Publications by authors named "Yueliang Shen"

16 Publications

  • Page 1 of 1

Neuroprotective effect of stroke pretreated MSCs against cerebral ischemia/reperfusion injury in rats.

World Neurosurg 2021 May 3. Epub 2021 May 3.

Department of General Medicine, The Affiliated Hospital of Hangzhou Normal University, Hangzhou, China. Electronic address:

Background: Mesenchymal stem cells (MSCs) have been shown to enhance neurological recovery after stroke. In this study, a middle cerebral artery occlusion (MCAO) rat model was designed to assess the neuroprotective effects of stroke pretreated MSCs on cerebral ischemia/reperfusion (I/R) injury.

Method: The MSCs were isolated and cultured in medium with 10% FBS, normal control serum (NS), or stroke serum (SS). Then these MSCs were injected into each group rats (n=6) 1 day after MCAO and continue feeding for 28 days. A battery of behavioral tests, TTC staining, hematoxylin and eosin staining, ELISA, and TUNEL assay were used to assess neural injury. Moreover, in order to detected the enhancement of neuronal regeneration and angiogenesis, immunofluorescence and western blotting were performed to assess the expression of trophic factor and growth factor.

Result: After treatment, the behaviour was improvement significantly. And the infarct area, brain lesion, and apoptosis cells were significantly decreased in the SS-MSCs group than others. It also modulated the inflammation by attenuating inflammatory cytokines. In addition, the number of neurogenesis positive cells, the expression of trophic factors and growth factors were significantly higher in the SS-MSCs group than others. At the same time, FBS-MSCs and NS-MSCs showed differences in the expression of trophic factors and growth factors, but the results were not as well as SS-MSCs.

Conclusion: SS-MSCs administration after the reperfusion led to neuroprotection by improving pathological changes, behavioral improvement, neurogenesis, suppression of apoptosis and inflammatory as well as angiogenesis.
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http://dx.doi.org/10.1016/j.wneu.2021.04.114DOI Listing
May 2021

MCC950 reduces neuronal apoptosis in spinal cord injury in mice.

CNS Neurol Disord Drug Targets 2020 Oct 5. Epub 2020 Oct 5.

Department of Basic Medicine Sciences, Zhejiang University School of Medicine, Hangzhou, Zhejiang. China.

Background: Traumatic spinal cord injury (SCI) is a severe condition usually accompanied by an inflammatory process that gives rise to uncontrolled local apoptosis and a subsequent unfavorable prognosis. One reason for this unfavorable outcome could be the activation of the NLRP3 inflammasome.

Objective: MCC950 is a specific inhibitor of NLRP3 that further inhibits the formation of the NLRP3 inflammasome. The purpose of this study was to determine whether the NLRP3 inflammasome was associated with the severity of local apoptosis and whether MCC950 could prevent neuronal apoptosis following SCI.

Methods: In this study, primary cortical neurons were cultured in vitro. With or without pretreatment/posttreatment with MCC950, neurons were subjected to oxygen-glucose deprivation (OGD) for 2 h and then reperfusion for 20 h. Immunofluorescence was used to determine the expression of NLRP3, ASC and cleaved caspase-1 in neurons. In vivo, SCI model mice were established with a 5 g weight-drop method. MCC950 was intraperitoneally injected at 0, 2, 4, 6, 8, 10, and 12 days after SCI. Basso Mouse Scale (BMS) scores and footprint assays were used to assess motor function. Paw withdrawal threshold and tail flick latency were used to assess somatosensory function. H&E, Nissl and TUNEL staining were used to measure histological changes and apoptosis at 3 days after SCI, and scar formation was observed by Masson staining and GFAP immunohistochemical analysis at 28 days after SCI.

Results: Immunofluorescence analysis confirmed that MCC950 inhibited OGD-induced activation of the NLRP3 inflammasome in neurons. Behavioral tests, Masson staining and GFAP immunohistochemical analysis showed that MCC950-treated mice had improved neuronal functional recovery and reduced scar formation at 28 days after SCI. H&E, Nissl and TUNEL staining confirmed that there were more living neurons and fewer apoptotic neurons in MCC950-treated mice than control mice at 3 days after SCI.

Conclusion: These results reveal that MCC950 exerts neuroprotective effects by reducing neuronal apoptosis, preserving the survival of the remaining neurons, attenuating the severity of the damage, and promoting the recovery of motor function after SCI.
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http://dx.doi.org/10.2174/1871527319666201005170659DOI Listing
October 2020

Microarray assay of circular RNAs reveals cicRNA.7079 as a new anti-apoptotic molecule in spinal cord injury in mice.

