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Objective To study the effect and mechanisms of berberine (BBR) on the proliferation of papillary thyroid cancer K1 cells induced by high glucose.Methods K1 cells were cultured under 5.5 mmol/L or 25 mmol/L glucose condition with or without different concentration of BBR (0,10,40 and 80 μmol/L) for 24 hours.The proliferations of K1 cells in each condition were detected by MTT.Western blot was used to measure the expression of nuclear factor erythroid 2-related factor 2 (Nrt2),phosphoinositide 3-kinase (PI3K),protein kinase B (Akt) and phosphorylated-Akt (p-Akt).The distribution pattern of Nrf2 in K1 cells was determined using immunofluorescent staining.Results Compared with 5.5 mmol/L condition,the proliferation rate [(126.64 ± 5.41) ％ vs (87.31 ± 3.67) ％],expression levels of PI3K (0.425 ±0.019 vs 0.272 ±0.039),p-Akt/Akt (0.446 ±0.021 vs 0.168 ±0.035) and Nrf2 (0.597 ± 0.014 vs 0.308 ± 0.026),and Nrf2 distribution (93.0％ vs 23.1％) in nuclear of K 1 cells under 25 mmol/L condition were significantly elevated,respectively (all P ＜0.01).Addition of BBR in 25 mmol/L condition dose dependently (10,40,80 μmol/L) lowered the proliferation rate of K1 cells [(111.76 ± 4.10)％,(70.03 ±2.18)％,(32.41 ±3.76)％ vs (126.64 ±5.41)％,all P＜0.05],and suppressed the expression of PI3K,p-Akt/Akt,Nrf2,and Nrf2 nuclear distribution (P ＜ 0.05).Conclusions BBR dose dependently inhibited the proliferation of high glucose-induced K1 cells.This effect was associated with the suppression on of PI3K/Akt signaling activation,Nrf2 expression and its nuclear translocation.
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MicroRNAs (miRNAs) are a class of endogenous;non-coding small RNA molecules;which can degradate target mRNA;or negatively regulate the expression of the corresponding target genes in the post transcriptional level through inhibiting target gene translation;inducing degradation and so on.MiRNAs exert important parts in the process of metabolism;cell growth;and development.MicroRNA 222 (miR-222) is an important member of microRNAs;which plays an important role in cell proliferation;differentiation;apoptosis and the development of a variety of biological tissues.Recent studies found that miR-222 could mediate a variety of physiological and pathological processes;and significantly influence the development of cardiovascular disease.MiR-222 has an important role in inflammatory response and apoptosis.Here;we reviewed the relationship between miR-222 and cardiovascular disease.
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Objective To assess the association of subclinical thyroid dysfunction with fractures. Methods Medline, Embase, Pubmed, Cochrane Library, CBM, CNKI, Wan Fang, and VIP databases were systematically searched from January 1990 to August 2015 to identify prospective cohort studies which have studied the risk of fracture in patients with subclinical thyroid dysfunction. The relative risks ( RR) of cohort studies were pooled respectively, depending on the result of heterogeneity test among the individual studies search. The Stata (version 13. 0) software was used for meta-analysis. Results Nine prospective cohort studies including 292460 participants were identified as eligible for the meta-analysis. RR of subclinical hyperthyroidism for fracture was 1. 39(95%CI 1. 24-1. 55);for hip fracture, RR was 1. 24(95%CI 1. 10-1. 40);for nonspine fracture, RR was 1. 32 (95%CI 1. 09-1. 60). Different gender for subclinical hyperthyroid was associated with higher fracture rates:for females, RR was 1. 15(95%CI 1. 04-1. 27); for males, RR was 1. 31 (95% CI 1. 08-1. 59). The incidence of fracture in patients with subclinical hyperthyroidism was higher during the follow-up. For subclinical hypothyroidism, the RR was 1. 21(95% CI 1. 03-1. 42). Subgroup analysis indicated that there were significant differences between endogenous/exogenous subclinical hyperthyroidism and euthyroid, but no differences between endogenous/exogenous subclinical hypothyroidism and euthyroid were found. Conclusion Subclinical hyperthyroidism is associated with an increased risk of fracture in the population, especially hip fracture and nonspine fracture. During the course of subclinical hyperthyroidism, the incidences of fracture should be noticed both in females and males. However, there is no evidence which could prove a definite association between subclinical hypothyroidism and the risk of fracture.
