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Objective To investigate the role and possible mechanism of combination use of chloroquine (CQ) with either dexamethasone (DEX) or radiation on multiple myeloma (MM) cell line U266 .Methods Cell viability of U266 treated with CQ alone ,or CQ combined with either DEX or radiation was measured by cell counting kit-8 (cck8) .CalcuSyn method was used to assess effect of drugs interaction .Cell viability and apoptosis of U266 pre-treated with CQ were also measured by cck8 and flow cytometry after radiation .Expression of B-cellymphoma-2 (Bcl-2) in U266 cells treated by CQ combined with DEX or radiation was determined by Western blot analysis .Results Either CQ or DEX displayed a dose dependent cell proliferation in-hibitory effect on U266 cells .Cytotoxic effect of DEX (125 μmol/L) on U266 cells was enhanced and expression of Bcl-2 pro-tein in U266 cells was decreased by combining with CQ (3 .9 μmol/L) .U266 cells were sensitized to radiation and cell death was induced by CQ (1 .0 μmol/L) .Conclusion CQ could sensitize cytotoxic effect of DEX or radiation on U 266 cells ,and the former was possibly related to down-regulation of Bcl-2 protein .
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Objective:Clonidine,by activating peripheral α-sbrenoceptors, produces transient pressor response after i.v.injection in anesthetized animals.Moxonidine, with at least 40-fold higher affinity to I1-imidazoline receptors than to α2-adrenoceptors,produces also a transient pressor response. This work was designed to investigate whether I1-imidazoline receptors are involved in this pressor effect of moxonidine. Methods:Female spontaneously hypertensive rats(SHRs,aged 14-16 weeks)were anesthetized with urethane.To observe the transient pressor responses,moxonidine 0.1,0.3,1.0mg/kg(intravenous,i.v),2.0μg(intracerebroventricular,i.c.v.)and 1.0,10.0mg/kg(intragastric,i.g.)were administrated in different groups of rats.To evaluate the roles of α1-adrenoceptors,α2-adrenoceptors and I1-imidazoline receptors in the transient pressor responses to moxonidine, prazosin(10.0μg/kg),yohimbine(2.0mg/kg),phentolamine(0.2mg/kg),idazoxan(1.0mg/kg)or yohimbine+idazoxan(2.0mg/kg+1.0mg/kg)were intravenously given to the animals before moxonidine 0.3mg/kg (i.v.).Results:It was found that i.v.moxonidine produced a greater pressor response than clonidine when producing a similar reduction of blood pressure.This effect of moxonidine was not influenced by prazosin, but was partly inhibited by yohimbine, phentolamine or idazoxan,and completely blocked by the combination of yohimbine and idzaxon.Neither i.c.v.injection nor i.g. administration of moxonidine induced transient pressor responses.Conclusion:The transient pressor response of i.v. moxonidine is mediated by both peripheral I1-imidazoline receptors and α2-adrenoceptors.
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Objective:Glucose-insulin-potassium(GIK) is clinically used for reducing mortality in acute myocardial infarction(MI). It is known that ventricular arrhythmia, left ventricular dysfunction and impaired baroreflex sensitivity(BRS) are the three major determinants for predicting the mortality after acute MI. The present work was designed to study the effects of GIK on BRS, ventricular arrhythmia, and left ventricular function in rats with coronary artery ligature. Sprague-Dawley rats were used and the myocardial infarction was produced by ligature of the left anterior descending artery. Five weeks after coronary artery ligation, BRS was measured in conscious state with a computerized blood pressure monitoring system and left ventricular function and electrocardiogram were determined in the anaesthetized state in the subacute phase of myocardial infarction. It was found that GIK did not affect the blood pressure and heart period in both conscious and anaesthetized rats. GIK did not enhance BRS, but reduced ventricular arrhythmia and improved left ventricular function by reducing left ventricular end diastolic pressure in anaesthetized rats with MI. It is proposed that reducing ventricular arrhythmia and improving left ventricular function contribute to the effect of GIK on reducing the mortality after MI.
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Objective: To determine the effect of K ATP on the reduction of blood pressure variability (BPV) caused by adenosine in conscious, freely moving sinoaortic denervated (SAD) rats. Methods: Using computerized analytic system of blood pressure (BP), five groups treated with adenosine, adenosine A 1 receptor agonist N 6 cyclopentyladenosine (CPA), A 2 receptor agonist 5′ N cyclopropyl carboxamido adenosine (CPCA), ATP sensitive K + channel (K ATP ) blocker glibenclamide, and CPCA with the K ATP blocked by glibenclamide in advance were used. BP, heart period (HP) and BPV were analyzed. Results: Both adenosine and CPCA significantly decreased BPV in SAD rats, but CPA had no influence on it. Glibenclamide markedly reduced BPV in SAD rats as well, furthermore, it might antagonize the effect of CPCA on BPV by blocking K ATP . Conclusion: K ATP plays an important role in the development of high BPV in SAD rats. [
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Objective:To investigate the effect of arterial baroreflex(ABR)on survival rate of rats with cecal ligation and puncture(CLP)-induced sepsis.Methods:Male Sprague-Dawley rats were divided into 2 groups:sham-operated rats(n=22)and sinoaortic denervated(SAD)rats(n=22).Four weeks after SAD rats were subjected to CLP-induced sepsis,the blood pressure and heart period(HP)were monitored for 12 hours in conscious state and the survival of rats was observed.Results:Both the diastolic and systolic blood pressue gradually decreased after CLP;the HP shortened first and then drastically prolonged until the death of rats.At 12 h after CLP the survival rate of SAD rats was lower than that of the sham-operated rats(59% vs 86%).Significant differences were found between the Kaplan-Meier survival curves of the rats in 2 groups(P
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Objective:To investigate the protective effect of Intravenous Injection of Radix Astragali seu Hedysari on acute myocardiac infarction (AMI) in anesthetized dogs. Methods: Twenty health dogs were treated by ligating descending anterior of coronary with two-step method. The changes of electrocardiogram before and after ligation were recorded. After 4 hours myocardium were taken out and dyed with NBT to make sure of the extent of myocardiac infarction.Results: Intravenous Injection of Radix Astragali seu Hedysari could decrease the lethality of AMI, ameliorated ST changes on electrocardiogram induced by AMI, and reduced infarction area. Conclusions: Intravenous Injection of Radix Astragali seu Hedysari is effective in the treatment of AMI in anesthetized dogs.