12 results on '"Chun-Ming Jiang"'
Search Results
2. Effect of Dopamine Receptor 1 on Apoptosis of Cultured Neonatal Rat Cardiomyocytes in Simulated Ischaemia/Reperfusion
- Author
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Yan Lin, Hong Li, Jun Gao, Yajun Zhao, Changqing Xu, Ye Tian, Li-Ping Han, Baofeng Yang, Chun-ming Jiang, Hongzhu Li, and Shu-xia Ma
- Subjects
Increased lactate dehydrogenase activity ,Agonist ,medicine.drug_class ,Blotting, Western ,Apoptosis ,Myocardial Reperfusion Injury ,Toxicology ,Mitochondria, Heart ,Fas ligand ,chemistry.chemical_compound ,Malondialdehyde ,Lactate dehydrogenase ,medicine ,Animals ,Myocytes, Cardiac ,Rats, Wistar ,Receptor ,Cells, Cultured ,Pharmacology ,L-Lactate Dehydrogenase ,biology ,Superoxide Dismutase ,Receptors, Dopamine D1 ,Cytochrome c ,Cytochromes c ,Receptors, Death Domain ,General Medicine ,Molecular biology ,Rats ,Disease Models, Animal ,Animals, Newborn ,Biochemistry ,chemistry ,Dopamine receptor ,Caspases ,biology.protein ,Calcium - Abstract
Dopamine receptors exist in many tissues, including rat cardiac tissue. However, the physiological importance of dopamine receptors in the homeostatic regulation of cardiac function is unclear. In this study, a model of ischaemia/reperfusion was established by culturing primary neonatal rat cardiomyocytes in ischaemia-mimetic solution for 2 hr, followed by incubation in normal culture medium for 24 hr. Lactate dehydrogenase activity, superoxide dismutase activity and malondialdehyde content were determined colorimetrically with a spectrophotometer. Apoptotic cell death was assayed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labelling staining and flow cytometry, and morphological alterations were observed with transmission electron microscopy. The intracellular free calcium concentration ([Ca2+]i) was measured by confocal laser scanning microscopy. Finally, the expression of dopamine receptor 1 (DR1), caspase-3, -8 and -9, Fas, Fas ligand and Bcl-2 and the release of cytochrome c were analysed by Western blot. The results showed that DR1 expression was increased markedly during ischaemia/reperfusion. Treatment with 10 microM SKF-38393 (DR1 agonist) significantly increased lactate dehydrogenase activity, decreased superoxide dismutase activity and increased malondialdehyde content in the culture medium. The DR1 agonist promoted the release of cytochrome c, accumulation of [Ca2+]i, and apoptosis induced by ischaemia/reperfusion. Furthermore, SKF-38393 up-regulated the expression of caspase-3, -8 and -9, Fas and Fas ligand, and down-regulated Bcl-2 expression. In contrast, 10 microM SCH-23390 (DR1 antagonist) had no significant effects on the above indicators. In conclusion, DR1 activation is involved in the apoptosis of cultured neonatal rat cardiomyocytes in simulated ischaemia/reperfusion through the mitochondrial and death receptor pathways.
