serum withdrawal, and this effect also inhibited by PI3K inhibitor (LY294002), NOS inhibitor (L-NAME)and estrogen receptor blocker(ICI 182,780), thus indicated that PI3K/Akt/NO pathway was involved the effect of estrogen on EPCs apoptosis. Moreover, E_2-BSA treatment increased phosphorylation of eNOS (p-eNOS). PI3K inhibitors (LY294002) also blocked these effects. [Conclusions] The results of present study suggested that mER mediated EPCs proliferation and apoptosis were related to the PI3K/Akt/eNOS pathway.
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Objective To explore the role of ERK1/2 protein in development of myocardial hypertrophy.Methods Myocardial cells were isolated from ventricles of 1～3-day-old neonate rats and purifed by a culture method.Neonate rat cardiomyocyte hypertrophic responses were assayed by measuring protein content,protein synthesis rate and cell surface area.Expression of protein ERK1/2 were detected by Western blot.Results Cell protein content,~3H-leucine(~3 H-Leu)incorporation and cell surface area increased by treating of cardiomyocytes with T(10~(-10)～10~(-6) mol/L)for 24 h.The maxium effect was observed at the concentration of 10~(-8) mol/L.The increase of cell protein content induced by T was inhibited by pretreating with flutamide(10~(-5) mol/L)for 2 h,while there was no effect on cardiomyocytes pretreating with flutamide alone.The increase of ~3H-Leu incorporation induced by T was blocked by PD98059(50 μmol/L).Expression of ERK1/2 was upregulated significantly by treating with testoster one for 24 h at the level of 10~(-8) mol/L.The increased expression of ERK1/2 induced by T was reversed by pretreating with flutamide(10~(-5) mol/L)for 2 h.Conclusion T with physio-concentration may induce cardiomyocyte hypertrophy and this effect was possibly mediated through the activation of ERK1/2 signalling.During this procession,T upregulated the protein expression of ERK1/2 mediated by androgen receptor.
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AIM: To investigate the effect of caveolin - 1 and phosphorylation of ERK1/2 on 17β - estradiol ( E_2 ) induced inhibition of vascular smooth muscle cells ( VSMCs ). METHODS: The proliferation in cultured VSMCs was determined by using [~3H ] - thymidine incorporation. The expressions of caveolin - 1, MKP -1 and ERK1/2 phosphorylation were measured by Western blotting. The expression of caveolin - 1 mRNA was measured by RT - PCR. RESULTS: Exposed to fetal calf serum ( FCS) for 24 h, the increase in proliferation of VSMCs was detected by [~3H] -thymidine incorporation. Pretreatment with various concentrations of E_2 for 24 h inhibited VSMC proliferation induced by FCS. The results of Western blotting and RT - PCR showed that pretreated with 17β - estradiol for 24 h reserved the decrease in caveolin - 1 induced by FCS. Western blotting results further proved that the expression of MKP - 1 was significantly increased and the expression of ERK1/2 phosphorylation was decreased after incubated with 17β - estradiol. CONCLUSION: 17β -estradiol increases caveolin - 1 and MKP - 1 expressions, and decreases ERK1/2 phosphorylation, leading to the inhibition of VSMC proliferation.
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We analyzed the minus of present medical education,basing on questionnaires of 1773 medical students,including the students' participation rates in lectures of multiple fields and their demands on future lectures.We gave some pieces of advice to solve the problems as well as some references to boost our lectures.
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The plan of three early educations is based on our real education condition, which builds a bridge between the traditional education and advanced education as a balance and breakthrough. It means the early involvement of clinic, the early involvement of scientific research and the early involvement of social practice.
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To improve the teaching of internal medicine,we analysed the results of clinical skill competition of interns on internal medicine and the current state of intern clinical skill learning including advantage and disadvantage.
