1.Effects of granulocyte colony-stimulating factor plus stem cell factor on the cardiac function of rats with acute myocardial infarction
Jirui CAI ; Renguang LIU ; Dongliang LIU
Chinese Journal of Tissue Engineering Research 2007;11(7):1394-1396
BACKGROUND: Mobilizing bone stem cell is popular because of no hurling, no immunological rejection and no extraction,cultivation and amplification of stem cells.OBJECTIVE: To investigate the effects of granulocyte colony-stimulating factor (G-CSF) and stem cell factor (SCF) on treating acute myocardial infarction (AMI) of rats.DESIGN: Randomized controlled study.SETTING: Laboratory of Pharmacology, Jinzhou Medical College.MATERIALS: A total of 32 healthy SD rats weighing (200+20) g were provided by the Animal Center of Jinzhou Medical College. Recombination human G-CSF (rhG-CSF) was provided by Shuanglu medicine factory, Beijing, and recombination human SCF (rhSCF) was provided by Diao Company, Chengdu.METHODS: The experiment was carried out in Jinzhou Medical Pharmacological Laboratory from July to November 2005.① Totally, 32 male SD rats were injected with 5 mg/kg ISO in left abdomen. After 3 hours, the rats were randomly divided into 4 groups with 8 in each group. Treatment group: The rats were injected with 1 mg/kg rhG-CSF and 1 mg/kg rhSCF under epidermis for 5 days. The concentration was 10 mg/kg. G-CSF group: The rats were injected with 1 mg/kg rhG-CSF and 1 mg/kg saline for 5 days. The concentration was 10 mg/kg. SCF group: The rats were injected with 1 mg/kg rhSCF and 1 mg/kg saline for 5 days. The concentration was 10 mg/kg. Control group: 2 mg/kg saline was injected under epidermis. ② After 14 days and 28 days from injecting ISO, one subgroup was weighted from every group.The rats were narcotized with 200 g/L urethane. After the heart's exposed, a tube filled with heparin sodium was inserted to left ventricle. Then tracked record the left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), maximal rising and descent velocity of left ventricular pressure (±dp/dr) using Medlab-u/Sc and kept the heart rate (HR) records. Tracheal cannula was pushed out; heart was cut off immediately; auricula and right ventricle were cut off; tissue was weighed with microbalance; left ventricle mass/body mass was calculated; myocardial remodeling was evaluated. Tissues were cut into sections, and pathological form and infarction area were observed under optic microscope. Infarction area in each group was analyzed with cellular image analyzer.MAIN OUTCOME MEASURES: Left ventricular function, myocardial infarction area, heart rate, ventricular remodeling and pathology of the cardiac muscle.RESULTS: All 32 rats were involved in the final analysis without any loss. ① Comparison of the left ventricular function:At 14 days after modeling, LVSP, LVEDP and ±dp/dr were higher in treatment group than those in other 3 groups (P <0.05); 28 days later, those indexes in the 4 groups were higher than those in the 4 groups at 14 days after modeling,and there was significant difference (P < 0.05). Those indexes in G-CSF group were higher than those in SCF group and control group at the two time points (P < 0.05). ② Comparison of infarction area, HR and the ventricular remodeling: At 14 and 28 days after modeling, infarction area and left ventricle weight were smaller and lighter in treatment group than those in other 3 groups (P < 0.05); 28 days later, infarction area in the 4 groups was smaller than those in the 4 groups at 14 days after modeling (P < 0.05). Those indexes in G-CSF group were less than those in SCF group and control group at the two time points. ③ Pathology results: At 14 and 28 days after modeling, there was no significant infarction car in treatment group and G-CSF group, and new capillary vessel and infiltration of fibroblast were found in the two groups. The density of capillary vessel in G-CSF group was less than that in treatment group. There were infarction scars and much lymphocyte in SCF group and control group. The nucleus was small, the color was deep, and plasma was less. New granulation tissue was not significant.CONCLUSION: Combining G-CSF with SCF can protect the ischemic cardial muscle and improve the heart function in rats. The function of combining G-CSF and SCF is better than singlly using G-CSF or SCF.
