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Objective:To investigate the effects of myeloid-derived growth factor(MYDGF) on inflammatory response and osteoclast differentiation of RAW264.7 cells.Methods:The RAW264.7 osteoclast precursor cells were cultured and treated with different concentrations of recombinant MYDGF protein(rMYDGF), and their cell viability was assessed using the MTT assay. RAW264.7 cells were induced with lipopolysaccharide(LPS) to induce inflammation, and the expression of inflammatory mediators and cell polarization were observed after intervention with rMYDGF. The RAW264.7 cells were induced for osteoclast differentiation using receptor activator of nuclear factor-κB ligand(RANKL), and rMYDGF was added for intervention. Osteoclast differentiation was evaluated by tartrate-resistant acid phosphatase(TRAP) staining. The osteoclast resorption pits and the number of actin rings(F-actin rings) were observed under a microscope. Reverse transcription PCR was performed to detect the expression of activated T cell nuclear factor 1(Nfatc1), cathepsin K(CTSK), and c-Fos genes during osteoclast differentiation. The protein phosphorylation levels of nuclear factor-κB(NF-κB) signaling pathway proteins were detected using Western blotting.Results:MTT assay showed that rMYDGF did not significantly inhibit the viability of RAW264.7 cell when the concentration was lower than 100 ng/mL. Moreover, rMYDGF inhibited the expression levels of inflammatory factors and M1 cell polarization after LPS stimulation. Compared with the control group, the number and area of TRAP positive cells, the number and area of bone resorption pit were decreased in rMYDGF intervention group respectively, as well as the area of the F-actin ring was reduced and its shape was incomplete after rMYDGF intervention. Furthermore, rMYDGF reduced the expression levels of osteoclast-specific marker genes and inhibited the phosphorylation of NF-κB signaling pathway protein IκBα during osteoclast differentiation.Conclusion:MYDGF inhibits the inflammatory response and osteoclast differentiation of RAW264.7 cells.
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Objective:To investigate the effect of alogliptin on bone loss in ovariectomized(OVX)mice.Methods:For animal experiments, thirty 8-week-old C57BL/6J female mice were divided into Sham group, OVX group, and OVX+ alogliptin group. OVX+ alogliptin group were administered with alogliptin in a dosage of 20 mg·kg -1·d -1 by gavage, Sham and OVX groups with equivalent saline. After 12 weeks intervention, serum bone anabolism indicators were detected, and Micro CT and HE staining were used to observe and analyze the bone trabecular structure of femur and tibia in mice. For in vitro experiments, bone marrow mesenchymal stem cells(BMSCs)were incubated with 100 μmol/L alogliptin for osteoblast differentiation. Alkaline phosphatase(ALP)and alizarin red S staining were used to determine the ALP activity and mineralization after osteogenic induction and culture. Real-time fluorescence quantitative PCR and Western blot were used to detect mRNA and protein expressions of osteoblast related genes. Results:Alogliptin intervention improved the biochemical indexes of bone anabolism and protected against bone microstructure deterioration to alleviate bone loss in OVX mice. Alogliptin stimulated osteoblast differentiation and elevated expression levels of Runt-related transcription factor 2(Runx2), ALP, osteocalcin, and osterix in in vitro experiments. Conclusion:Alogliptin can alleviate bone loss in OVX mice.