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AIM: To study the roles and mechanisms of ERKs and intracellular free calcium in cardiomyocyte hypertrophic response induced by endothelin-1(ET-1). METHODS: (1) Neonatal rat cardiomyocyte hypertrophic response was assayed by measuring cell surface area and protein content; (2) ERKs activity was determined by Whatman Paper Filter method; (3) Intracellular free calcium concentration (［Ca2+］i) was measured using Fura-2/AM as a fluorescent indicator. RESULTS: (1) ET-1 could increase total protein production, surface area, ERKs activity and ［Ca2+］i in cultured cardiomyocyte in dose-dependent manner at concentrations ranging from 10-9 to 10-7 mol/L. And this effect could be abolished by BQ123, an antagonist of ETA receptor, partly inhibited by PTX, but not by BQ788, an antagonist of ETB receptor.（2）The activation of ERKs and the increase of ［Ca2+］i induced by ET-1 were obviously inhibited by PD98059, a selective ERKs kinase inhibitor, and nifedipine, a calcium channel blocker, respectively. Both antagonists partially inhibited ET-1-stimulated cardiomyocyte hypertrophic response. (3) Staurosporine, a selective PKC inhibitor, could inhibit ET-1-stimulated cardiomyocyte hypertrophic response and increase of ［Ca2+］i, but not affect the activation of ERKs. CONCLUSION: Cardiomyocyte hypertrophic response induced by ET-1 is mediated by ETA receptor coupled to PTX-sensitive G-protein, which involves at least two signalling pathways: PKC-mediated increase of ［Ca2+］i , and PKC-independent activation of ERKs.
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AIM:To investigate the effect of caveolin-1 and phosphorylation of ERK1/2 on 17?-estradiol (E2) induced inhibition of vascular smooth muscle cells (VSMCs). METHODS:The proliferation in cultured VSMCs was determined by using [3H]-thymidine incorporation. The expressions of caveolin-1,MKP-1 and ERK1/2 phosphorylation were measured by Western blotting. The expression of caveolin-1 mRNA was measured by RT-PCR. RESULTS:Exposed to fetal calf serum (FCS) for 24 h,the increase in proliferation of VSMCs was detected by [3H]-thymidine incorporation. Pretreatment with various concentrations of E2 for 24 h inhibited VSMC proliferation induced by FCS. The results of Western blotting and RT-PCR showed that pretreated with 17?-estradiol for 24 h reserved the decrease in caveolin-1 induced by FCS. Western blotting results further proved that the expression of MKP-1 was significantly increased and the expression of ERK1/2 phosphorylation was decreased after incubated with 17?-estradiol. CONCLUSION:17?-estradiol increases caveolin-1 and MKP-1 expressions,and decreases ERK1/2 phosphorylation,leading to the inhibition of VSMC proliferation.
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AIM: To investigate the effect of 17?-estradiol(E2) on myocardial hypertrophy induced by endothelin-1(ET-1) and the related mechanism.METHODS: Myocardial cells from neonate rats were cultured in vitro and myocardial hypertrophy model was established with ET-1.The effects of 17?-estradiol on myocardial hypertrophy were observed.The role of ERK1/2 in the effects of 17?-estradiol was also detected.RESULTS: Compared with control group,ET-1 increased cell protein content,cell surface area and -Leucine(-Leu) incorporation.Pretreatment with E2 for 24 h could inhibit the increase in cell protein content,cell surface area and -Leu incorporation induced by ET-1.ET-1 significantly stimulated ERK1/2 activity,which was prevented by pretreatment with E2.Tamoxifen,estradiol receptor antagonist,partially inhibited the effect of E2.The ability of ET-1 to stimulate -Leu incorporation was significantly blocked by PD98059,which could enhance the inhibitory effect of E2 on the increase of -Leu incorporation in cardiomyocytes induced by ET-1.CONCLUSION: E2 can inhibit cardiomyocyte hypertrophy induced by ET-1.This effect is mediated by estrogen receptor.ERK1/2 signal pathway is closely correlated with the inhibitory effect of E2 on cardiomyocyte hypertrophy induced by ET-1.
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Estrogen has widespread biological actions. Besides sexual organs, estrogen plays an important role in cardiovascular system, central nervous sy s tem and bone tissue. However, the mechanisms of estrogen action are very complex and not fully understood. The actions of estrogen are not identical and even co mpletely different in some organs system. In this review, we will focus on the n ew development of molecular mechanisms of estrogen action.