- Published
- 2008
3. [Effects of edaravone on the expression of GRP78, Caspase-12, and neuron apoptosis in juvenile rat hippocampus after status convulsive]
- Author
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Guang-Qian, Li, Hai-Ping, Wang, and Chun-Ming, Jiang
- Subjects
Male ,Rats, Sprague-Dawley ,Seizures ,Edaravone ,Animals ,Apoptosis ,Hippocampus ,Antipyrine ,Caspase 12 ,Heat-Shock Proteins ,Rats - Abstract
To observe the expression of GRP78 (glucose regulated protein, GRP78), Caspase-12 and the change of neuron apoptosis in the juvenile rat hippocampus after status convulsive (SC), and to explore the effect of edaravone on them.One hundred and ninety-five juvenile male Sprague-Dawley (SD) rats were randomly divided into normal saline control group (NS group), status convulsive group (SC group) and edaravone treatment group (ED group). Each group was further divided into five subgroups in different executed time points after SC. The rats in status convulsive group were kindled into epilepsy by lithium-pilocarpine method. Expression of GRP78 mRNA and caspase-12 mRNA was detected with reverse transcription-polymerase chain reaction (RT-PCR) method. Expressions of GRP78 and caspase-12 protein were detected with immunohistochemical methods. The neuron apoptosis was observed by TdT-mediated dUTP nick end labeling (TUNEL).(1) Measured by immunohistochemistry the value of OD of GRP78 (0.1480 ± 0.0164, 0.1682 ± 0.0114, and 0.1540 ± 0.0102, respectively, 12 h - 48 h points) and caspase-12 (0.1325 ± 0.0165, 0.1794 ± 0.0213, 0.1525 ± 0.0423, and 0.1309 ± 0.0199, respectively, 12 h-72 h points) positive cells in the SC group increased, there was a significant difference compared with NS group (GRP78: 0.1214 ± 0.0147, 0.1272 ± 0.0177, and 0.1260 ± 0.0157, respectively, 12 h-72 h points. Caspase-12: 0.1050 ± 0.0121, 0.1041 ± 0.0151, 0.1058 ± 0.0222, and 0.1036 ± 0.0186, respectively, 12 h - 72 h points) (P0.01, or P0.05). By ED intervention GRP78 (0.1550 ± 0.0131, 0.1886 ± 0.0154, and 0.1721 ± 0.0151, respectively, 12 h - 48 h points) positive cells value of the OD increased as compared with SC group (P0.01, or P0.05). and caspase-12 (0.1211 ± 0.0184, 0.1545 ± 0.0205, and 0.1085 ± 0.0219, respectively, 12 h, 24 h and 72 h points) positive cells value of the A decreased as compared with SC group (P0.01, or P0.05). (2) Measured by RT-PCR, the expression of GRP78 mRNA and caspase-12 mRNA trend was similar to protein. (3) The TUNEL positive cells in hippocampus CA(1) of SC group (11.41 ± 2.37) were more than that of NS group after the SC 12 h (P0.01), reached its highest level at 48 h (28.78 ± 5.11), after the intervention with edaravone (8.98 ± 2.22, 13.09 ± 2.54 and 20.57 ± 4.89, respectively, 12 h-48 h points), TUNEL positive cells showed a significant drop in SC group at 12 h-48 h time points (P0.01, or P0.05), but still significantly higher than that of the NS group (6.22 ± 1.50, 6.57 ± 1.61 and 6.72 ± 1.14, respectively) (P0.01, or P0.05), at the 4 h time point (NS group 6.29 ± 1.49, SC group 6.61 ± 1.71, ED group 5.75 ± 1.41) among the three groups, no significant difference in TUNEL positive cells was found (P = 0.759).The expression of GRP78 and caspase-12 increased after SC. Edaravone increased expression of GRP78 and decreased expression of caspase-12 in hippocampus rat with pilocarpine-induced seizures, reduced the number of neuronal apoptosis. These results suggest that edaravone may have protective effect against the hippocampal damage caused by status convulsive.
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- 2011
4. Role of dopamine D2 receptors in ischemia/reperfusion induced apoptosis of cultured neonatal rat cardiomyocytes
- Author
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Guangdong Yang, Rui Wang, Lina Wang, Shuzhi Bai, Changqing Xu, Guang-Wei Li, Hongzhu Li, Yan Lin, Jin Guo, Hong Li, Jun Gao, Hong-Xia Li, Yajun Zhao, Chun-ming Jiang, Weihua Zhang, Li-ping Han, Baofeng Yang, Lingyun Wu, and Ye Tian
- Subjects
Male ,Agonist ,medicine.medical_specialty ,medicine.drug_class ,Endocrinology, Diabetes and Metabolism ,Clinical Biochemistry ,Myocardial Ischemia ,Ischemia ,lcsh:Medicine ,Apoptosis ,Myocardial Reperfusion Injury ,Fas ligand ,Internal medicine ,Dopamine receptor D2 ,medicine ,Animals ,Myocytes, Cardiac ,Pharmacology (medical) ,Rats, Wistar ,Receptor ,Molecular Biology ,Bromocriptine ,Cells, Cultured ,Biochemistry, medical ,Receptors, Dopamine D2 ,Chemistry ,Research ,lcsh:R ,Biochemistry (medical) ,Cell Biology ,General Medicine ,medicine.disease ,Rats ,Dopamine D2 Receptor Antagonists ,Endocrinology ,Animals, Newborn ,Haloperidol ,Calcium ,Reperfusion injury ,medicine.drug - Abstract
