Objective To observe and preliminarily explore the effects of Deferasirox (DFX) on lipid peroxidation and ferroptosis in human retinal endothelial cells (HREC). MethodsA cell experimental study. Divided the in vitro cultured HREC into normal glucose (NG) group, high glucose (HG) group, NG+DFX group, HG+DFX group, NG+DFX+ferric ammonium citrate (FAC) group, and HG+DFX+FAC group. Light microscope was used to observe the morphology of the cells; cell proliferation was detected by Cell Counting Kit-8 assay, and Calcein-AM staining was used to detect the unstable iron pool (LIP) content; enzyme-linked immunosorbent assay reader was used to detect the reactive oxygen species (ROS), malondialdehyde (MDA), glutathione (GSH), and oxidized glutathione (GSSG); Western blot was used to detect the relative protein expression of Glutathione Peroxidase 4 (GPX4) and Solute Carrier Family 7 Member 11 (SLC7A11). Two-tailed Student t test was used for comparison between the two groups; one-way ANOVA was used for comparison between multiple groups. ResultsCompared with the HG group and the HG+DFX+FAC group, the cell proliferation rate and the contents of GSH and the relative protein expression of GPX4, and SLC7A11 in the HG+DFX group were significantly increased, and the differences were statistically significant (F=150.70, 21.02, 26.09, 52.62; P＜0.001). The contents of LIP, ROS, MDA, and GSSG were significantly decreased, and the differences were statistically significant (F=807.20, 16.94, 31.62, 19.21; P＜0.001). ConclusionsHigh glucose significantly induces an increase in LIP, lipid peroxidation, and ferroptosis in HREC. Deferasirox inhibits lipid peroxidation and ferroptosis in HREC by downregulating LIP levels.
In order to understand the change of free radicals in the course of injury and regeneration of nerve, the sciatic nerve of Wistar rat was crushed to, prepare the model of nerve injury and measured the content of Malondialdehyde (MDA) and superoxide dismutase (SOD) of the nerve. Thirty rats were used in this study. The sciatic nerve on one side was crushed, the contralateral sciatic nerve was served as control. According to the time of assessment (2,4,6,11,21 days after crushing), the rats were divided into 5 groups. The MDA concentration of the controlwas 19.65±0.27 and that of the crushing groups at different time were 21.25±0.36, 21.98±0.35, 22.77±0.38, 23.73±0.13, 23.92±0.44, respectively (nmol/100mg pro, x±s), while the SOD concentration of the control was 119.18±0.58 and that of the crushing groups at different time were 144.85±1.70, 136.14±1.71, 130.58±0.57, 126.41±0.98, 122.36±0.79, respectively (ug/mg pro, x±s), In the experimental groups, all the MDA concentrations were markedly higher than that of the control Plt;0.01, t-test) and tended to increase with the time passing by. The SOD concentrations in the experimental groups were also higher than that of the control Plt;0.01, t-test) and tended to decrease with the time passing on. The study suggested that after crushing or ligation of the nerve, the free radicals would increase.
The contents of lipid peroxides(LPO)and vitamin E(V.E)and some functional index and histologic changes in the lungs from the the rabbit models of acute cholangitis of severe type(ACST)were measured dynamically.The results revealed that the V.E content decreased strikingly from 6 hours and the LPO level increased progressivelg from 12 hours in the lungs.Simultanuosly,the congestion and neutrophil infiltreation in the lung mesenchyme,and the endothelial cell damage and thrombosis in the lung blood capillaries had been observed.These suggest that acute lung injury induced by ACST is referable to the lipid peroxidation damage to the lung blood capillaries which is due to increased LPO and decreased antioxidants including V.E.