Brain Res Bull 2020 11 1;164:157-171. Epub 2020 Sep 1.

Department of Neurosurgery, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China. Electronic address:

Traumatic spinal cord injury (SCI) can lead to motor disturbance, sensory deficit, or autonomic dysfunction. The role of circRNAs in the pivotal physiopathological processes of SCI has been demonstrated recently. However, no similar research has been performed to explore the circRNAs involved in apoptosis after SCI. The differentially expressed circRNAs in mice spinal cord three days after SCI were originally detected with microarray assay (n = 4/group). Subsequently, potential apoptosis-related circRNAs were predicted by comprehensive bioinformatics analysis. In total, 1131 circRNAs varied (>2-fold change, p < 0.05) in the injured mice spinal cord. The characters of these circRNAs were summarized. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis was applied to predict the primary function of these circRNAs. 148 circRNAs were found to be correlated to the apoptosis injury progress in after SCI. Moreover, an apoptosis-related ceRNA network was constructed. In loss-of-function experiments, cicRNA.7079 knockdown enhanced apoptosis in NSC-34 motor neurons. This study may contribute to new insights into the mechanism of apoptosis after SCI. The anticipation of anti-apoptosis circRNA. 7079 may provide potential research targets for SCI in mice.
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http://dx.doi.org/10.1016/j.brainresbull.2020.08.004DOI Listing
November 2020

Identification of mitochondrial function-associated lncRNAs in septic mice myocardium.

J Cell Biochem 2021 Jan 12;122(1):53-68. Epub 2020 Aug 12.

Department of Basic Medicine Sciences, Zhejiang University School of Medicine, Hangzhou, China.

The present study aimed to analyze long noncoding RNA (lncRNA) and messenger RNA (mRNA) expression profiles in septic mice heart and to identify potential lncRNAs and mRNAs that be responsible for cardiac mitochondrial dysfunction during sepsis. Mice were treated with 10 mg/kg of lipopolysaccharides to induce sepsis. LncRNAs and mRNAs expression were evaluated by using lncRNA and mRNA microarray or real-time polymerase chain reaction technique. LncRNA-mRNA coexpression network assay, Gene Ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were performed. The results showed that 1275 lncRNAs were differentially expressed in septic myocardium compared with those in the control group. A total of 2769 mRNAs were dysregulated in septic mice heart, most of which are mainly related to the process of inflammation, mitochondrial metabolism, oxidative stress, and apoptosis. Coexpression network analysis showed that 14 lncRNAs were highly correlated with 11 mitochondria-related differentially expressed mRNA. Among all lncRNAs and their cis-acting mRNAs, 41 lncRNAs-mRNA pairs (such as NONMMUG004378 and Apaf1 gene) were enriched in GO terms and KEGG pathways. In summary, we gained some specific lncRNAs and their potential target mRNAs that might be involved in mitochondrial dysfunction in septic myocardium. These findings provide a panoramic view of lncRNA and might allow developing new treatment strategies for sepsis.
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http://dx.doi.org/10.1002/jcb.29831DOI Listing
January 2021

Local application of MDL28170-loaded PCL film improves functional recovery by preserving survival of motor neurons after traumatic spinal cord injury.

Neurosci Lett 2019 02 5;694:161-167. Epub 2018 Dec 5.

Department of Basic Medicine Sciences, School of Medicine, Zhejiang University, Hangzhou, 310058, China. Electronic address:

Neuronal death and organization degeneration can happen inordinately after spinal cord injury (SCI), which lead to nerve dysfunction. We aimed to determine whether local application of a cell permeable calpain I inhibitor (MDL28170) can promote SCI recovery by increasing neuronal cell viability. MDL28170-loaded polycaprolactone (PCL) film was fabricated. Scanning electron microscopy showed the surface of PCL film was smooth with holes (diameter at μM level). The PCL film was non-toxic, biological compatibility, and had good neuron adhension and slow release characteristic. MDL28170 increased VSC4.1 motor neurons' viability under tunicamycin (an endoplasmic reticulum stress) induced injury. In a traumatic SCI rat model, MDL28170-loaded PCL film reduced the area of lesion cavity, and promoted recovery of locomotor behavior. Moreover, the expression of GAP-43 was upregulated after MDL28170-loaded PCL film treatment. Thus, our findings demonstrated that localized delivery of MDL28170 could promote SCI recovery by inhibiting endoplasmic reticulum stress, preserving survival of the motor neurons, which may point out a promising therapeutic target for treating SCI patient.
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http://dx.doi.org/10.1016/j.neulet.2018.12.006DOI Listing
February 2019

Local Delivery of β-Elemene Improves Locomotor Functional Recovery by Alleviating Endoplasmic Reticulum Stress and Reducing Neuronal Apoptosis in Rats with Spinal Cord Injury.