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Objective:To observe the main clinical features and outcomes of type 2 diabetes mellitus patients after infection with COVID-19 and to compare them with those without diabetes mellitus.Methods:A single-center retrospective observational study was conducted in 88 in-patients who were diagnosed as COVID-19 from January 1 to February 26, 2020. They were divided into diabetic group and non-diabetic group, with 44 patients in each group. Patients′ medical history, laboratory examination, in-hospital treatment plan, and disease outcome were collected and compared.Results:The clinical symptoms of diabetic patients were varied, mainly fever(75.0%), cough(75.0%), fatigue(52.3%), and so on. The systolic blood pressure(SBP)was higher [131.50(120.00, 140.75) vs 125.00(120.00, 131.75)mmHg, 1 mmHg=0.133 kPa, P=0.021] and the oxygenation was lower [96.00%(94.25%, 97.00%) vs 97.00%(95.00%, 98.00%), P=0.038] at admission compared with the non-diabetic group. Hypertension and chronic kidney disease were more common in diabetic group. Fasting blood glucose [7.64(6.12, 15.43) vs 5.62(5.25, 6.50)mmol/L, P<0.01], interleukin-6(IL-6)[19.85(6.50, 43.38) vs 10.80(3.03, 20.90)pg/ml, P=0.046] in diabetic group were significantly higher than those in non-diabetic group. Secondary infection(27.3% vs 9.1%, P=0.027), ARDS(22.7% vs 4.5%, P=0.013)and shock(4.5% vs 0%, P<0.01)were more likely to occur in the diabetic group. More patients were treated with mechanical ventilation in the diabetic group(20.5% vs 4.5%, P=0.024). The diabetes group was more likely to progress to critical type(20.5% vs 4.5%, P=0.024), and the time to progress to critical state was shorter [3(1.75, 5.25) vs 6(3.00, 12.00)d, P=0.019). The duration of severe symptoms was longer in the diabetic group [26.5(15.00, 31.50) vs 9(8.00, 13.00)d, P=0.026]. Conclusion:The clinical symptoms of type 2 diabetes patients with COVID-19 are diverse. They are often combined with diseases such as hypertension and chronic kidney disease. The inflammatory reaction is more obvious and has more COVID-19 related complications and is more likely to progress into a persistent severe condition in a short time.
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Objective To investigate the effect of myeloid-derived growth factor ( MYDGF) on the secretion of glucagon-like peptide 1 ( GLP-1) in type 2 diabetic mice and its mechanism. Methods A type 2 diabetes model was established by injecting streptozotocin into C57BL/6J wild type ( WT) mice and MYDGF knockout ( KO) mice, which were divided into diabetic group ( WT-D, KO-D) and non-diabetic group ( WT-ND, KO-ND) . Six weeks later, the relevant indicators were detected. Next, those mice were divided into wild-type diabetes group (WT-GFP), wild-type diabetes MYDGF intervention group (WT-MYDGF), knockout type diabetes group (KO-GFP), and knockout type MYDGF intervention group ( KO-MYDG ) according to whether or not the AAV-MYDGF intervention was performed. The wild-type non-diabetic mice were used as a blank control group to observe the effects of MYDGF on biochemical indexes, GLP-1 secretion, and mitogen-activated protein kinase kinase ( MEK)/extracellular regulated protein kinases ( ERK) signal pathway in mice. Results After 6 weeks of intervention, there was no significant difference in the glucose and lipid metabolism indexes between WT-ND and KO-ND groups ( P>0.05) . Compared with WT-D group, fasting plasma glucose (FPG), HbA1C, and blood lipid levels in KO-D group were increased, while gcg, pc3 mRNA, and GLP-1 secretion levels were decreased (all P<0.05). Compared with the WT-GFP group, FPG, HbA1C , and blood lipid levels were decreased in WT-MYDGF group, while gcg and pc3 mRNA, and GLP-1 secretion levels were increased (all P<0.05). KO group revealed a result similar to that in WT group after MYDGF intervention. Western blotting showed that the phosphorylation level of ERK1/2 was lowered in KO diabetic mice compared with WT diabetic mice, which was enhanced in WT and KO mice after MYDGF intervention. Conclusions MYDGF promotes the secretion of GLP-1 by activating MEK/ERK signaling pathway, thereby delaying the development of diabetes.