Background Myocardial ischemia/reperfusion injury is the major cause of morbidity and mortality for cardiovascular diseases. Dopamine D2 receptors are expressed in cardiac tissues. However, the roles of dopamine D2 receptors in myocardial ischemia/reperfusion injury and cardiomyocyte apoptosis are unclear. Here we investigated the effects of both dopamine D2 receptors agonist (bromocriptine) and antagonist (haloperidol) on apoptosis of cultured neonatal rat ventricular myocytes induced by ischemia/reperfusion injury. Methods Myocardial ischemia/reperfusion injury was simulated by incubating primarily cultured neonatal rat cardiomyocytes in ischemic (hypoxic) buffer solution for 2 h. Thereafter, these cells were incubated for 24 h in normal culture medium. Results Treatment of the cardiomyocytes with 10 μM bromocriptine significantly decreased lactate dehydrogenase activity, increased superoxide dismutase activity, and decreased malondialdehyde content in the culture medium. Bromocriptine significantly inhibited the release of cytochrome c, accumulation of [Ca2+]i, and apoptosis induced by ischemia/reperfusion injury. Bromocriptine also down-regulated the expression of caspase-3 and -9, Fas and Fas ligand, and up-regulated Bcl-2 expression. In contrast, haloperidol (10 μM) had no significant effects on the apoptosis of cultured cardiomyocytes under the aforementioned conditions. Conclusions These data suggest that activation of dopamine D2 receptors can inhibit apoptosis of cardiomyocytes encountered during ischemia/reperfusion damage through various pathways.
- Published
- 2011
5. Calcium-sensing receptors induce apoptosis in cultured neonatal rat ventricular cardiomyocytes during simulated ischemia/reperfusion
- Author
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Zhuo-Ran Zhang, Li-Ping Han, Chun-ming Jiang, Wei-ming Li, Changqing Xu, Rui Wang, Hongzhu Li, and Ying-Bo Qu
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Heart Ventricles ,chemistry.chemical_element ,Apoptosis ,Gadolinium ,Myocardial Reperfusion Injury ,Biology ,Calcium ,Confocal scanning microscopy ,Calcium in biology ,Fas ligand ,Microscopy, Electron, Transmission ,Myocyte ,Animals ,Myocytes, Cardiac ,Receptor ,Cells, Cultured ,Flavonoids ,Cell Biology ,General Medicine ,Molecular biology ,Rats ,Disease Models, Animal ,chemistry ,Animals, Newborn ,Calcium-sensing receptor ,Apoptosis Regulatory Proteins ,Receptors, Calcium-Sensing - Abstract
Calcium-sensing receptors (CaSRs) are G-protein coupled receptors which regulate systemic calcium homeostasis and also participate in cell proliferation, differentiation and apoptosis. We have previously shown that CaSR can induce apoptosis in isolated rat adult hearts and in normal rat neonatal cardiomyocytes. However, no knowledge exists concerning the role of CaSR in apoptosis induced by ischemia and reperfusion in neonatal cardiac myocytes. Therefore, in the present study, we incubated primary neonatal rat ventricular cardiomyocytes in ischemia-mimetic solution for 2 h, then re-incubated them in a normal culture medium for 24 h to establish a model of simulated ischemia/reperfusion (I/R). We assayed the apoptotic ratio of the cardiomyocytes by flow cytometry; observed morphological alterations by transmission electron microscope; analyzed the expression of caspase-3, Bcl-2, CaSR, extracellular signal-regulated protein kinase (ERK), and Fas/Fas ligand (FasL) by Western blotting; and measured the concentration of intracellular calcium by Laser Confocal Scanning Microscopy. The results showed that simulated I/R increased the expression of CaSR and cardiomyocyte apoptosis. GdCl3, a specific activator of CaSR, further enhanced CaSR expression, along with increases in intracellular calcium and apoptosis in cardiomyocytes during I/R. Activation of CaSR down-regulated Bcl-2 expression, up-regulated caspase-3 and Fas/FasL expression and stimulated ERK1/2 phosphorylation. In summary, CaSR is involved in I/R injury and apoptosis of neonatal rat ventricular cardiomyocytes by inhibiting Bcl-2, inducing calcium overload and activating the Fas/FasL death receptor pathway.