Cell Physiol Biochem 2018 30;49(2):595-609. Epub 2018 Aug 30.

Department of Neurosurgery, Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, China.

Background/aims: Spinal cord injury (SCI) is a serious global problem that leads to permanent motor and sensory deficits. This study explores the anti-apoptotic and neuroprotective effects of the natural extract β-elemene in vitro and in a rat model of SCI.

Methods: CCK-8 assay was used to evaluate cell viability and lactate dehydrogenase assay was used to evaluate cytotoxicity. A model of cell injury was established using cobalt chloride. Apoptosis was evaluated using a fluorescence-activated cell sorting assay of annexin V-FITC and propidium iodide staining. A rat SCI model was created via the modified Allen's method and Basso, Beattie, and Bresnahan (BBB) scores were used to assess locomotor function. Inflammatory responses were assessed via enzyme-linked immunosorbent assay (ELISA). Apoptotic and surviving neurons in the ventral horn were respectively observed via terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining and Nissl staining. Western blotting was used to measure protein expression.

Results: β-elemene (20 μg/ml) promoted cell viability by activating phosphorylation of the PI3K-AKT-mTOR pathway. β-elemene reduced CoCl2-induced cellular death and apoptosis by suppressing the expression levels of CHOP, cleaved-caspase 12, 78-kilodalton glucose-regulated protein, cleaved-caspase 3, and the Bax/Bcl-2 ratio. In the rat model of SCI, Nissl and TUNEL staining showed that β-elemene promoted motor neuron survival and reduced neuronal apoptosis in the spinal cord ventral horn. BBB scores showed that β-elemene significantly promoted locomotor behavioral recovery after SCI. In addition, β-elemene reduced the ELISA-detected secretion of interleukin (IL)-6 and IL-1β.

Conclusion: β-elemene reduces neuronal apoptosis by alleviating endoplasmic reticulum stress in vitro and in vivo. In addition, β-elemene promotes locomotor function recovery and tissue repair in SCI rats. Thus, our study provides a novel encouraging strategy for the potential treatment of β-elemene in SCI patients.
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http://dx.doi.org/10.1159/000492996DOI Listing
September 2018

β-Elemene Enhances GAP-43 Expression and Neurite Outgrowth by Inhibiting RhoA Kinase Activation in Rats with Spinal Cord Injury.

Neuroscience 2018 07 9;383:12-21. Epub 2018 May 9.

Department of Basic Medicine Sciences, School of Medicine, Zhejiang University, Hangzhou 310058, China. Electronic address:

RhoA signaling pathway inhibitors such as Y27632 (a ROCK inhibitor) have recently been applied as treatments for spinal cord injury (SCI) because they promote neurite outgrowth and axonal regeneration in neurons. β-Elemene, a compound that is extracted from a natural plant (Curcuma zedoary), influences the expression level of RhoA protein. Whether it can promote neurite outgrowth in motor neurons or enhance locomotor recovery in SCI remains unclear. Here, we initially demonstrated that β-elemene promotes neurite outgrowth of ventral spinal cord 4.1 (VSC4.1) motoneuronal cells and primary cortical neurons. Pull-down assays showed that β-elemene significantly inhibits the activation of RhoA kinase. Western blotting assays suggested β-elemene markedly inhibits the phosphorylation of limk and confilin and significantly increases the expression level of GAP-43. Then, in a rat model of SCI, hematoxylin-eosin and myelin staining showed that β-elemene reduces the area of lesion cavity and spares the white matter. BBB scores showed β-elemene significantly promotes locomotor behavioral recovery. In addition, western blotting assays and immunofluorescence staining demonstrated that the expression level of GAP-43 is upregulated by β-elemene treatment in vivo. Thus, our study provided an encouraging novel strategy for the potential treatment of SCI patients with β-elemene.
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http://dx.doi.org/10.1016/j.neuroscience.2018.04.045DOI Listing
July 2018

Update on biomaterials for prevention of epidural adhesion after lumbar laminectomy.

