Therapeutic Effect of Recombinant Human Stem Cell Factor on Rhesus Monkeys with Severe Acute Radiation Sickness / 中国实验血液学杂志

<p><b>OBJECTIVE</b>To study the therapeutic effect of rhSCF early administration on rhesus monkeys with severe acute radiation sickness(ARS).</p><p><b>METHODS</b>Twelve adult monkeys totally exposed to 7.0 GyCo were divided into radiation control and SCF groups, and monkeys in SCF group were subcutaneously injected recombinant human SCF(rhSCF) 200 µg/kg at half an hour and 24 hour after irradiation, while the radiation control monkeys were injected physiological saline. Survival was monitored and hematopoiesis was evaluated at 40 days following early treatment.</p><p><b>RESULTS</b>6 animals treated with rhSCF all survived, while 2 in irradiated controls survived on 40 day after radiation. rhSCF treatment promoted hematopoiesis recovery significantly, increased the nadir of white blood cells, neutrophils and platelets, and simplified supportive care in ARS rhesus monkeys.</p><p><b>CONCLUSION</b>RhSCF injection soon after TBI taken shows an significant therapeutic efficiency on rhesus monkeys with severe acute radiation sickness.</p>

New drugs for treatment of severe acute radiation sickness: Research advances / 国际药学研究杂志

Through efforts of several generations over the past half century, great advances have been achieved in the development of radiation countermeasures for the acute radiation sickness (ARS). Convergent studies have disclosed numerous radioprotectants with significant radioprotective efficacy which include granulocyte colony stimulating factor (G-CSF), granulocyte macrophage colony stimulating factor (GM-CSF), thrombopoietin (TPO), interleukin-12, derivatives of the bacterial flagellin, androst-5-ene-3β, 17β-diol (AED), beclomethasone 17, 21-dipropionate (BDP), vitamin E (and its)derivatives, and genistein. particularly, the two growth factors G-CSF and TPO show greater radioprotective effects. In this paper, we summarize the radioprotective effects of compounds or biological agents on severe ARS (SARS), which have been evaluated in large animal models or assembled into a nuclear accident emergency treatment medicine box, and review their research advances in recent years.

Effect of VEGF, P53 and telomerase on angiogenesis of gastric carcinoma tissue

OBJECTIVE@#To investigate the effect of vascular endothelial growth factor (VEGF), P53 and telomerase on angiogenesis in gastric carcinoma tissue.@*METHODS@#A total of 95 surgical resection samples of gastric cancer tissue after pathological diagnosis are collected to observe the VEGF, P53 and telomerase expression using immunohistochemical methods. Relationship between their expression and its influence on angiogenesis in gastric carcinoma tissue were analyzed.@*RESULTS@#Microvascular density (MVD) and the expression of VEGF, P53 and telomerase were positively correlated. Expression of VEGF and P53 protein were related to tumor type and lymph metastasis, and also a correlation was observed between P53 and VEGF. The telomerase expression had no correlation with VEGF, and P53.@*CONCLUSIONS@#VEGF angiogenesis has a angiogenesis promoting effect on gastric cancer tissue development and plays an important role in tumor generation and metastasis. Mutant P53 promotes the tumor angiogenesis generation by adjusting VEGF. Telomerase has a certain role in promoting activity of angiogenesis through different way rather than P53.