- Published
- 2007
6. Effects of polyamines on apoptosis induced by simulated ischemia/reperfusion injury in cultured neonatal rat cardiomyocytes
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Baofeng Yang, Hongzhu Li, Changqing Xu, Yajun Zhao, Li-Ping Han, Yan-qiao Zhang, Weiming Zhao, Li Zhang, Weihua Zhang, and Chun-ming Jiang
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Ischemia ,Apoptosis ,Confocal scanning microscopy ,Biology ,Rats, Sprague-Dawley ,chemistry.chemical_compound ,Microscopy, Electron, Transmission ,medicine ,Polyamines ,Animals ,Myocytes, Cardiac ,Cells, Cultured ,TUNEL assay ,Cytochrome c ,Cytochromes c ,Cell Biology ,General Medicine ,medicine.disease ,Molecular biology ,Rats ,Spermidine ,chemistry ,Animals, Newborn ,Proto-Oncogene Proteins c-bcl-2 ,Caspases ,Reperfusion Injury ,Putrescine ,biology.protein ,Calcium ,Reperfusion injury - Abstract
We incubated neonatal Sprague-Dawley rat cardiomyocytes in primary culture in a medium simulating ischemia (consisting of hypoxia plus serum deprivation) for 2 h, then re-incubated them for 24 h in normal culture medium to establish a model of simulated ischemia/reperfusion (I/R) injury. Apoptotic cell death was measured by MTT assay, TUNEL staining and flow cytometry. Morphological alterations were assessed by transmission electron microscopy, the expression of caspases-3 and -9 and Bcl-2 and the release of cytochrome c by Western blotting, and the intracellular free-calcium concentration ([Ca2+]i) by laser confocal scanning microscopy. The results showed that pretreatment with 10 micromol/l spermine or spermidine significantly inhibited apoptosis in the I/R cells, suppressed the expression of caspases-3 and -9 and cytochrome c release, up-regulated Bcl-2 expression and decreased [Ca2+]i. However, pretreatment with 10 micromol/l putrescine had the opposite effects. Evidence for this "double-edged" effect of polyamines on apoptosis in I/R-injured cardiomyocytes is presented for the first time. It may suggest a novel pharmacological target for preventing and treating cardiac ischemia/reperfusion injury.
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- 2007
7. [Association between calcium-sensing receptor protein expression and rat cardiomyocyte apoptosis]
- Author
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Yi-Hua, Sun, Chang-qing, Xu, Hong, Li, Sa, Shi, Wei-hua, Zhang, Ya-jun, Zhao, Yan-qiao, Zhang, Wei-min, Han, Li-ping, Han, Chun-ming, Jiang, Quan-feng, Li, and Rui, Wang
- Subjects
Male ,Caspase 3 ,Myocardium ,Animals ,Apoptosis ,Female ,Myocytes, Cardiac ,RNA, Messenger ,Rats, Wistar ,Receptors, Calcium-Sensing ,Rats ,Signal Transduction - Abstract
To investigate the relationship between calcium-sensing receptor protein (CaSR) expression and rat cardiomyocyte apoptosis and related signal transduction pathways.The CaSR, BCl2, Caspase3 protein and ERK1/2 phosphorylation or non-phosphorylation were detected by Western blot. Cardiomyocyte apoptosis was detected by flow cytometry and immunofluorescence.CaSR protein was detected in rat cardiac tissue and CaSR activator gadolinium (GdCl3) induced cardiomyocyte apoptosis and increased ERK1/2 phosphorylation and expression of BCl2 and activated Caspase3. The selective mitogen-activated protein kinase (MAPK) inhibitor PD98059 abolished gadolinium -induced ERK1/2 activation and BCl2 expression, further increased the activation of Caspase3 and cardiomyocyte apoptosis.Our results demonstrate the CaSR existence in cardiomyocytes and CaSR activation by gadolinium can induce myocyte apoptosis by activating Caspase3 and tyrosine protein kinase pathway.