J Orthop Translat 2018 Apr 7;13:41-49. Epub 2018 Mar 7.

Department of Basic Medical Sciences, Zhejiang University School of Medicine, Hangzhou 310058, China.

Lumbar laminectomy often results in failed back surgery syndrome. Most scholars support the three-dimensional theory of adhesion: Fibrosis surrounding the epidural tissues is based on the injured sacrospinalis behind, fibrous rings and posterior longitudinal ligaments. Approaches including using the minimally invasive technique, drugs, biomaterial and nonbiomaterial barriers to prevent the postoperative epidural adhesion were intensively investigated. Nevertheless, the results are far from satisfactory. Our review is based on various implant biomaterials that are used in clinical applications or are under study. We show the advantages and disadvantages of each method. The summary will help us to figure out ideas towards new techniques. The translational potential of this article: This review summarises recent biomaterials-related clinical and basic research that focuses on prevention of epidural adhesion after lumbar laminectomy. We also propose a novel possible translational method where a soft scaffold acts as a physical barrier in the early stage, engineered adipose tissue acts as a biobarrier in the later stage in the application of biomaterials and adipose-derived mesenchymal stem cells are used for prevention of epidural adhesion.
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http://dx.doi.org/10.1016/j.jot.2018.02.001DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5892378PMC
April 2018

Interaction among hERG channel blockers is a potential mechanism of death in caffeine overdose.

Eur J Pharmacol 2017 Apr 16;800:23-33. Epub 2017 Feb 16.

Chinese Herb Medicine Division, The Nurturing Station for the State Key Laboratory of Subtropical Silviculture, Zhejiang Agriculture and Forestry University, 88 North Circle Road, Lin'an 311300, PR China. Electronic address:

Caffeine overdose death is due to cardiac arrest, but its mechanism has not been explored in detail. In this study, our data showed that caffeine significantly prolonged the heart rate-corrected QT interval (QTc) of rabbits in vivo (P<0.05; n=7). Caffeine was also found to be a hERG channel blocker with an IC of 5.04mM (n=5). Although these two findings likely link caffeine overdose death with hERG channel blockade, the amount of caffeine consumption needed to reach the IC is very high. Further study demonstrated that addition another hERG blocker could lower the consumption of caffeine significantly, no matter whether two hERG blockers share the same binding sites. Our data does not rule out other possibility, however, it suggests that there is a potential causal relationship between caffeine overdose death with hERG channel and the interaction among these hERG blockers.
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http://dx.doi.org/10.1016/j.ejphar.2017.02.018DOI Listing
April 2017

Barium chloride impaired Kir2.1 inward rectification in its stably transfected HEK 293 cell lines.

Eur J Pharmacol 2014 May 12;730:164-70. Epub 2014 Mar 12.

Chinese Herb Medicine Division, The Nurturing Station for the State Key Laboratory of Subtropical Silviculture, Zhejiang Agriculture and Forestry University, 88 North Circle Road, Lin'an 311300, PR China. Electronic address:

Kir2.1 channel is a typical inward rectified channel with little outward currents when the membrane depolarized. Barium blocks the inward Kir2.1 currents in a voltage-dependent manner. However, in this study we found that barium would impair the rectification and open Kir2.1 outward currents at a depolarized voltage, causing increment of outward current amplitudes by 43±7% (n=5, P<0.01) after 200s barium application. In the meanwhile, a higher barium concentration did block the outward currents by 17.5±4.3% (n=4, P<0.01) and temporarily twisted current upward tendency. The increment was likely barium specific since both calcium and Kir2.1 specific blocker, Chloroethylclonidine (CEC), did not enhance the current amplitudes. The rectification of Kir2.1 was not recovered by washing barium off, which suggested a non-competitive mechanism. Since the currents occurred at phase 1, 2 of cardiac action potential, it would likely shorten the action potential plateau and it would decrease QT duration in electrocardiography (ECG).
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http://dx.doi.org/10.1016/j.ejphar.2014.02.025DOI Listing
May 2014

[Research on a novel method for the evaluation of left ventricular diastolic function].

Sheng Wu Yi Xue Gong Cheng Xue Za Zhi 2010 Apr;27(2):270-3

Zhejiang University School of Medicine, National Education Base for Basic Medical Sciences, Hangzhou 310058, China.

