Objective:To explore the establishment of radiation-induced heart damage (RIDH) SD rat models caused by irradiation of 15Gy/3f and the changes in early detection indicators, and evaluate the effect of irradiation combined with recombinant human endostatin (Endostar).Methods:75 adult male SD rats were randomly divided into the blank control group (C group), Endostar group (E group), 25Gy irradiation group (MHD 25 group), 15Gy irradiation group (MHD 15 group) and 15Gy irradiation combined with Endostar group (MHD 15+ E group), respectively. Blood sample was taken to measure the CK, CK-MB, LDH and CRP at 24h, 48h and 15d after corresponding interventions. After cardiac echocardiography at 1, 3 and 6 months, 5 rats in each group were randomly sacrificed and myocardial tissues were collected for HE and Masson staining. Two-way ANOVA was employed for statistical analysis. Results:Compared with group C, myocardial fibrosis were observed in the MHD 15 group at 6 months ( P<0.05), which occurred later than that in the MHD 25 group. Ejection fraction (EF) and fractional shortening (FS) were significantly decreased after 3 months in each irradiation group (all P<0.05), whereas the degree of decrease was similar among all groups (all P>0.05). The expression levels of myocardial enzymes and inflammatory cytokines did not significantly differ among different groups (all P>0.05). Conclusions:In the early stage, exposure to 15Gy/3f irradiation can cause cardiac function damage in SD rat hearts, such as the reduction of EF and FS, and even lead to myocardial fibrosis in the late stage, which is delayed and less severe than high-dose irradiation. Irradiation combined with Endostar has no significant effect on radiation myocardial injury in rats.

Objective: Radiation-induced heart disease (RIHD) is a concern during radiation therapy (RT). In past decades, recombinant human endostatin (rE) has widely been used for the treatment of non-small cell lung cancer. However, the incidence of rE-associated cardiovascular toxicity is substantial and previously under-recognised. Materials and methods: Sprague-Dawley rats were placed into the following experimental groups: RT (25Gy), rE (6mg/kg), rE (12mg/kg), RT (25Gy)+ rE (6mg/kg), RT (25Gy)+ rE (12mg/kg) and blank control groups. Hematoxylin and eosin staining (HE), Masson trichrome staining, Western blotting (TGF-beta 1, Smad2/3, collagen-I) and real-time PCR (TGF-beta 1, Smad2, Smad3, collagen-I) were performed to. Result: During autopsy, interstitial fibrosis could reliably be detected and quantified following irradiation and irradiation combined with recombinant endostatin hearts after follow-up times of 3 and 6 months. Based on Western blotting results, TGF-beta 1 and collagen-I was increased 3 and 6 months after irradiation and irradiation combined with recombinant endostatin on cardiac tissue. Real-time PCR results indicate that TGF-beta 1, Smad2, Smad3 and collagen-I increased 3 and 6 months after irradiation and irradiation combined with recombinant endostatin on cardiac tissue. Conclusion: The studied parameters could be used in future experiments for testing protective agents for the prevention of radiation heart injury and the toxicity of recombinant human endostatin.

Objective:The experimental animal model was established to unravel the mechanism of radiation-induced myocardial fibrosis and validate the role of recombinant human endostatin in aggravating the process of radiation-induced myocardial fibrosis via the TGF-β 1, Smad 2 and Smad 3 signaling pathways. Methods:Sixty male adult Sprague-Dawley rats were randomly divided into the following groups: radiotherapy (RT)25 Gy, recombinant human endostatin (RE) 6 mg/kg, RE 12 mg/kg, RT 25 Gy+ RE 6 mg/kg, RT 25 Gy+ RE 12 mg/kg and blank control groups. Five rats were sacrificed in each group at 1 and 3 months after interventions. The myocardial tissues were collected. The pathological changes were observed by Hematoxylin and eosin staining. The degree of fibrosis was assessed by Masson trichrome staining. The expression levels of TGF-β 1, Smad 2, Smad 3 and Collagen-I mRNA and protein were quantitatively measured by real-time PCR and Western blotting. Results:At 3 months after intervention, Masson trichrome staining revealed that the collagen deposition in the RT 25Gy and RT 25Gy+ RE (6 and 12 mg/kg) groups was more significant than that in the control group. In addition, The expression levels of TGF-β 1, Smad 2, Smad 3 and Collagen-I mRNA and protein in these groups were significantly up-regulated compared with those in the control group. Conclusions:Radiation with a total physical dose of 25 Gy can induce myocardial fibrosis in the SD rat models. TGF-β 1 and Smad 2 signaling pathways are the common signaling pathways of myocardial fibrosis induced by radiation combined with recombinant human endostatin.