Effects of angiotensin converting enzyme inhibitor, angiotensin II type I receptor blocker and their combination on postinfarcted ventricular remodeling in rats / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Transforming growth factor (TGF) beta(1)-Smads signal plays an important role in cardiac remodeling following myocardial infarction (MI). In addition, both angiotensin converting enzyme inhibitor (ACEI) and angiotensin II type I receptor blocker (ARB) can effectively prevent left ventricular remodeling. The current study focused on whether the combination of ACEI and ARB is more beneficial for preventing ventricular remodeling and whether Smad proteins mediate this beneficial effect.</p><p><b>METHODS</b>MI was induced by ligating the left anterior descending coronary artery in rats. Twenty-four hours after ligation, the survived rats were randomly divided into five groups and treated for 8 weeks: placebo group, ACEI group (benazepril 10 mg.kg(-1).d(-1)), ARB group (irbesartan 50 mg.kg(-1).d(-1)), ACEI + ARB group (benazepril 10 mg.kg(-1).d(-1) + irbesartan 50 mg.kg(-1).d(-1)) and control group (sham-operated rats). After 8 weeks, we examined the following indexes: the ratio of ventricular weight to body weight (VW/BW), left ventricular end diastolic dimension (LVDd), ejection fraction (EF), fractional shortening (FS), ratio of E-wave to A-wave velocity, collagen of noninfarcted zone, the mRNA expression of TGFbeta(1), Smad 2, and Smad 3 by RT-PCR in noninfarcted zone, the protein expression of Smad 2 and Smad 3 in noninfarcted zone by Western blot.</p><p><b>RESULTS</b>VW/BW significantly increased in the placebo groups compared with that in the control group (P < 0.01). This increase was limited in ACEI, ARB, and combined groups (P < 0.01 compared with placebo group). There was no significant difference among the three actively treated groups. Collagen was increased in placebo group (5.68 +/- 0.5)% compared with that in control group (P < 0.01). ACEI, ARB and combined treatment attenuated this increase of collagen [(4.3 +/- 0.5)%, (3.5 +/- 0.5)%, (3.2 +/- 0.4)%] in comparison with that in placebo group (P < 0.01 respectively). Combined treatment showed more significant effect on collagen deposition. EF and FS significantly decreased, LVDd and E/A significantly increased in placebo group compared with that in control group (P < 0.01 respectively). ACEI, ARB and combined treatment ameliorated these indexes (P < 0.01 compared with placebo group). The mRNA expression of TGFbeta(1), Smad 2, and Smad 3 (0.700 +/- 0.045, 0.959 +/- 0.037 and 0.850 +/- 0.051) increased in placebo group compared with that in control group (P < 0.01). ACEI, ARB and combined treatment normalized the increase (P < 0.01). Furthermore, ARB and combined treatment proved to be more effective in decreasing TGF beta(1) and Smad mRNA expression than ACEI treatment (P < 0.01). The expression of Smad 2 and Smad 3 protein increased in placebo group compared with that in control group (P < 0.01). ACEI, ARB and combined treatment normalized the increase (P < 0.01). Furthermore, ARB and combined treatment proved to be more effective than ACEI alone (P < 0.01).</p><p><b>CONCLUSIONS</b>TGFbeta(1)-Smads signal activation is correlated with ventricular remodeling following MI. ACEI and ARB treatment prevents ventricular remodeling by inhibiting expression of Smad 2 and Smad 3. ARB and combined treatment are more effective than ACEI alone.</p>

Relationship between expression of Smad and ventricular remodeling after myocardial infarction in rats / 中华心血管病杂志

<p><b>OBJECTIVE</b>To investigate the relationship between expression of Smad3, Smad7 and ventricular remodeling in rats after myocardial infarction.</p><p><b>METHODS</b>Myocardial infarction was induced by left anterior descending coronary artery ligation in rats (n = 11) and sham-operated rats were used as control (n = 10). The rats were sacrificed 8 weeks later. Heart weight/body weight (HW/BW), mean blood pressure, left ventricular end diastolic pressure (LVEDP), collagen content in the un-infarcted area were examined. The mRNA levels of transforming growth factor (TGF)beta(1), Smad 3, Smad7 were determined by RT-PCR.</p><p><b>RESULT</b>Compared with controls, the level of HW/BW, LVEDP and collagen content were significant increased. The mRNA expression of TGFbeta(1) and Smad3 was significantly increased in areas of myocardial infarction, border of the infarction, interventricular septum and right ventricle. The expression of Smad7 mRNA in these areas was decreased.</p><p><b>CONCLUSION</b>These results indicated that TGFbeta(1)-Smads signaling was correlated to the ventricular remodeling after myocardial infarction. Smad3 might promote the process while Smad7 inhibit the process.</p>