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- 2006
8. Involvement of calcium sensing receptor in myocardial ischemia/reperfusion injury and apoptosis*
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Yi-Hua Sun, Rui Wang, Chun-ming Jiang, Changqing Xu, and Weihua Zhang
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Myocardial ischemia ,Apoptosis ,business.industry ,medicine ,Calcium-sensing receptor ,Pharmacology ,Cardiology and Cardiovascular Medicine ,Adenosine A3 receptor ,medicine.disease ,business ,Molecular Biology ,Reperfusion injury - Published
- 2007
9. Erratum to 'Calcium-sensing receptor induces apoptosis in cultured neonatal rat ventricular cardiomyocytes during simulated ischemia/reperfusion' [Cell Biol Int 32 (2008) 792-800]
- Author
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Wei-Min Li, Chun-ming Jiang, Ying-Bo Qu, Hongzhu Li, Changqing Xu, Li-Ping Han, Zhuo-Ran Zhang, and Rui Wang
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Neonatal rat ,medicine.anatomical_structure ,Chemistry ,Apoptosis ,Simulated ischemia ,INT ,Cell ,medicine ,Cell Biology ,General Medicine ,Calcium-sensing receptor ,Cell biology - Published
- 2009
10. Role of dopamine D2 receptors in ischemia/reperfusion induced apoptosis of cultured neonatal rat cardiomyocytes.
- Author
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Hong-zhu Li, Jin Guo, Jun Gao, Li-ping Han, Chun-ming Jiang, Hong-xia Li, Shu-zhi Bai, Wei-hua Zhang, Guang-wei Li, Li-na Wang, Hong Li, Ya-jun Zhao, Yan Lin, Ye Tian, Guang-dong Yang, Rui Wang, Ling-yun Wu, Bao-feng Yang, and Chang-qing Xu
- Subjects
DOPAMINE receptors ,ISCHEMIA ,APOPTOSIS ,CARDIOVASCULAR diseases ,CELL death - Abstract
Background: Myocardial ischemia/reperfusion injury is the major cause of morbidity and mortality for cardiovascular diseases. Dopamine D
2 receptors are expressed in cardiac tissues. However, the roles of dopamine D2 receptors in myocardial ischemia/reperfusion injury and cardiomyocyte apoptosis are unclear. Here we investigated the effects of both dopamine D2 receptors agonist (bromocriptine) and antagonist (haloperidol) on apoptosis of cultured neonatal rat ventricular myocytes induced by ischemia/reperfusion injury. Methods: Myocardial ischemia/reperfusion injury was simulated by incubating primarily cultured neonatal rat cardiomyocytes in ischemic (hypoxic) buffer solution for 2 h. Thereafter, these cells were incubated for 24 h in normal culture medium. Results: Treatment of the cardiomyocytes with 10 μM bromocriptine significantly decreased lactate dehydrogenase activity, increased superoxide dismutase activity, and decreased malondialdehyde content in the culture medium. Bromocriptine significantly inhibited the release of cytochrome c, accumulation of [Ca2+ ]i , and apoptosis induced by ischemia/reperfusion injury. Bromocriptine also down-regulated the expression of caspase-3 and -9, Fas and Fas ligand, and up-regulated Bcl-2 expression. In contrast, haloperidol (10 μM) had no significant effects on the apoptosis of cultured cardiomyocytes under the aforementioned conditions. Conclusions: These data suggest that activation of dopamine D2 receptors can inhibit apoptosis of cardiomyocytes encountered during ischemia/reperfusion damage through various pathways. [ABSTRACT FROM AUTHOR]- Published
- 2011
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11. Effect of Dopamine Receptor 1 on Apoptosis of Cultured Neonatal Rat Cardiomyocytes in Simulated Ischaemia/Reperfusion.