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AIM: To study the protective effect of aerobic exercise on cardiac dysfunction in mice and its mechanism, and to provide theoretical and practical basis for the exercise therapy of diabetic cardiac dysfunction .METH-ODS:The mice were divided into normal control non-exercise (NNC) group, normal control exercise (ENC) group, dia-betic non-exercise (NDM) group and diabetic exercise (EDM) group.At the end of the experiment , the cardiac function was evaluated by echocardiography .The pathological changes of the myocardial tissues and the development of fibrosis were observed.The mRNA expression of ANP, and the protein levels of PI3K (p110α) and Akt were determined.RESULTS:The decrease in cardiac function of diabetic mice was observed , and the cardiac function recovered after exercise interven-tion (P<0.05).Under light microscope with HE and Masson staining , the myocardial structure in NDM group was in ex-treme disorder , cell arrangement was not neat , and the degree of fibrosis increased , but the myocardial damage was im-proved in ENC group .Compared with NNC group , the mRNA expression of ANP in the myocardium of diabetic mice was up-regulated (P<0.05).The protein levels of PI3K (p110α) and Akt were decreased (P<0.05), and the cascade was inactivated.Compared with NDM group , the mRNA expression of ANP was down-regulated and the protein levels of PI 3K (p110α) and Akt were up-regulated in EDM group (P<0.05).CONCLUSION:Diabetes results in myocardial damage in mice, and reduces cardiac function .Exercise intervention alleviates the heart dysfunction induced by high glucose via activating PI3K( p110α)/Akt signaling pathway to protect the structure and function of the myocardium .
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Objective To investigate the protective effects of aerobic exercise and miR-222 expression in myocardium of diabetic mice. Methods C57BL/ 6 mice were divided into 4 groups: normal non-exercise group (SC), normal exercise group(EC), non-exercise diabetic group(SD), and exercise diabetic group(ED). After the diabetic model was established successfully, EC and ED underwent a swimming training for 5 weeks. By the end of the experiment, light microscope was used to observe the pathological changes of heart, RT-PCR for myocardial miR-222 expression, and Western blot for phosphatase and tensin homolog deleted on chromosome ten ( PTEN ), phosphatidylinositol 3-kinase (PI3K), and protein kinase B (Akt) protein expressions in myocardial tissue. Results (1) Under the light microscope, the diabetic mice had a significant change in myocardial structure, with great disorder in the cell arrangement. After exercise intervention, the lesion was alleviated. (2) MiR-222 expression was increased in the myocardium of normal mice and DM mice after exercise (all P<0. 05); (3) Compared with SC group, PTEN expression was increased and PI3K/ Akt expressions were inhibited in myocardium of diabetic mice(all P <0. 05). After exercise intervention, the expression of PTEN reduced( P < 0. 05) and PI3K/ Akt pathway was reactivated in myocardium of diabetic mice (all P<0. 05). Conclusion Exercise intervention may protect the myocardium under high glucose via inducing miR-222 and activating PI3K/ Akt signaling pathway.
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Objective To investigate the effects of interlukin-22 (IL-22) on diabetic renal fibrosis and its possible mechanisms. Methods C57 BL/ 6 mice were randomized to normal control group ( NC group), diabetic nephropathy control group ( DN group), recombinant interlukin-22 ( rIL-22) group, and interlukin-22 antibody (Anti-IL-22) group. 8 weeks after successful establishment of diabetes model, mice were injected intraperitoneally with 200 ng/ g rIL-22, Anti-IL-22 or equal 0. 1% bovine serum albumin (BSA) twice a week for 4 weeks. After the intervention, blood glucose, kidney function and 24 h urine microalbumin creatinine ratio were measured. Renal pathological changes and collagen deposition were observed under the light microscope, and semiquantitative assessment of renal sclerosis and fibrosis were evaluated at the same time. The mRNA expression of transforming growth factor ( TGF)-β1 was determined by realtime PCR. The protein expressions of α-smooth muscle actin (α-SMA), E-cadherin, and fibronetin (FN) were examined by Western blotting. The protein expressions of collagenⅢ were examined by immunohistochemical analysis. Results After 4 weeks of intervention, the 24 h urine microalbumin creatinine ratio decreased significantly in the Anti-IL-22 group ( P<0. 05). Renal tubular epithelial cells vacuolar degeneration, protein cast formation, and glomerular mesangial expansion were observed under the light microscope. And the lesions were more severe in the rIL-22 group, whereas improved in the Anti-IL-22 group. Meanwhile, the collagen deposition was in accordance with the tubular injury score. Moreover, TGF-β1 gene expression increased significantly in the rIL-22 group (P<0. 01). α-SMA and E-cadherin, epithelial-mesenchymal transition (EMT) markers, increased or decreased significantly in the rIL-22 group respectively (P<0. 05). FN and collagen Ⅲ, extracellular matrix ( ECM ) proteins, increased significantly in the rIL-22 group as well ( P <0. 05). Conclusions IL-22 may induce renal tubular epithelial cells TGF-β1 high expression. As a consequence, this contributes to EMT occurance and ECM accumulation, eventually accelerating the progression of diabetic renal fibrosis.