Objective To investigate the protective effect and mechanism of erythropoietin (EPO) on injury of human retinal pigment epithelial (hRPE) cell induced by hydrogen peroxide (H2O2). Methods Take subcultured hFRPE cells as study target. They were treated with 800 mu;mol/L of H2O2 for 3 hours to establish the cell injury model. The cultured cells were divided into three groups：control group, simply injury group and therapeutic group which again divided into 10 IU/ml, 20 IU/ml, 40 IU/ml,60 IU/ml subgroups according to the concentration of recombinant human erythropoietin(rhEPO). NF-kappa;B was measured by immunohistochemistry. The content of Malondialdehyde(MDA) which was the product of cellular lipid peroxidation and the releasing rate of lactate dehydrogenase（LDH）were estimated by chromatometry. Results H2O2 could elevate the level of MDA and the releasing rate of LDH, compared simply injury group with control group, the differences were significant.(tLDH＝29.746,tMDA＝20.426,Plt;0.05); Compared all of therapeutics groups with simply injury group, the releasing rate of MAD and LDH were decreased obviously, the differences were significant.（LDH t10IU＝5.770，t20IU＝12.774，t40IU＝19.818，t60IU＝24.833，Plt;0.05；MDA t10IU＝5.345，t20IU＝10.278，t40IU＝18.571，t60IU＝20.247，Plt;0.05）; The correlative analysis results of each therapeutic subgroup were: ①the concentration of rhEPO had negative correlation with the relation rate of LDH and the content of MDA(r=-0.976，P=0.024； r=-0.968，P=0.032) ; ②the concentration of rhEPO had positive correlation with the nuclear translative rate of NF-kappa;B(r=0.998，P=0.002); ③the nuclear translative rate of NF-kappa;B had negative correlation with the content of MDA(r=－0.954，P=0.046). Conclusion EPO can protect hFRPE cells from the injury of H2O2, the mechanism may be related to the activation of NF-kappa;B.
Objective To observe the protective effects of Na2SeO3 on the damage of retinal neuron induced by microwave. Methods Cultured fluids of retinal neuron were divided into 4 groups,including 1 group of control, according to the concentration of Na2SeO3 in cultured fluid and then exposed to 30 mW/cm2 microwave for 1 hour.The targets of lipid peroxidation and the concentration of selenium in cells were measured.Apoptosis detection was taken by TUNEL detection kit. Results The activity of SOD and GSH-Px rised,meanwhile the content of MDA and the amount of apoptosis cells decreased in 1times;107 mol/L group compared with the group without Na2SeO3.The other groups was superior in antioxdant capacity to 1times;107 mol/L group. Conclusion Na2SeO3 might be possessed of the effect of protecting the damage of retinal neuron induced by microwave. (Chin J Ocul Fundus Dis,2000,16:97-99)
ObjectiveTo investigate the correlation between epileptic seizure and lipid metabolism and nutritional index in patients with glioma.Methods380 patients with glioma admitted to Linyi People's Hospital Affiliated to Shandong University from January 2017 to December 2019 were selected. According to whether the first symptom is epilepsy or not, patients with glioma were divided into epileptic group (n=72) and control group (n=308). Combined with the basic demographic information, lipid metabolism and nutrition indicators in the medical records, the two groups of patients were analyzed retrospectively.ResultsThe mean age of epileptic group was (39.38±13.40) years, and the sex ratio was 1.88∶1. The mean age of the control group was (46.25±15.97) years, and the sex ratio was 1.20∶1. Chi-square test results showed that there was a statistical correlation between gender, alcohol consumption, history of hypertension and seizures (χ2=0.813, P<0.05). The results of multiple logistic regression analysis showed that there were differences in age, weight, LDL-C and potassium between the epilepsy group and the control group (P<0.05).ConclusionMale, age, weight, LDL-C and abnormal potassium concentration are risk factors for epilepsy in patients with brain tumor, and effective prevention and treatment measures should be taken in time for patients with abnormal lipid metabolism and nutritional indicators.
To study the lipid peroxidation injury and the protecting effect of vitamin E emulsion on liver function following acute cholangitis. During the operation and 24 hours after operation, vitamin E emulsion or placebo emulsion was infused via mesenteric vein in rats suffering acute cholangitis. The contents of malondialdehyde (MDA), superoxide dismutase (SOD) and adenosine triphosphate (ATP) in the liver tissue and serum were measured at 48hrs after operation. Results: As compared with the placebo emulsion group, MDA and mGOT contents in the liver tissue and serum decreased significantly, but SOD activity increased dramatically in the VE emulsion group. ATP content in the infected lobe was much higher than those in the placebo emulsion group. Conclusion: Intravenous infusion of large dose of vitamin E emulsion may reduce the lipid peroxidation reaction in acute cholangitis, and have protecting effect.
