Objective To observe the effect of celecoxib on the expression vascular endothelial growth factors (VEGF) in diabetic rats. Methods Thirty-six wistar rats were used to establish the diabetic models by intraperitoneal injection with streptozotocin. The diabetic rats were divided into 2 groups: diabetic group (n=18) and celecoxib group (n=18). Celecoxib (50 mg/kg) was administered orally to the rats in celecoxib group and the physiological saline with the same volume was given orally to the rats in diabetic group. Eighteen else rats were in normal control group. All of the rats were executed 3 months later. The expression of VEGF protein was detected by immunohistochemistry method. Reverse transcription-polymerase chain reaction（RT-PCR） analysis was used to examine the expression of retinal VEGF mRNA and cyclooxygenase-2 mRNA. Results Lower positive expression of VEGF mRNA and cyclooxygenase-2 mRNA, weakly positive action of immunohistochemistry of VEGF, and lower expression of VEGF protein were detected in normal control group; in the diabetic group, the expression of VEGF mRNA and cyclooxygenase-2 mRNA increased obviously comparing with which in the control group (Plt;0.05), and the bly positive action of immunohistochemistry of VEGF and increased expression of VEGF protein were detected (Plt;0.01); in celecoxib group, the expression of VEGF mRNA was lower than that in the diabetic group (Plt;0.05), the expression of cyclooxygenase-2 mRNA didnprime;t decrease much (Pgt;0.05), the positive action of immunohistochemistry of VEGF decreased, and the expression of VEGF protein decreased (Plt;0.01). Conclusion By inhibiting the activation of cyclooxygenase-2, celecoxib can inhibit the expression of retinal VEGF mRNA and protein in diabetic rats induced by streptozotocin. (Chin J Ocul Fundus Dis,2007,23:265-268)
Objective To observe the serum betatrophin levels in patients with type 2 diabetes mellitus (T2DM) and to explore the role of betatrophin in the pathogenesis of diabetic retinopathy (DR). Methods A total of 59 patients with T2DM (DM group) and 14 healthy controls (NC group) were enrolled in the study. Vision, slit lamp microscope, indirect ophthalmoscope, fluorescein fundus angiography were performed on all the subjects. According to the results of the examination combined with the international DR clinical staging criteria, the patients were divided into no DR (Non-DR) group, non-proliferative DR (NPDR) group, and proliferative DR (PDR) group, with 30, 20 and 9 patients in each, respectively. The fasting blood glucose (FPG), insulin (FIN), C-peptide, glycated hemoglobin (HbA1c), total cholesterol (TC), triglyceride (TG), high-density lipoprotein (HDL-C), low-density lipid Protein (LDL-C) levels were detected. The level of betatrophin in serum was determined by enzyme-linked immunosorbent assay. The correlation between betatrophin and other indicators was analyzed by Spearman correlation. The influencing factors of PDR were analyzed by logistic regression. Results Compared with subjects in the NC group, the level of FPG (F=-4.316, P＜0.001), FIN (F=2.142, P=0.001), HbA1c (F=-5.726, P＜0.001), TC (t=3.609, P=0.010), LDL-C (t=0.000, P=0.003), and betatrophin (F=-2.263, P=0.024) were significantly increased and HDL-C level (F=-3.924, P＜0.001) was decreases in the DM group. The difference of TG level between two groups was not statistically significant (F= -1.422, P=0.155). Compared with the Non-DR group and the NPDR group, the serum C-peptide (F=7.818, P=0.020) and betatrophin levels (F=12.141, P=0.002) were significantly increased in the PDR group. Spearman correlation analysis showed that the levels of betatrophin in the DM group was positively correlated to TC (r=0.304, P=0.019). The serum levels of betatrophin was positively correlated to body mass index in the Non-DR group (r=0.513, P=0.004). Furthermore, in the PDR group, a significant positive correlation was observed between the serum betatrophin levels and diastolic blood pressure (r=0.685, P=0.042). Logistic regression analysis showed that the duration of diabetes, serum C-peptide and betatrophin levels were risk factors for PDR. After controlling for the duration and serum C-peptide, the PDR risk for betatrophin levels great than or equal to 1.0 ng/ml was 12 times as much as betatrophin levels less than 1.0 ng/ml in T2DM patients. Conclusions The serum betatrophin content of patients with T2DM is abnormal. Betatrophin may be involved in the occurrence and development of PDR.