Objective To observe the concentrations of NO , MAD and SOD , and the expression of eNOS in the prefrontal cortex of rats with chronic unpredictable mild stress , thus to detect the effect and mechanism of anti -depression effect of metoprolol.Methods Forty SD rats were randomly divided into 4 groups, control group, model group, model plus metoprolol group , and control plus metoprolol group .The rats were exposed to the chronic unpredictable mild stress ( CUMS) and isolation to create a depression model .Open field test and sucrose water consumption test were performed to observe the behavior of animals after intragstric administration with metoprolol ( in control plus metoprolol and model plus metoprolol groups ) or distilled water ( in control and model groups ) for 22 days.The expression of eNOS mRNA was measured with RT-PCR, as the expression of eNOS and eNOS -ser1179 protein was detected by Western blot .The con-centrations of NO , SOD and MDA were assessed by ELISA .Results Compared with the model group , the model plus metoprolol group were significantly lower in the concentrations of NO (6.12 ±1.05 μmol/mg) and MDA (8.21 ±1.25μmol/mg);and higher in concentration of SOD (55.59 ±11.07 U/mg).Compared with the model group, there was sig-nificantly higher expression in eNOS protein , eNOS mRNA and eNOS-ser1179 protein in model plus metoprolol ( P<0.05).Conclusion The metoprolol have positive effects in depression rats , which could be related with the decrease of the oxidative stress in the brain .

Obiective To investigate the effects of antidepressant therapy on whole regulating function of serotonin and tryptophan hydroxylase 2 system in ovariectomized(OVX) rats with depressive disorder.Methods seventy-two female Sprague-Dawley rats were used as subjects.The rats were randomly divided in-to 8 groups as following:Sham operation group (Sn),depression group (Dn),the OVX group (On),OVX with depression group (ODn),OVX with depression + sertraline group (ODs),OVX with depression + citalopram group(ODx),OVX with depression+ venlafaxine group(ODw),OVX with depression+ reboxetine group(0Dr).Rats in group OVX and group OVX with depression were ovariectomized.Rats in group with depression were exposed to the chronic unpredictable mild stress (CUMS).Open-field test and sugar consumption experiment were tested on all rats before the experiment and the 28th day of experiment.The expression of TPH2 mRNA was measured with RT-PCR,and the expression of TPH2 protein was detected by Western blot.The concentration of 5-HT was detected by ELISA.Results (1) After exposure of CUMS,the scores of motion and percentage of sugar consumption experiment in Dn group were decreased contrast to the Sn group (P＜0.05),and the scores in ODn group were decreased compared with the on group(P＜0.05).(2)The protein and gene expression of THP2 in On and Dn group were decreased contrast to the Sn group (P＜0.05).The protein and gene expression of THP2 in ODn were decreased compared with the on group (P＜0.05).The protein and gene expression of THP2 in ODs (protein (0.68±0.07);gene (0.87±0.09)),ODx (protein (0.71 ±0.05);gene (0.84±0.17)),ODw(protein (0.69±0.04);gene (0.88±0.16)) and ODr(protein (0.53±0.07);gene (0.70±0.15)) were increased compared with the ODn(protein (0.31±0.09);gene (0.56±O.16)) group (P＜0.05).(3)The concentration of 5-HT of hippocampus and serum in Dn and On group were decreased contrast to the Sn group (P＜0.05).The concentration of 5-HT of hippocampus and serum in ODs,ODx,ODw and ODr group was increased compared with the ODn group (P＜0.05).Conclusion The antidepressants can up-regulate the expression of THP2 and the concentration of 5-HT in the OVX rats with depressive disorder.Sertralin is stronger however Reboxetine Mesylate is the poorest.