2.Effects of ShenFu injection on endothelial function of rabbits with myocardial ischemia-reperfusion injury
Xupeng JIN ; Lianyi GUO ; Renguang LIU
Medical Journal of Chinese People's Liberation Army 2008;33(7):841-843
Objective To investigate the changes of endothelial function during myocardial ischemia and reperfusion (I/R) injury of rabbits, and the protection of ShenFu injection (SFI) for the injury, as well as the related mechanism. Methods Twenty one Japanese white rabbits were randomly divided into 3 groups (7 each): sham operated group (A), I/R group (B) and SFI-treated I/R group (C). The activity of serum endothelial nitric oxide synthase(eNOS), the concentrations of serum nitric oxide products (NOP) and plasma endothelin (ET) before ligation of coronary artery, 40min after ischemia and 40min after reperfusion were determined. The concentration of total superoxide dismutase (T-SOD) and malonyl-dialdehyde (MDA) in myocardial tissue were determined. Ultrastructure of myocardial cell was observed by electro microscope. Results 1) Serum eNOS and NOP decreased and plasma ET increased ingroup B than that ingroup A after 40min of ischemia (P<0.01), even more significant after 40min of reperfusion. NOP was correlated positively with ETafter 40min of ischemia (P<0. 05) and after 40min of reperfusion ( P<0. 01). In 40min after reperfusion, T-SOD was decreased and MDA was increased ingroup B than that in group A, significantly (P<0. 01). NOP were correlated positively with T-SOD, while were correlated negatively with MDA (P<0.05). ET was correlated positively with MDA, while was correlated negatively with T-SOD (P<0.05). Ultrastructure of myocardial cell changed abnormally. 2) SFI can increase eNOS and NOP after 40min ischemia and 40min reperfusion, and decrease ET after 40min reperfusion, significantly (P<0. 01). SFI can increase T-SOD and decrease MDA significantly (P<0. 01), the abnormality of myocardial cells can be relieved obviously. Conclusion SFI can improve the endothelial function in which free radicals are involved, and prevent myocardial tissue from I/R injury.
3.The study on examination methods of clinical electrocardiology in medical postgraduates training
Yingjie ZHANG ; Renguang LIU ; Hong XIAO
Chinese Journal of Medical Education Research 2003;0(03):-
How to improve the teaching quality is urgent and significant at present.Based on reforming the teaching methods,the authors have studied the new methods of medical postgraduate examination since 2005 including the assessments on practical skills,the level of mastering knowledge,self learning and innovating ability and the criterion of giving a mark,which have been applied for three years and achieved the aim and the effect in clinical electro-cardiology teaching.
4.Effects of salvia miltiorrhiza bone-setting capsule on fracture healing in a rat model of closed femoral fractures
Xiqiang WANG ; Renguang SUN ; Shirun SUN ; Jun SUN ; Yongmei WANG ; Taijian LIU ; Huijun DU ; Feng PAN
Chinese Journal of Tissue Engineering Research 2016;20(5):622-627
BACKGROUND:Salvia miltiorrhiza bone-setting capsule is a traditional Chinese medicine for the treatment of fractures due to activating blood circulation to dissipate blood stasis, reducing sweling and pain. OBJECTIVE: To observe the effects of Salvia miltiorrhiza bone-setting capsule on the fracture healing in a rat model of closed femoral fractures. METHODS: Rats were randomly divided into salvia miltiorrhiza bone-setting capsule group, physiological saline group and normal group. In the salvia miltiorrhiza bone-setting capsule group and physiological saline group, rat models of closed femoral fractures were prepared, and then given physiological saline and salvia miltiorrhiza bone-setting capsule 2 pils by intragastric administration. In the normal group, rats were housed normaly. At 7, 14 and 28 days after fractures, hematoxylin-eosin staining conditions, serum osteocalcin, the expression of colagen type I, and the expression of protein and mRNA calus transforming growth factor-beta 1 were observed in the salvia miltiorrhiza bone-setting capsule group and physiological saline group. RESULTS AND CONCLUSION: (1) Hematoxylin-eosin staining demonstrated that at 7 days after fractures, no significant difference was found in pathological changes of femoral fracture in salvia miltiorrhiza bone-setting capsule group and physiological saline group. At 14 and 28 days after fractures, pathological repair was more obvious in the salvia miltiorrhiza bone-setting capsule group than in the physiological saline group. (2) At 3 and 7 days after fractures, serum osteocalcin and the expression of type I colagen were significantly increased in the salvia miltiorrhiza bone-setting capsule group and physiological saline group (P < 0.05), and the expression trend was consistent in both groups. The expression was always higher in the salvia miltiorrhiza bone-setting capsule group than in the physiological saline group, and significant differences were found at 14 and 28 days after fractures (P < 0.01). (3) Transforming growth factor beta 1 expression reached a peak at 3 days after fractures, gradualy reduced, increased at 14 days (the second peak), and diminished at 28 days in the salvia miltiorrhiza bone-setting capsule group and physiological saline group. The expression trend of transforming growth factor beta 1 was consistent in the salvia miltiorrhiza bone-setting capsule group and physiological saline group. At 7, 14 and 28 days, the transforming growth factor beta 1 expression was higher in the salvia miltiorrhiza bone-setting capsule group than in the physiological saline group. (4) Results showed that salvia miltiorrhiza bone-setting capsule could promote fracture healing, and its mechanism was probably associated with serum osteocalcin, the expression of colagen type I and transforming growth factor-β1.