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Objective: To explore the change of activities of the cardiac autonomic nervous system in the EMG biofeedback with the quantified index of heart rate variability(HRV). Methods: Various physiological signals such as ECG、EEG、EMG were recorded by Synchronous Multi-Signal Recording Biofeedback System, and HRV analysis was applied to the extracted ECG signals. Thirty healthy young men received the tests. Results:Compared with the resting state, when the subjects entered biofeedback state, the values of low frequency power, indicator of the sympathetic activity decreased while the values of high frequency power (indicator of the vagal activity) increased, and the values of low frequency power/high frequency power ratio, the marker of the sympatho-vagal balance decreased too. During the later treatment sessions (after 7-10 times treatments) the change exhibited statistical difference and achieved one stable level (low frequency power, baseline 3.98?0.21, 3.82?0.15, 3.93?0.16, 3.91?0.23, test state 3.55?0.32, 3.51?0.29, 3.93?0.16, 3.39?0.26, t=-6.85～-3.68,P
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Objective: To study the mechanism of electromyographic (EMG) biofeedback. Methods: The EMG and electroencephalographic (EEG) signals were recorded dynamically during the course of EMG biofeedback. Changes of EMG amplitude and frequency during EMG biofeedback were assessed with linear analysis. We also applied the nonlinear analysis, approximate entropy (ApEn) of EMG signals and Cross Approximate entropy (Cross-ApEn) between EMG and EEG signals, to assess regularities in EMG and correlation between EMG and EEG. Results: With the processing of EMG biofeedback, the maximum, minimum and mean amplitude of EMG signals decreased significantly (F=3.85~25.59,P
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AIM: To study the roles and mechanisms of ERKs and intracellular free calcium in cardiomyocyte hypertrophic response induced by endothelin-1(ET-1). METHODS: (1) Neonatal rat cardiomyocyte hypertrophic response was assayed by measuring cell surface area and protein content; (2) ERKs activity was determined by Whatman Paper Filter method; (3) Intracellular free calcium concentration ([Ca 2+ ]i) was measured using Fura-2/AM as a fluorescent indicator. RESULTS: (1) ET-1 could increase total protein production, surface area, ERKs activity and [Ca 2+ ]i in cultured cardiomyocyte in dose-dependent manner at concentrations ranging from 10 -9 to 10 -7 mol/L. And this effect could be abolished by BQ123, an antagonist of ET A receptor, partly inhibited by PTX, but not by BQ788, an antagonist of ET B receptor.(2)The activation of ERKs and the increase of [Ca 2+ ]i induced by ET-1 were obviously inhibited by PD98059, a selective ERKs kinase inhibitor, and nifedipine, a calcium channel blocker, respectively. Both antagonists partially inhibited ET-1-stimulated cardiomyocyte hypertrophic response. (3) Staurosporine, a selective PKC inhibitor, could inhibit ET-1-stimulated cardiomyocyte hypertrophic response and increase of [Ca 2+ ]i, but not affect the activation of ERKs. CONCLUSION: Cardiomyocyte hypertrophic response induced by ET-1 is mediated by ET A receptor coupled to PTX-sensitive G-protein, which involves at least two signalling pathways: PKC-mediated increase of [Ca 2+ ]i , and PKC-independent activation of ERKs. [
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AIM: To investigate the effect of caveolin-1 on the endothelin-1 (ET-1)-induced vascular smooth muscle cells (VSMC) proliferation. METHODS: The -thymidine (TdR) incorporation, immunofluorescence assays and western blotting were used in this study. RESULTS: The ETA receptor specific antagonist BQ123 inhibited the increase in TdR incorporation in response to ET-1 on VSMC. Immunofluorescence assays showed that caveolin-1 was mostly distributed in plasmalemma of VSMC. After 24 h treatment of VSMC with ET-1, the expression of caveolin-1 in VSMC was significantly decreased. Western blotting showed that ET-1 inhibited the expression of caveolin-1 in VSMC, BQ123 reversed the effect of ET-1. CONCLUSION: Caveolin-1 was mostly distributed in plasmalemma of VSMC. ET-1 downregulated caveolin-1 expression in VSMC via ETA receptor.