The etiology and pathogenesis of age-related macular degeneration (AMD) are unclear and difficult fot treatment. Some genetic research evidences in recent years have shown that the relationship between lipid metabolism-related gene polymorphism and AMD is statistically significant; it has also been found that blood lipid levels are related to AMD, and lipid-lowering drugs may have the effect of delaying the development of AMD in clinically. Abnormal lipid metabolism may play an important role in the occurrence and development of AMD. Clarifying the role of lipid metabolism in the occurrence and development of diseases will help reveal the pathogenesis of diseases and promote early diagnosis, monitoring and prevention of diseases, and provide an entry point for treatment.
Objective To explore the relationship between the structure and function of galectin-3， lipid metabolism disorders， and investigate the expression of galectin-3 in the occurrence and progress of lower limb arteriosclerosis block disease. Methods Related articles were reviewed. Results Galectin-3 participates in inflammatory reaction and lipid metabolism disorders， regulates the cell growth， differentiation， adhesion， apoptosis， and angiogenesis， and palys a role in the occurrence and progress of arteriosclerosis obliterans. Conclusion Galectin-3 is correlation with the occurrence， progress， and the prognosis of arteriosclerosis obliterans.
Objective To assess the efficacy and safety of lipid-modifying agents for metabolism syndrome.Methods We searched The Cochrane Library, MEDLINE, EMbase, the China Biological Medicine Database, VIP and CMAC to 2007. We also did some handsearching and additional searching. Randomized controlled trials of lipidmodifying therapy for metabolic syndrome were included. Two reviewers independently extracted data from the eligible studies and evaluated the quality of the included studies. Meta-analyses were performed for the results of homogeneous studies using The Cochrane Collaboration’s RevMan 4.2.9 software. Results A total of 11 studies involving 1 422 patients with metabolic syndrome were included. The results indicated that there was no significant difference in TG between rosuvastatin and atorvastatin. However, rosuvastatin was more effective than atorvastatin on HDL-c improvement. Atorvastatin decreased TG levels greater than simvastatin, but simvastatin was superior to atorvastatin in HDL-c improvement. Two trials comparing fenofibrate with placebo were heterogeneous for some outcomes: one found no significant difference in improvements to HOMA-index, but the other trial indicated that fenofibrate was superior to placebo in improving QUICKI. However, the two trials revealed that fenofibrate favorably affected TG [WMD= – 1.77, 95%CI (– 2.21, – 1.33)] and HDL-c [WMD= 6.62, 95%CI (2.07, 11.17)] compared with placebo. No significant differences among atorvastatin, fenofibrate, alone or in combination, were observed in the proportion of metabolic syndrome reduction [RR=0.99, 95%CI (0.84, 1.16); RR=1.03, 95%CI (0.88, 1.20); RR=1.01, 95%CI (0.87, 1.18)]. Atorvastatin plus fenofibrate was superior to atorvastatin alone in TG and HDL-c improvement. Simvastatin-fenofibrate combination produced greater effectiveness in improving of HDL-c and TG compared with simvastatin alone. The fenofibrateorlistat combination was similar to fenofibrate in reducing metabolic syndrome [RR=1.15, 95%CI (0.68, 1.95)] and TG improvement, but was more effective than fenofibrate in HOMA-index improvement. This review of the clinical trials shows that the majority of lipid-modulating drugs did not have favorable effects on FPG, BP, BMI and WC. Six studies reported side effects, showing that the side effects for lipid-regulating drugs were mild to moderate, and well tolerated.Conclusion Our results suggest that lipid-regulating drugs in general exhibit beneficial effects on TG and HDL-c, but not on blood glucose and central obesity. The therapeutic effects of lipid-regulating drugs on blood pressure and insulin sensitivity are uncertain and have no positive effects on FPG, BMI and WC. There is insufficient evidence in this review to recommend the use of lipid-modifying drugs for metabolic syndrome due to low methodological quality, small ssamplesize and limited number of the trials. More high-quality and large-scale randomized controlled trials are required.