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Objective To investigate the effects of interlukin-22 (IL-22) on diabetic renal fibrosis and its possible mechanisms. Methods C57 BL/ 6 mice were randomized to normal control group ( NC group), diabetic nephropathy control group ( DN group), recombinant interlukin-22 ( rIL-22) group, and interlukin-22 antibody (Anti-IL-22) group. 8 weeks after successful establishment of diabetes model, mice were injected intraperitoneally with 200 ng/ g rIL-22, Anti-IL-22 or equal 0. 1% bovine serum albumin (BSA) twice a week for 4 weeks. After the intervention, blood glucose, kidney function and 24 h urine microalbumin creatinine ratio were measured. Renal pathological changes and collagen deposition were observed under the light microscope, and semiquantitative assessment of renal sclerosis and fibrosis were evaluated at the same time. The mRNA expression of transforming growth factor ( TGF)-β1 was determined by realtime PCR. The protein expressions of α-smooth muscle actin (α-SMA), E-cadherin, and fibronetin (FN) were examined by Western blotting. The protein expressions of collagenⅢ were examined by immunohistochemical analysis. Results After 4 weeks of intervention, the 24 h urine microalbumin creatinine ratio decreased significantly in the Anti-IL-22 group ( P<0. 05). Renal tubular epithelial cells vacuolar degeneration, protein cast formation, and glomerular mesangial expansion were observed under the light microscope. And the lesions were more severe in the rIL-22 group, whereas improved in the Anti-IL-22 group. Meanwhile, the collagen deposition was in accordance with the tubular injury score. Moreover, TGF-β1 gene expression increased significantly in the rIL-22 group (P<0. 01). α-SMA and E-cadherin, epithelial-mesenchymal transition (EMT) markers, increased or decreased significantly in the rIL-22 group respectively (P<0. 05). FN and collagen Ⅲ, extracellular matrix ( ECM ) proteins, increased significantly in the rIL-22 group as well ( P <0. 05). Conclusions IL-22 may induce renal tubular epithelial cells TGF-β1 high expression. As a consequence, this contributes to EMT occurance and ECM accumulation, eventually accelerating the progression of diabetic renal fibrosis.
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Humanumbilicalveinendothelialcells(HUVECs)weretreatedwith3nmol/Lliraglutidefor10, 15, 30, 45, 60, 90, 120, 150, 180, 210, 240, and 270 minutes at the concentrations of 5. 5 or 30 mmol/L glucose. Western blot analysis was used to detected protein expression and phosphorylation of insulin receptor substrates-1 ( IRS-1 ) and endothelial nitric oxide synthase ( eNOS ) . The results showed that the baseline level of phosphorylated-eNOS/eNOS was lower in high glucose group than that in normal group(0. 239 ± 0. 016 vs 0. 400 ± 0. 02,P<0. 05). Liraglutide time-dependently increased phosphorylated-eNOS/eNOS and phosphorylated-IRS-1/IRS-1 levels at 5. 5 or 30 mmol/L glucose.
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Objective To investigate the role of AT1 receptor autoantibody (AT1-AA) in the inhibitory action of irbesartan on endoplasmic reticulum stress (ERS)-related apoptotic signals in rat kidney with diabetic nephropathy (DN).Methods DN model rats were induced by high-sugar and high-fat diet plus intraperitoneal injection of streptozotocin,and the serum level of AT1-AA was detected by ELISA.These DN rats with positive or negative AT1-AA were divided into DN group and irbesartan treated group.After 4 weeks of irbesartan treatment,TUNEL staining was used to detect renal cell apoptosis.The protein and mRNA expressions of ERS chaperone protein glucose-regulated protein 78 (GRP78) and ERS-associated apoptosis proteins were determined by Western blot and RT-PCR.Results Compared with NC group,the apoptosis rate of renal cells in DN group was obviously increased,along with the increased expressions of GRP78,C/EBP homology protein (CHOP),phosphorylated c-Jun N-terminal kinase (JNK),and Caspase12 protein and mRNA (all P＜0.01).The cell apoptosis and protein and mRNA levels of these genes were significantly decreased after irbesartan treatment (all P＜ 0.01),especially in AT1-AA positive DN rats(all P＜0.05).The renal cell apoptosis rate,and protein and mRNA levels of these four genes in AT1-AA positive DN group were much greater than those in AT1-AA negative DN group (all P＜0.05).Conclusions AT1-AA may be involved in ERS-related cell apoptosis in the kidney of DN rats,and play a role in irbesartan-improved renal function via inhibiting ERS-associated CHOP-JNK-Caspase12 apoptotic signals and renal cell apoptosis.
