The selenium levels in plasma and liver of rats suffered from 3rd degree burn of 20% BSA on dorsum were significantly decreased, plasma VE dropped too, while the VE contents of RBC and liver were as high as those in control group. After giving 2.3?g selenium/100g bw as selenite to the burned rats, the VE contents of RBC and liver as well as plasma were then decreased as compared with control. The content of plasma total sulfhydryl group decreased more in selenium-supplemented group than in burned control.These results indicated that the requirement of VE probably increased after supplementation of selenium in burned rats.

Objective To observe the effect of arsenic trioxide on the apoptosis of synovium and IL-l, TNF-? in CIA rat. Methods Seventy-two rats were divided into normal control, model, and As2O3 treatment groups. The experimental models of collagen induced arthritis rats were used as the experimental moldels. The knees′ synovium, cartilage and bone tissue of the rat were taken out, then observed with light microscope and electron microscope and apoptosis were measured by TUNEL after the 15th day of treatment. Meanwhile the level of IL-1 and TNF-? were measured with ELISA kit. Results The pathological injury were improved and the apoptosis of synoviocytes were increased in the As2O3 treatment group, compared with the model group. IL-1 and TNF-? levels were decreased in the arsenic trioxide treatment groups, especially in the Ⅴ and Ⅵ groups (P

BACKGROUND: Angiotensin Ⅱ has been found to induce atrial electrical remodeling, which can be blocked or inhibited by allicin.OBJECTIVE: To study the effects of allicin on angiotensin Ⅱ-induced calcium channel current and intracellular free calcium concentration in human atrial myocytes.DESIGN: A randomized controlled study based on human atrial myocytes freshly isolated.SETTING: Cardiology department of a military medical university of Chinese PLA.METHODS: This study was carried out from June 2003 to June 2004 in the Laboratory of Cardiology Department, Xijing Hospital, the Fourth Military Medical University of Chinese PLA. Ten patients with congenital heart disease who underwent extracorporeal circulation surgery were included in the study. Among them, there were 6 males and 4 females with the average age of 15 ± 6 years. Tissue samples were taken from their right auricle and sent to the lab, where the atrial myocytes were freshly isolated. There were four co-administration of angiotensin Ⅱ (0. 1 μmol/L)and allicin(50 μmol/L).The conventional whole-cell configuration of the patch-clamp technique was used to detect membrane electric current of Ca2 + in L type. Confocal microscope was used with Fluo-3/AM as calcium indicator to detect changes of intracellular free calcium concentration immediately and 15 minutes after drug intervention, respectively.MAIN OUTCOME MEASURES: The peak density of electric current of Ca2 + in L type and alteration of fluoresence intensity of intracellular free calcium concentration.electric current of Ca2 + in L type in human atrial myocytes was significantly increased by angiotensin Ⅱ of 0. 1 μmol/L[( - 12. 77 ± 1. 61) vs ( -5.78affect electric current of Ca2+ in L type in human atrial myocytes group, the peak density of electric current of Ca2 + in L type was significantly lower than that in angiotensin Ⅱ group[ ( - 8.75 ± 0.97) pA/pF, P ＜ 0. 05 ].in angiotensin Ⅱ group was significantly higher than that in control and allicin groups[(2 610.1±112.6, (299.2±27.3)%; 653.9±42.5, 0;simultaneously with angiotensin Ⅱ, the alteration of intracellular fluoresence intensity was much lower than that in angiotensin Ⅱ group[ ( 1284.9 ± 85.2,(96.5±8.4)%;P ＜0.05].CONCLUSION: Allicin antagonizes angiotensin Ⅱ-induced increase in the peak density of electric current of Ca2+ in L type and intracellular calcium overload, which may relieve atrial electrical remodeling.

BACKGROUND: Vascular smooth muscle cell(VSMC) is one of the major cell components of vascular wall and its pathologic effects in atherosclerosis has been verified and recognized. How to inhibit VSMC proliferation and migration becomes one of the hotspots in the researches regarding the prevention of coronary heart disease(CHD).OBJECTIVE: To observe the impacts of diethyl-2, 6-diethyl-4-furny-1,4-dihydropyridine-3, 5-dicarboxylate(EFDP) on angiotensin Ⅱ (Ang Ⅱ)-induced VSMC proliferation.DESIGN: A randomized controlled study based on VSMC of rabbit' s thoracic aorta cultured in vitro.SETTING: Department of cardiology in a military medical university of Chinese PLA.MATERIALS: The study was conducted in the Laboratory of Cardiology of Xijing Hospital of the Fourth Military Medical University of Chinese PLA between August 2003 and June 2004. Five New Zealand rabbits were selected for the harvest of VSMC. Animal cells were randomly divided into control group, Ang Ⅱ group and Ang Ⅱ + EFDP group(EFDP group).METHODS: New Zealand rabbits were fed by high-fat food. Thoracic aorta was harvested for the separation and culture of VSMC after the injury in thoracic aorta intima by sacculus. The experiment introduced the cultured rabbit VSMC to observe the impacts of EFDP on VSMC DNA synthesis and its time effect during VSMC proliferation promoted by Ang Ⅱ by 3H-TdR method.MAIN OUTCOME MEASURES: 3H-TdR intensity of radio activity in cells of each group to display the DNA synthesis during VSMC proliferation process.RESULTS: Ang Ⅱ could promote the synthesis of rabbit VSMC DNA, which hit its peak at the 36th hour compared with that of control group(358. 00± 49.01 vs 272.42 ± 54.96, P ＜ 0. 01 ) . EFDP had significant inhibitive effects on Ang Ⅱ-induced VSMC proliferation, which also displayed a significant dose-dependent relationship, i.e. with the elevation of EFDP concentration, its inhibitive rate on VSMC proliferation also gradually increased. At the 36th hour, 78.40 μ mol/L of EFDP had more significant effect than that of 0. 08 μmol/L of EFDP(281.50 ± 15.28 vs 349. 25 ±32.10, P＜ 0. 05).CONCLUSION: EFDP can significantly inhibit Ang Ⅱ-induced rabbit VSMC proliferation with certain dose-effect dependency and time responses,which provides a theoretical gist for the primary rehabilitative prevention of atherosclerosis.