The methods for evaluating left ventricular diastolic function completely and simply are lacking in our country at present. To solve this problem, we presents in this paper a novel method, which is developed according to certain algorithms and mathematic models and is carried out by a MATLAB program. This method mainly obtains dP/dt loops, and calculates four important indices, including left ventricular end-diastolic pressure (LVEDP), Maximal decrease in velocity of left ventricular pressure (--(dP/dt)max), Time constant of ventricular isovolumic relaxation (tau) and Chamber stiffness (Kd), according to the changes of left ventricular pressure. The results obtained from the experiment of isolated rat hearts during ischemia/reperfusion have demonstrated the usefulness and validity of this method. Therefore, with the use of tau and Kd as indicators, this is a sensitive and effective method for evaluating the left ventricular diastolic function, and it can be applied to early detection of left ventricular diastolic dysfunction.
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April 2010

Protection of myocardium in streptozotocin-induced diabetic rats by water extracts of Hsian-tsao (Mesona procumbens Hemsl.).

Asia Pac J Clin Nutr 2008 ;17(1):23-9

School of Medicine, Zhejiang University, 388 Yuhangtang Road, and The Second Affiliated Hospital of Zhejiang University, Hangzhou 310058, P.R. China.

The myocardial protective effects of water extracts from Hsian-tsao (Mesona procumbens Hemsl.) on diabetic rats were investigated. Thirty Sprague-Dawley male rats were randomly divided into three groups, "control group" (n=10) with intraperitoneal saline injection, "diabetic group" (n=10) with 60 mg of intraperitoneal streptozotocin injection per kg of body weight and "Hsian-tsao group" (n=10) with intragastric administration of Hsian-tsao extracts every day for 4 weeks after intraperitoneal streptozotocin injection. Body weight and blood sugar concentrations were measured before and after model induction in the three groups. Thrombospondin-1 (TSP-1) expressions in the myocardium were monitored by immunohistochemistry and rt-RT-qPCR analysis. Myocardial ultrastructural changes were also analyzed by us-ing transmission electron microscopy. Our results demonstrated that diabetic myocardial ultrastructural changes included myofibrillar disarrangements, mitochondria disruption, and an increase in nuclear membrane invaginations. These damages were significantly less severe in the Hsian-tsao group compared with the diabetic group. A significant increase of the TSP-1 expression was also observed in the hearts of the diabetic rats (p<0.01), but it was relatively lower in the Hsian-tsao group than in the diabetic group (p<0.01). It suggested that Hsian-tsao treatment in the diabetic rats effectively prevented the pathological alterations in the myocardium and decreased TSP-1 expression.
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September 2008

Hemin-induced Erk1/2 activation and heme oxygenase-1 expression in human umbilical vein endothelial cells.

Free Radic Res 2007 Sep;41(9):990-6

Department of Physiology, Zhejiang University School of Medicine, Hangzhou, China.

Hemin has been reported to be protective in the pathological process, but its protective mechanisms have not been precisely defined. Hemin could induce Erk1/2 phosphorylation in astrocyte. Erk1/2 phosphorylation has been proved to be involved in many growth signals cellular transduction. However, little study has been conducted as to the relationship between hemin and Erk1/2 activation in human umbilical vein endothelial cells (HUVECs). The present study aimed to investigate the relationship between hemin and Erk1/2 phosphorylation in HUVECs. The results showed that low concentration of hemin induced and sustained phosphorylation of Erk1/2 for a long time. The HO inhibitor protoporphyrin IX zinc (II) abrogated phosphorylation of Erk1/2 induced by hemin. Biliverdin, one of the metabolites of hemin, obviously induced the Erk1/2 phosphorylation in HUVECs. Both hemin and biliverdin promoted HUVEC cell growth. The results strongly suggested that hemin could induce and sustain Erk1/2 phosphorylation in HUVECs by way of HO-1 induction and biliverdin produced from HO-1 catalysing hemin degradation.
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http://dx.doi.org/10.1080/10715760701468740DOI Listing
September 2007

Activation of Mitochondrial ATP-Sensitive Potassium Channel Contributes to Protective Effect in Prolonged Myocardial Preservation.

Conf Proc IEEE Eng Med Biol Soc 2005;2005:4027-30

Dept. of Phys., Zhejiang Univ. Sch. of Med., Hangzhou.