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[Summary] Berberine is akind of alkaloids extracted from Chinese herb medicine in cludingphellod endron ,coptis and radix berberidis .In recent years ,the pharmacological effects of berberinewas investigated extensively including anti-infection ,anti-arrhythmia ,protection of ischemic myocardium ,anti-hypertension , anti-tumor ,anti-HIV .And there are increasing reports about its hypoglycemic effect ,but its mechanism remains unclear .Here we summarize the possible mechanism of hypoglycemic effect and clinical efficacy of berberine .
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Objective To study the relationship of angiotensin Ⅱ type 1 receptor (AT1R) autoantibody (AT1-AA) and renal cell apoptosis induced by caspase-12 in diabetic nephropathy (DN)rats.Methods High-sucrose and high-fat diet and intraperitoneal injection of streptozotocin (35 mg/kg) were utilized to establish DN rat model.Serum AT1-AA was detected by enzyme-linked immunosorbent assay (ELISA) and renal cell apoptosis was detected by TUNEL staining.Furthermore,the mRNA levels of the endoplasmic reticulum stress (ERS) chaperone protein glucose regulated protein 78 (GRP78) and ERS-associated apoptosis protein caspase-12 were measured by real-time quantitative PCR.Additionally,the levels of GRP78 and caspase-12 protein were measured by Western blotting.Results The renal cell apoptosis rate in DN group was increased significantly (P ＜ 0.01),and the renal cells apoptosis rate in AT1-AA positive DN group was higher than that in AT1-AA negative DN group [(20.05±1.71)％ vs (13.24±4.93)％,P ＜ 0.01].The mRNA expressions of GRP78 and caspase-12 in DN group,in comparison to NC group,were increased significantly (P ＜ 0.01),as well as the proteins (P ＜ 0.01).And the expression of these mRNA and proteins had significant increment in AT1-AA positive DN rats when compared with AT1-AA negative DN rats (P ＜ 0.05).Conclusions AT1-AA can induce ERS in the renal tissue of DN rats,and promote renal cell apoptosis likely via the modulation of caspase-12 signaling pathway.
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Objective To explore the relationship of autoantibodies against G protein coupled angiotensin Ⅱ-1 receptor (AT1 R),α1-adrenergic and β1-adrenergic receptors (α1 R and β1 R) with thyrotoxicosis heart disease (THD).Methods The epitopes of the second extracellular loop ofAT1 R (165-191),α1 R (192-218),and β1 R(197-222) were synthesized for screening autoantibodies from 277 participants by ELISA.237 patients with thyrotoxicosis were subdivided into thyrotoxicosis treatment group (n =148) and thyrotoxicosis recovery group (n =89),or into THD group (n =46) and simple hyperthyroidism group (n =191).40 healthy subjects were served as control group.Results (1) The positive rates of autoantibodies against AT1 R,α1 R and β1 R in thyrotoxicosis patients were higher than those in the control subjects (31.6％ vs 12.5％,27.8％ vs 10.0％,and 23.6％ vs 7.5％,all P＜0.05).The positive rates of the three autoantibodies in the patients with Graves' disease were higher compared with thyrotoxicosis caused by other reasons (36.3％ vs 19.7％,32.2％ vs 16.7％,and 28.1％ vs 12.1％,all P＜0.05).(2) In thyrotoxicosis treatment group,the positive rates of autoantibodies against AT1 R and α1 R were higher than those in the hyperthyroidism recovery group (40.5％ vs 16.9％ and 33.1％ vs 19.1％,both P＜0.05).(3) The incidence of autoantibodies against AT1 R and α1 R in THD were significantly higher compared with simple hyperthyroidism (52.2％ vs 26.7％ and 43.5％ vs 24.1％,both P＜0.05).Conclusions Autoantibodies against AT1 R,α1 R,and β1 R may play important roles in the pathogenesis of hyperthyroidism,which may be involved in the progression of THD.