ObjectiveTo investigate the role of apelin, glycosylated hemoglobin (HbA1c), cholesterol (TC), triglyceride (TG), High density lipoprotein cholesterol (HDLC), low density lipoprotein cholesterol (LDLC) in the development and progress of diabetic retinopathy (DR). MethodsThe serum concentration of apelin, HbA1c, TC, TG, HDLC and LDLC were measured in 30 normal control subjects and 90 patients with type 2 diabetic mellitus, including 30 cases without DR (NDR), 30 with non-proliferative DR (NPDR), 30 with proliferative DR (PDR). These data were analyzed by SPSS for windows 13.0. ResultsThe serum concentration of apelin, HbA1c, TC, HDLC, LDLC were significantly higher in NDR, NPDR, PDR group than those in control group (F=403.06, 5.45, 4.27, 201.56, 4.90;P < 0.05). The serum concentration of TG has no significantly difference (F=2.19, P > 0.05). The serum concentration of apelin, HbA1c, TC, LDLC were significantly higher in NDR, NPDR, PDR group than those in control group (t=0.30, 0.58, 0.79;P < 0.05), the serum concentration of HDLC were significantly lower than those in control group(t=0.79, P < 0.01). There were significantly positive correlation between the progression of DR and the serum concentration of apelin, HbA1c, TC, LDLC(r=0.962, 0.562, 0.935;P < 0.05). There were significantly negative correlation between the progression of DR and the serum concentration of HDLC(r=-0.753, P < 0.01). There were correlation between apelin and HbA1c, LDLC and HDLC(r=0.956, 0.741, -0.691;P < 0.01). ConclusionOur data demonstrated that serum apelin levels increased significantly in patients with diabetic retinopathy, and are closely related to blood sugar, blood lipid metabolic abnormalities.
Objective To observe the changes of expression of glutamine synthetase (GS) in early diabetic ratsprime; retina and investigate its possible mechanism. Methods Three groups of streptozotocininduced diabetic models of SpragueDawley (SD) rats with different diseased courses, ie, 1 month, 2 months, and 3 months, respectively, with 8 rats in each group, and 8 normal ones as control were examined. The expressions of GS, interleukin-1beta; (IL-1beta;) and c-Jun in retina in the 4 groups were detected by indirect immunofluorescence and western blotting techniques. Meanwhile, different doses of IL-1beta;（0,100,500,and 1000 ng/ml） were injected into the vitreous cavities of 32 normal rats (8 rats in each group), and 24 hours later, the expressions of GS and c-Jun in retina were detected by the same methods. Results The expression of GS in retina did not changed in control group or in 1 month and 2 months group, but decreased obviously in 3 months group comparing with which in the control group (Plt;0.01).The expressions of c-Jun and IL-1beta; in retina in control group were very low, but increased gradually in diabetic rats in 1-3 months group, which significantly differed from which in the control group (Plt;0.01). Vitreous injection with IL-1beta; (500 and 1000 ng/ml) down regulated the expressions of GS, and the expression of c-Jun increased in a dose-dependent way after injection with IL-1beta; at the concentration of 100 ng/ml. Conclusions In early diabetic ratsrsquo; retina, IL-1beta; may down regulate the expression of GS. The possible mechanism may be the activation of c-Jun by IL-1beta;. (Chin J Ocul Fundus Dis,2007,23:260-264)
Objective To investigate the relationship between diabetic retinopathy (DR) and coronary atherosclerosis (CAS) in type 2 diabetes patients and other risk factors of DR. Methods A total of 118 patients of type 2 diabetes with DR (DR group), 120 patients of type 2 diabetes without DR matched in age and sex (non-DR group), and 86 normal controls (control group) were enrolled in this study. The body mass index (BMI), blood pressure (BP), fasting blood-glucose (FPG), glycosylated haemoglobin (HbA1C), total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterin (LDL-C), creatinine, estimate glomerular filtration rate (eGFR) and urinary albumin excretion rate(UAER) in all the subjects were measured. Meanwhile, the incidence of CAS in the three groups was detected by 64slice multidetector computed tomography angiography (MDCTA). Assume concurrent DR as dependent variable, clinical indicators and laboratory parameters as independent variable, the risk factors were determined by Logistic regression analysis. In addition, CAS as dependent variable, DR as fixed factor, analysis of covariance was used to investigate the relationship between CAS and DR. Results The incidence of CAS in DR group was higher than that in nonDR group and control group, the differences were statistically significant (chi;2=26.9,35.5;P＜0.05). The results of Logistic regression analysis showed that systolic BP, BMI, CAS, myocardial infarction and UAER were key risk factors for DR ［odds ratio (OR)=1.02, 0.89, 4.50, 3.89, 1.34;P＜0.05］. There was a negative relationship between BMI and DR. The results of analysis of covariance showed that there was significant correlation between CAS and DR (OR=5.31, 95% confidence interval=2.62-10.60; P＜0.05). Conclusion CAS is independently associated with DR in type 2 diabetes patients. In addition, the other risk factors for DR include systolic BP, BMI, myocardial infarction and UAER.