To find a better strategy for effective donor organ preservation, here we used a model of long-term hypothermia preservation of rat hearts to investigate the cardioprotective effects of diazoxide, a selective opener of mitochondrial ATP-sensitive potassium channel (mitoKATP ). Cardiac function was impaired by 8-hour ischemic preservation following 30 minutes of reperfusion. Treatment with diazoxide significantly attenuated the decline of myocardial contractility, and decreased the lactate dehydrogenase leakage and myocardial edema. Diazoxide also prevented the loss of activity of mitochondrial superoxide dismutases and sarcolemmal Na+/K+ ATPase during ischemia or reperfusion period, respectively. These effects of diazoxide could be abolished by a selective mitoKATp blocker 5-hydroxydecanoate. The results suggest that diazoxide, as a supplementation in cardioplegic solution, could enhance myocardial protection by opening mitoKATp channel, and better maintenance of mitochondrial anti-oxidative enzyme.
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http://dx.doi.org/10.1109/IEMBS.2005.1615345DOI Listing
October 2012

An in vitro rat diaphragmatic fatigue model induced by combined hypoxic and hypercapnic acidosis and the effect of salmeterol.

Pharmacol Res 2006 Feb 28;53(2):171-6. Epub 2005 Nov 28.

Department of Respiratory Medicine, First Affiliated Hospital, Medical School of Zhejiang University, Hangzhou 310003, China.

Hypoxia or hypercapnia impairs diaphragmatic contractility and induces fatigue. However, little is known about the combined effect of hypoxic and hypercapnic acidosis (HHA) on diaphragmatic fatigue. In this study, a gas mixture (21% O2, 12% CO2 and 67% N2) was used to produce HHA-induced rat diaphragmatic fatigue. Force-frequency relationships and twitch characteristics including peak twitch tension (PTT), time to peak tension (TPT), half relaxation time (1/2RT), maintaining tension (MT) and direct-muscle-stimulation tension (MST) were measured in diaphragm preparations from male SD rats. The HHA gas mixture attenuated force at all frequencies (5-120 Hz) and decreased PTT, MT and MST significantly. Aminophylline, a positive control drug, blocked the negative inotropic effect of HHA in a dose-dependent manner. Moreover, salmeterol, a long-acting beta2-adrenoceptor agonist, inhibited the harmful effect of HHA at high frequencies (40-120 Hz), but without effect on MT and MST. These results suggest that an in vitro HHA-induced rat diaphragmatic fatigue model could be established by aerating with the gas mixture, which may be an optimal model to screen effective drugs for diaphragmatic fatigue. Furthermore, salmeterol may play a protective role in HHA-induced impairment.
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http://dx.doi.org/10.1016/j.phrs.2005.10.008DOI Listing
February 2006

[Electrophysiologic study of the biphasic effects of cyclovirobuxine D on arrhythmias].

Zhongguo Zhong Xi Yi Jie He Za Zhi 2004 Nov;24(11):1010-3

Department of Cardiology, The First Affiliated Hospital of Medical College, Zhejiang University, Hangzhou (310003).

Objective: To explore the possible mechanism of cyclovirobuxine D (CVB-D) in countering and inducing arrhythmia, by way of studying its electro-physiological effect on ventricular papillary muscles of rats in vitro.

Methods: The transmembrane potential of rat's isolated right ventricular papillary muscles were recorded using conventional glass micro-electrode technique.

Results: (1) CVB-D in concentration of 13.3-63.3 micromol/L, showed prolonging effect on the action potential repolarization time, mainly the action potential duration 50 (APD50), APD70 and APD90, in dose-dependent manner, in concentration of 33.3-63.3 micromol/L, it could inhibit the resting potential, action potential amplitude (APA) and maximum depolarization velocity (Vmax) in dose-dependent manner. (2) CVB-D also showed time-dependent effect, the effect initiated 10 min after 20 micromol/L was perfused in ventricular muscle, the APD50, APD70 and APD90 were potentiated gradually along with prolongation of action time and reached the peak at 30-40 min, without any potentiation thereafter. (3) CVB-D could markedly prolong the effective refractory period (ERP) of action potential, increase the ratio of ERP/APD. (4) CVB-D in concentration of 33.3 micromol/L could induce frequent, multifocal spontaneous arrhythmia in some cells when the action time was longer than 45 min.

Conclusion: CVB-D has the action of anti-ventricular arrhythmia, the mechanism is correlated with the prolongation of APD and ERP of ventricular muscle as well as the increase of ERP/APD ratio, while it also has the effect of inducing arrhythmia, the mechanism might be concerned with excessive prolongation of APD and the inhibition on RP, APA and Vmax.
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November 2004