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Objective To observe the effects of doxazosin on the expression of type Ⅰ and type Ⅲ collagen fiber in autoantibodies against α1-adrenergic receptors (α1-AA) positive diabetic rats,and to investigate the protective mechanism of doxazosin on cardiomyopathy of diabetic rats.Methods After establishment of diabetes model with streptozocin,diabetic rats were randomly divided into diabetic group (group A,n =10),doxazosin treated group (group B,n =10),α1-AA mediated group (group C,n =8),α1-AA plus doxazosin treated group (group D,n =8).Group C and group D were injected α1-AA (100 μg/100 g) by caudal vein at 0,4,8,12,and 16 weeks.Doxazosin (0.36 mg · kg-1 · d-1) was administered by lavage for 16 weeks in group B and group D,and other groups were given the same volume of saline every day.Expressions of type Ⅰ and type Ⅲ collagen fibers in myocardium of left ventricle were detected by immunohistochemical staining.Pathological changes in the myocardium were observed by both light and electron microscopes.Changes in collagen fiber in myocardium were detected by Van Gieson staining.Results Among various groups,there was no significant difference in blood glucose levels (P ＞ 0.05).After the intervention of doxazosin,body weight in group B and group D was greater than that of group A and group C (P＜0.05 or P＜0.01).Expression of type Ⅰ and type Ⅲ collagen fibers in myocardium in group D was lower than that in group C (P＜0.05).Expression of type Ⅰ and type Ⅲ collagen fibers in group B was lower than that in group A (P＜0.05) as well.Myocardial pathological changes in group C were most serious,showing reduced mitochondrial,vacuolar degeneration,and interstitial collagen hyperplasia.Cardiomyopathy in group D and group B was less marked as compared with that in group C and group A,respectively.Myocardial collagen fiber in group C was significantly increased and showed poor alignment.Compared with group C,myocardial collagen deposition in group D was obviously reduced.Conclusions Doxazosin may suppress type Ⅰ and type Ⅲ collagen expressions in myocardium of α1-AA mediated diabetic rats,resulting in alleviation of myocardial fibrosis and protection of myocardium in diabetic rats.
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To observe the relationship between positive rate of β1-adrenergic and AT1 receptors autoantibodies with serum concentration of cystatin C in 371 patients with diabetic nephropathy patients,107 patients with type 2 diabetes,and 47 subjects as healthy control.In patients with diabetic nephropathy,the positive rates of the β1 and AT1 receptors autoantibodies were significantly higher than those in patients with type 2 diabetes and normal controls.The titers of β1 and AT1 receptors autoantibodies in diabetic nephropathy patients with abnormal cystatin C were significantly higher than those with normal cystatin C concentration.These findings suggested that β1 and AT1 receptors autoantibodie may play important roles in the pathogenesis of diabetic nephropathy.
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Objective To make a status survey on type2 diabetic patients with metabolic Syndrome in middle-aged inhabitants.Methods 338 inpatients with type 2 DM including 179 male and 159 female,aged 46?5 years,with complete records in the computer database.Results The prevalent rates of the complications in group of 40～yrs type2 diabetic patients were 17.8% combined with coronary atherosclerotic heart disease,50.9% with hypertension,18.1% with left ventricular dilatation,53.6% with hypertriglyceridemia,46.2% with lower HDL,54.7% with obesity and 38.8% with metabolic Syndrome,respectively.These prevalent rates in the 40-year-old group were all lower than those in groups above 60 years,and the rates was higher in patients whose BMI was above 25(kg/m2).Conclusion There was high prevalence in type 2 diabetic patients with metabolic Syndrome,and was related with the age and obesity.Obesity was an independent risk factor for MS.
