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Objective To investigate the effect of exercise on calcium modulin in myocardial sarcoplasmic re-ticulum of animal type 1 diabetes model in rat. Methods A total of 40 Spragne-Dawley rats were randomly dividedinto 4 groups : a normal control group, an exercise training group, a diabetes group and a diabetes plus exercise-traininggroup. At the end of 4- week-exercise training after the establishment of the diabetes model by intraperitoncal injectionof sterptozotocin, the animals were sacrificed and the level of blood glucose, insulin, blood fat and glycosylated serumprotein were tested. The gene expression of calcium modulin proteins was measured by reverse transcription-polymerasechain reaction, and the Western blotting technique was used to measure the protein of sarcoplasmic endoplasmic reticu-lure Ca<'2+> -ATPase (SERCA2) and phaspholamban (PLB). Results The level of biochemical indicator of exercisegroup is not affected when comparing with that of the control group, but significantly changed in diabetic group ( P <0. 01 ) ; The level of blood glucose, insulin, blood fat and glycosylated serum protein were ameliorated in diabetic rats inthe exercise training group. No significant changes in mRNA level of SERCA2, PLB and ryanodine receptor type 2(RYR2) were observed between control and diabetic group, the same to protein expression of SERCA2 and PLB. Butexpression of calcium modulin mRNA was significantly increased in exercise group and diabetic rats in the exercisetraining group comparing with that of the control and diabetic groups ( P < 0.01 ), the same to protein expression ofSERCA2 and PLB. Conclusion Exercise exerted good protective effects on the myocardial injury with 1 type diabetesrat, which might attribute to the upregnlated expression of SERCA2, PLB and RYR2 in diabetic rat heart.
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Aim To observe the dysfunction of myocardial nuclear calcium transport in rat myocardial injury and effects of taurine on it . Methods The model of myocardial damage was induced by subcutaneous injection of isoproterenol (ISO,5 mg?kg-1?d-1). Myocardial nuclei were purified with Sucrose density centrifugation and identified zymologically. The activity of Ca2+_ATPase was measured zymologically and calcium uptake was assayed with 45Ca2+ isotope.Results Compared with the control, the Ca2+_ATPase activity of myocardial nuclear in ischemia group was decreased by 18.1%(P
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Objective: To observe the protective effect of ligustrazine on myocardial ischemia rat induced by isoproterenol. Methods : The model of myocardial ischemia was induced by subtcuaneous injection of isoproterenol (ISP, 5mg?kg -1 ) into rats and repeated the same dose 24 hours later. The activities of Ca 2+ -ATPase、Ca 2+ -Mg 2+ -ATPase and the contents of Ca 2+ in the myocardial mitochondria were observed, respectively. The changes of protein expression of bcl-2 and bax genes were detected by immunohistochemical staining. Results : In the ligustrazine treated group, as compared with those of the model, the activities of Ca 2+ -ATPase、Ca 2+ -Mg 2+ -ATPase in the myocardial mitochondria increased significantly( P 0.05). Conclusion : Ligustrazine possesses protective effects against myocardial ischemia injury via increasing the activities of Ca 2+ -ATPase、Ca 2+ -Mg 2+ -ATPase in the myocardial mitochondria and influencing the expression of bcl-2.
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AIM: To study the effects of Liquestrazin on succinic dehydrogenase (SDH) and cytochrome oxidase (CCO) in the myocardial mitochondria of the ischemia-reperfusion rats and its mechanism. METHODS:Model of myocardial ischemia-reperfusion injury was produced by coronary artery ligation . The rats were devided into sham operation control (SC), ischemia-reperfusion (IR) and ischemia-reperfusion protected with Liqustrazin (IR+L) group . Activity of SDH,CCO,SOD and GSH?PX and contents of malondialdehyde (MDA),Cyt aa 3,Cyt c and phospholipid(PL) were observed respectively . RESULTS: As compared with ischemia-reperfusion group (IR), IR+L group showed significantly increased activity of SDH, CCO,SOD and GSH?PX (P
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AIM Taurine can regulate Asp、 Glu、 GABA from rat cortical synaptosomes. But its mechanism is unclear. The release regulated effects were investigated through analysis of GABA receptors.METHODS Bicuculline、Phaclofen、Baclofen were added in a Krebs Ringer buffer with resuspended synapotomes.Endogenous Asp、 Glu and GABA release during the 5 min superfusion were measured by high perfusion liquid chromatography using percolumn durivatization with Dans Cl. RESULT Phaclofen,but not bicucullion baclofen, counteracted the inhibition of GABA overflow,although the inhibition of Asp and Glu overflow was not attenuated. CONCLUSION Taurine inhibits the depolarization evoked release of GABA through the activation of presynaptic autoreceptors and taurine also acts on presynaptic sits of Asp Glu nerve terminals to inhibit their evoked release in rat cerebral cotex.