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Hong-zhu Li, Li-ping Han, Chun-ming Jiang, Hong Li, Ya-jun Zhao, Jun Gao, Yan Lin, Shu-xia Ma, Ye Tian, Bao-feng Yang, and Chang-qing Xu
- Subjects
DOPAMINE receptors ,APOPTOSIS ,HEART cells ,ISCHEMIA ,REPERFUSION injury ,ANIMAL models in research ,LACTATE dehydrogenase ,SUPEROXIDE dismutase ,MALONDIALDEHYDE ,SPECTROPHOTOMETERS - Abstract
Dopamine receptors exist in many tissues, including rat cardiac tissue. However, the physiological importance of dopamine receptors in the homeostatic regulation of cardiac function is unclear. In this study, a model of ischaemia/reperfusion was established by culturing primary neonatal rat cardiomyocytes in ischaemia-mimetic solution for 2 hr, followed by incubation in normal culture medium for 24 hr. Lactate dehydrogenase activity, superoxide dismutase activity and malondialdehyde content were determined colorimetrically with a spectrophotometer. Apoptotic cell death was assayed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labelling staining and flow cytometry, and morphological alterations were observed with transmission electron microscopy. The intracellular free calcium concentration ([Ca
2+ ]i ) was measured by confocal laser scanning microscopy. Finally, the expression of dopamine receptor 1 (DR1), caspase-3, -8 and -9, Fas, Fas ligand and Bcl-2 and the release of cytochrome c were analysed by Western blot. The results showed that DR1 expression was increased markedly during ischaemia/reperfusion. Treatment with 10 µM SKF-38393 (DR1 agonist) significantly increased lactate dehydrogenase activity, decreased superoxide dismutase activity and increased malondialdehyde content in the culture medium. The DR1 agonist promoted the release of cytochrome c, accumulation of [Ca2+ ]i , and apoptosis induced by ischaemia/reperfusion. Furthermore, SKF-38393 up-regulated the expression of caspase-3, -8 and -9, Fas and Fas ligand, and down-regulated Bcl-2 expression. In contrast, 10 µM SCH-23390 (DR1 antagonist) had no significant effects on the above indicators. In conclusion, DR1 activation is involved in the apoptosis of cultured neonatal rat cardiomyocytes in simulated ischaemia/reperfusion through the mitochondrial and death receptor pathways. [ABSTRACT FROM AUTHOR]- Published
- 2008
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12. LPS induces cardiomyocyte injury through calcium-sensing receptor
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Gan Han, Xiao-xie Li, Zhu-ying Wang, Hong-yu Wang, Chun-ming Jiang, Xue-yan Liu, and Zhi-mei Jiang
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Lipopolysaccharides ,medicine.medical_specialty ,Clinical Biochemistry ,Lipopolysaccharide ,Apoptosis ,Adamantane ,Gadolinium ,Cardiomyocyte ,Biology ,Calcium in biology ,Article ,Superoxide dismutase ,Rats, Sprague-Dawley ,chemistry.chemical_compound ,Internal medicine ,Lactate dehydrogenase ,Malondialdehyde ,Quinoxalines ,Calcium-sensing receptor ,medicine ,Myocyte ,Animals ,Myocytes, Cardiac ,Calcium Signaling ,Receptor ,Molecular Biology ,Cells, Cultured ,IL-6 ,L-Lactate Dehydrogenase ,Interleukin-6 ,Superoxide Dismutase ,Tumor Necrosis Factor-alpha ,General Medicine ,Cell Biology ,Rats ,Endocrinology ,chemistry ,TNF-α ,biology.protein ,Tumor necrosis factor alpha ,Receptors, Calcium-Sensing - Abstract
Calcium-sensing receptor (CaSR) belongs to the family C of G-protein coupled receptors. We have previously demonstrated that CaSR could induce apoptosis of cultured neonatal rat ventricular cardiomyocytes in simulated ischemia/reperfusion. It remains unknown whether the CaSR has function in lipopolysaccharide (LPS)-induced myocardial injure. The aim of this study was to investigate whether the CaSR plays a role in LPS-induced myocardial injury. Cultured neonatal rat cardiomyocytes were treated with LPS, with or without pretreatment with the CaSR-specific agonist gadolinium chloride (GdCl3) or the CaSR-specific antagonist NPS2390. Release of TNF-α and IL-6 from cardiomyocytes was observed. Levels of malonaldehyde (MDA), lactate dehydrogenase (LDH), and activity of superoxide dismutase (SOD) were measured. In addition, apoptosis of the cardiomyocytes, [Ca(2+)]i and level of CaSR expression were determined. The results showed that LPS increased cardiomyocytes apoptosis, [Ca(2+)]i, MDA, LDH, TNF-α, IL-6 release, and CaSR protein expression. Compared with LPS treatment alone, pretreatment with GdCl3 further increased apoptosis of cardiomyocytes, MDA, LDH, TNF-α, IL-6 release, [Ca(2+)]i, and the expression of the CaSR protein. Conversely, pretreatment with NPS2390 decreased apoptosis of cardiomyocytes, MDA, LDH, TNF-α, IL-6 release, [Ca(2+)]i and the expression of the CaSR protein. These results demonstrate that LPS could induce cardiomyocyte injury. Moreover, LPS-induced cardiomyocyte injury was related to CaSR-mediated cardiomyocytes apoptosis, TNF-α, IL-6 release, and increase of intracellular calcium.
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