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Objective To explore the role of the autoantibodies against ?_1-adrenergic receptor(?_1-receptor)in the development of hypertension with renal failure.Methods The epitopes of the second extracellular loop of ?_1-receptor were synthesized and used respectively to screen sera autoantibodies from patients with hypertension with renal failure(61 cases),hypertension without renal failure(58 cases) and healthy blood donors(40 cases,control) by ELISA method.Results The positive rates of the autoantibodies ?_1-receptor(69%,42/61) in patients with hypertension with renal failure were higher than those of patients with hypertension without renal failure(19%,11/58) respectively(P
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Objective To explore the role of the autoantibodies against angiotensin Ⅱtype 1 receptor(AT1-receptor) and ?1-adrenergic receptor(?1-receptor)in the development of chronic glomerulonephritis(CGN) with renal failure.Methods The epitopes of the second extracellular loop of AT1 receptor(165-191),?1 receptor(192-21),M2 receptor(169-191) were synthesized and used respectively to screen sera autoantibodies from patients with chronic renal failure(n=66),hypertension without renal failure(n=58) and healthy blood donors(n=40,control) by ELISA.Results In patients of chronic glomerulonephritis with renal failure,the positive rates of the autoantibodies against AT1-receptor and ?1-receptor were 56.1% and 53.0% respectively.The positive rates were all higher than those in patients of the hypertension without renal failure(the positive rates were 15.5% and 12.1%,respectively) and in the healthy donors(10% and 12.5%,respectively)(P
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<p><b>OBJECTIVE</b>To investigate the relationship between angiotensin converting enzyme (ACE) gene and exercise-induced silent myocardial ischemia (SI) in patients with type 2 diabetes mellitus.</p><p><b>METHODS</b>One hundred and eight patients suffering from type 2 diabetes mellitus with normal rest electrocardiograph and 50 healthy individuals were selected randomly. SI was diagnosed with treadmill exercise test and ACE genotypes were detected with PCR.</p><p><b>RESULTS</b>(1) The control group and type 2 diabetes mellitus group had similar distribution of ACE genotypes and alleles (P>0.05). Compared with the non-SI group, the SI group had significantly higher ACE D allele prevalence (Chi-square=4.501, P<0.05); however, the two groups had similar prevalence of ACE genotypes (P>0.05). (2) There were no significant differences in clinical characteristics and serum lipoproteins among the three ACE genotypes (II, DD,ID) of type 2 diabetes mellitus (P>0.05). (3) The prevalence of SI in DD group was found to be 68.2%, which was significantly higher than that in II genotype group (39.5%, Chi-square=4.593, P<0.05).</p><p><b>CONCLUSION</b>ACE D allele increases the risk of SI in type 2 diabetes mellitus.</p>
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Adult , Aged , Female , Humans , Male , Middle Aged , Diabetes Mellitus, Type 2 , Blood , Genetics , Exercise , Physiology , Gene Frequency , Genetic Predisposition to Disease , Genetics , Genotype , Lipoproteins , Blood , Myocardial Ischemia , Diagnosis , Genetics , Peptidyl-Dipeptidase A , Genetics , Polymerase Chain ReactionABSTRACT
Objective To investigate the effect of ?-lipoic acid on the expression levels of intercellular adhesion molecule-1 (ICAM-1) in human umbilical vein endothelial cells under high glucose concentration. Methods Human umbilical vein endothelial cells (ECV304) were randomized into control (NG) group,high glucose (HG) group and ?-lipoic acid group. Cells in the 3 groups were incubated for 48h with 5.5mmol/L glucose,30mmol/L glucose,30mmol/L glucose + ?-lipoic acid in a series of concentrations (50,100,200?mol/L),respectively. The activity of superoxide dismutase (SOD) in the supernate was determined by the method of xanthine oxidase,and the content of malondialdehyde (MDA) was measured with thiobarbituric acid as the substrate. The level of ICAM-1 in the supernate was determined by enzyme-linked immunosorbent assay (ELISA). The expressive levels of ICAM-1 mRNA were determined by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR). Results Compared with the control group,the activity of SOD declined significantly and the contents of MDA and ICAM-1 increased in umbilical vein endothelial cells in HG group (P
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Objective To explore the roles of autoantibodies against ?1 adrenoceptor(?1-receptor)and M2 cholinergic receptor(M2-receptor)in patients with chronic renal insufficiency.Methods The epitopes of the second extracellular loop of ?1 receptor and M2 receptor were synthesized and used respectively to detect the sera autoantibodies against ?1 receptor and M2 receptor by enzyme linked immunosorbent assay(ELISA) in 76 patients with chronic renal insufficiency,60 cases with hypertension and 40 healthy controls.Results In patients with chronic renal insufficiency,the positive rates of the autoantibodies against ?1-receptor and M2-receptor were 56.7% and 38.1% respectively,which were much higher than those of patients with hypertension(18.3% and 11.7%) and higher than those of healthy controls(17.5% and 15.0%)(all P