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Objective:To investigate the relationship between the levels of vascular endothelial growth factor (VEGF) and homocysteine (Hcy) in serum and diabetic retinopathy (DR) and diabetic nephropathy (DN).Methods:A total of 211 patients with type 2 diabetes mellitus (T2DM) who were treated in Beijing Tongren Hospital from February to July 2019 were selected as the case group, including 72 patients with T2DM (T2DM group), 45 patients with DR (DR group), 49 patients with DN (DN group), 45 patients with DR and DN (DR+DN group); 76 healthy people were selected as the control group. The levels of serum VEGF and Hcy were measured in all subjects. The course of diabetes, body mass index, waist to hip ratio, fasting blood glucose, glycosylated hemoglobin (HbA 1c), triglyceride(TG), total cholesterol(TC), low density lipoprotein-cholesterol(LDL-C), high density lipoprotein-cholesterol(HDL-C), urinary microalbumin/creatinine (ACR), urinary immunoglobulin G/creatinine (IGU/CR), urinary transferrin/creatinine (TRU/CR), urinary α1-microglobulin/creatinine (α1/CR), serum urea nitrogen, serum creatinine, hypersensitive C-reactive protein (hCRP) and erythrocyte sedimentation rate (ESR) were also observed in the case group. Results:The VEGF level of the T2DM group, DR group, DN group and DR+DN group was 90.02(61.24, 118.52), 124.38(81.50, 170.28), 133.19(78.84, 168.49), 124.08(79.82, 187.33)ng/ml respectively, which were significantly higher than that of the control group 50.31(21.10,67.74)ng/ml(all P<0.05); Compared with the T2DM group, the VEGF level in the DR group, DN group and DR+DN group increased significantly (all P<0.05). The level of Hcy in the DN group and DR+DN group [(12.58±3.66), (11.91±2.42) μmol/L, respectively] was higher than that in the control group [(10.44±2.09) μ mol/L], and the difference was statistically significant ( P<0.05). There was no statistically significant difference in VEGF and Hcy levels in different stages of DR ( U=264.00, t=-0.43, P>0.05). The Hcy level of DN patients in the group of massive proteinuria was higher than that in the group of microalbuminuria [(15.00±1.87) vs (11.79±3.76) μmol/L, t=-2.82, P=0.01].VEGF was positively correlated with ACR, TRU/CR and IGU/CR ( r=0.23, 0.19, 0.17, all P<0.05),while Hcy was positively correlated with serum urea nitrogen, serum creatinine, ACR, TRU/CR, IGU/CR and α 1/CR ( r=0.35, 0.44, 0.22, 0.19, 0.21, 0.29, all P<0.05). Conclusions:The level of VEGF in the serum of DR and DN patients increased, suggesting that VEGF may play a role in the development of DR and DN, but there was no significant difference in the level of VEGF in patients with different stages of DR and different urinary albumin excretion rate of DN.The level of serum Hcy in DN patients increased, and that was higher in massive proteinuria group, suggesting that serum Hcy may have clinical significance in the diagnosis and monitoring of DN.
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BACKGROUND:Current research data have shown that patients with epilepsy are often accompanied by complications such as cognitive impairment. Recent studies have demonstrated that melatonin has an inhibitory effect on epilepsy, but its underlying mechanism is unknown. OBJECTIVE: To investigate the effects of melatonin on the cognitive function and GluR2 expression in the hippocampus of rat models of epilepsy, and further study the mechanism of melatonin against epilepsy. METHODS: Rat models of chronic epilepsy were established by intraperitoneal injection of lithium chloride-pilocarpine, and intraperitonealy injected with sufficient amount of physiological saline and melatonin respectively. Control group was set for observation. RESULTS AND CONCLUSION:At 4 and 6 weeks after modeling, the GluR2 expression level in the hippocampus of rats in the epilepsy + melatonin group was significantly higher than that in the epilepsy group (P < 0.05); the GluR2 expression level in the synaptic membrane of hippocampal CA1 region of rats in the control and epilepsy + melatonin groups was significantly higher than that in the epilepsy group (P < 0.05). At 4 days after modeling, compared with epilepsy group and epilepsy + physiological saline group, the escape latency, operation time, active avoidance latency, passive avoidance latency of rats in the epilepsy + melatonin group were significantly decreased (P< 0.05), the correct rate and active avoidance number were significantly increased (P < 0.05). These results demonstrate that melatonin can improve the cognitive function of rat models of epilepsy by up-regulating the expression of GluR2 in the synaptic membrane of hippocampal CA1 region.