Effect of implantation of cardiosphere-derived cells combined with rat heart tissue-derived extracellular matrix on acute myocardial infarction in rats / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate whether heart tissue-derived extracellular matrix (ECM) promotes the differentiation of cardiosphere-derived cells (CDCs) implanted in rat infracted myocardium to improve the cardiac structure and function.</p><p><b>METHODS</b>Rat CDCs were cultured by cardiac explant methods, and ECM was prepared by decelluariztion method. In a Wistar rat model of acute myocardial infarction established by ligating the left anterior descending branch, IMDM solution, ECM suspension, 10CDCs in IMDM solution, or 10CDCs in ECM suspension were injected into the infracted rat myocardium (6 rats in each group). The cardiac function of the rats was evaluated by cardiac ultrasonography, and the percentage of positive heart fibrosis area after infarction was determined with Masson staining. The differentiation of implanted CDCs in the infarcted myocardium was detected using immunofluorescence assay for the markers of cardiac muscle cells (α-SA), vascular endothelial cells (vWF) and smooth muscle cells (α-SMA).</p><p><b>RESULTS</b>Three weeks after acute myocardial infarction, the rats with injection of CDCs in ECM showed the highest left ventricular ejection fraction (LVEF) and percentage of fraction shortening with the lowest percentage of positive heart fibrosis area; implantation of CDCs with ECM resulted in significantly higher rates of CDC differentiation into cardiac muscle cells, vascular endothelial cells and smooth muscle cell (P<0.05).</p><p><b>CONCLUSION</b>Heart-tissue derived ECM significantly promotes the differentiation of CDCs implanted in the infracted myocardium into cardiac muscle cells, vascular endothelial cells and smooth muscle cells to improve the cardiac structure and cardiac functions in rats.</p>

Antagonistic Effect of N-acetylcysteine on Hepatic Mitochondria Damage Induced by Cadmium in Rats / 环境与健康杂志

Objective To study the antagonistic effect of N-acetylcysteine(NAC)on the damage of hepatic mitochondria of rats induced by cadmium in vitro.Methods The mitochondria were prepared from the clean Wistar rats' whole liver by using differ ential centfifugation.The mitochondria were incubated in the assay buffer containing different concentration of CdCl_2 (10,100,1 000,10 000 ?mol/L)at 37 ℃ for 1 h.The effect of NAC(500 ?mol/L)was studied at a CdCl_2 concentration of 1 000 ?mol/L.The incubation buffer was collected and the level of GSH,cytochrome C and the activity of Mn-SOD were determined. Results Compared with the control group,the level of GSH and Mn-SOD in 100,1 000,10 000 ?mol/L CdCl_2 groups were significantly decreased,the content of cytochrome C in 1 000,10 000 ?mol/L CdCl_2 groups were significantly increased(P

[Experimental study on the effects of BSO, GSH, vitamin C and DMPS on the nephrotoxicity induced by mercury].

OBJECTIVE: To study the renal toxicity caused by mercury administrated once and to observe the effects of buthionine sulfoximine (BSO), gluthionein (GSH), vitamin C (VC), and sodium 2,3-dimercato-1-propanesulfonate (DMPS) pretreatment on the nephrotoxicity of mercury. METHODS: Sixty-four Wistar rats were divided randomly into eight groups, i. e., control group, low, middle and high dose mercury groups and BSO, GSH, VC, DMPS pretreatment groups. The low, middle, and high dose mercury group rats were subcutaneously (sc) injected with 0.75, 1.5, and 2.5 mg/kg HgCl2, respectively. The BSO pretreatment group rats were intraperitoneally (ip) injected with 0.5 mmol/kg BSO and four hours later sc administrated with 0.75mg/kg HgCl2. The GSH, VC and DMPS pretreatment group rats were ip injected with 3 mmol/kg GSH, 4mmol/kg VC, 200 micromol/kg DMPS, respectively, and two hours later sc administrated with 2.5 mg/kg HgCl2. The control group rats were sc injected with saline at corresponding time. The volume of injection was 5 ml/kg body weight. The 12 h urine samples were collected after 12 hours. After 48 hours, the blood samples were collected and then centrifuged to get the serum. The liver and renal cortex were also removed. Mercury contents in the liver, renal cortex, and urine samples were measured. Urinary NAG, ALP, LDH activities, urinary protein and BUN contents were also determined. RESULTS: Mercury concentrations in the liver, renal cortex, and urine samples increased with mercury dose increasing. Mercury contents in the renal cortex presented evident dose-effect relationship. Mercury concentrations in the liver of high-dose mercury group were higher significantly than that of low, middle-dose mercury group, and control group. The concentrations of urinary mercury in the middle and high dose mercury groups were higher significantly than that of control group. Compared with 0.75mg/kg HgCl2 alone group, BSO pretreatment increased mercury concentrations in the liver, but decreased the concentrations in the renal cortex and urine. Mercury concentrations in the liver of GSH, VC and DMPS pretreatment groups were lower than that of 2.5 mg/kg HgCl2 alone group. Urinary NAG, ALP, LDH activities, urinary protein and BUN contents increased with mercury dose increasing, and the values in the animals of 2.5 mg/kg HgCl2 mercury group were higher significantly than that of control, 0.75 and 1.5 mg/kg HgCl2 groups. Urinary NAG, ALP activities, urinary protein and BUN contents in the rats of BSO pretreatment were higher than that of 0.75 mg/kg HgCl2 alone group and control group. Compared with 2.5 mg/kg HgCl2 alone group, urinary NAG, ALP, LDH activities, urinary protein and BUN contents decreased significantly. CONCLUSION: Mercury concentrations in the liver, renal cortex, and urine of the rats increased with mercury dose increasing. BSO pretreatment could enhance the renal toxicity induced by mercury, however, GSH, VC, and DMPS pretreatment had antagonistic effects on nephrotoxicity of the mercury.