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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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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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Objective To investigate the effects of growth differentiation factor 11 ( GDF11 ) on β-cell function in db/db mice and its possible mechanism. Methods Twenty eight-week-old male db/db mice were randomizedtoi.p. administration of GDF11(0.3mg·kg-1·day-1)or equivalent PBS(n=10)for 6 weeks.10age-matched male db/m were used as normal control, received equivalent PBS injection for 6 weeks. Blood glucose levels, body weights and food intake were monitored weekly. IPGTT and glucose-stimulated insulin secretion ( GSIS) were analyzed. After 6 weeks of intervention, serum HbA1C , TG, TC, and FFA were measured respectively. The concentrations of hormones in serum and pancreas were evaluated. The mRNA expression of Pdx-1, MafA, Nkx6. 1, and insulin2 were determined by RT-PCR. The expression of phosphorylated Smd2 (P-Smad2), Smad2 in islet were examined by western blot. Results Compared with NC group, GDF11 administration decreased FBG, HbA1C , modified lipid profiles. GDF11 improved glucose tolerance and augmented GSIS. Moreover, GDF11 increased serum insulin and pancreatic insulin content, while decreased serum glucagon concentration. The expression of Pdx-1, MafA, Nkx6. 1, and Insulin2 were significantly increased in GDF11 group. GDF11 elevated the expression of P-Smad2 in islets. Conclusion s GDF11 may preserve β-cell function and facilitate the secretion and production of insulin. Diminishing the metabolic abnormalities, alleviating the secretion of glucagon, as well as maintaining the key transcript factor activation may contribute to the amelioration of β-cell function after GDF11 administration. Smad2 pathway may be related to the protective effects of GDF11.
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Objective To investigate the effects and possible mechanism of growth differentiation factor 11 (GDF11)on angiogenesis in diabetic hindlimb ischemia. Methods Sixty SD rats were used in this study. Diabetes was induced by intraperitoneal injection of streptozotocin. 3 days after streptozotocin administration, 40 rats with plasma glucose concentration≥16.7 mmol/L were selected in the subsequent experiments. 12 weeks after diabetes was induced,the left femoral artery and all the sides branches were dissected free and excised. After resection of the left femoral artery,rats were randomized to four groups:PBS group(n=10),GDF11 group(n=10),IgG Ab group (n=10),or GDF11 Ab group(n=10). After 0,7,and 14 days,the serial blood flows were measured by a Laser Doppler perfusion image(LDPI)analyzer. To detect capillary endothelial cell,the sections of muscles were reacted with anti-CD31 monoclonal antibodies,and subsequently reacted with Cy3-conjugated anti-rabbit IgG antibody. The expression levels of HIF1α and VEGF were detected by western blotting. Results In GDF11 group significantly increased the blood perfusion and capillary density of ischemia hindlimb of the diabetic rats were found,which was correlated to an increased level of HIF1α and VEGF. In contrast, GDF11 Ab could lead to the opposite effects. Conclusion GDF11 treatment promotes the recovery of diabetic hindlimb ischemia, which may be related to the improvement of expression of HIF1 alpha and VEGF.
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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 effect of growth differentiation factor 11 ( GDF11 ) on aorta in apolipoprotein E-Null( ApoE-/-) mice and its possible mechanisms. Methods Four-week-old healthy male ApoE-/-mice were fed with high-fat diet for 1 week and were then divided into 4 groups:vehicle group(n=10), GDF11 group (n=10),adeno-associated virus-green fluorescent protein group(AAV-GFP group, n=10), and AAV-GDF11 group ( n=10 ) . The mice received intraperitoneal injection with phosphate buffered saline, GDF11 protein, a single injection of purified AAV-GDF11 or AAV-GFP through the tail vein, respectively. After 4 weeks, serum GDF11/8 level and endothelium-dependent vasodilatation were detected. After 12 weeks, serum GDF11/8, interleukin-6 (IL-6), tumor necrosis factor-α( TNF-α), total cholesterol ( TC), triglycerides ( TG), oxidized low density lipoprotein(ox-LDL), and free fatty acids(FFA)levels were measured, the plaque areas in aortic enface and cross sections were measured by oil red O or HE staining, the macrophages/T lymphocytes infiltration in plaques were detected with immunohistochemistry, and the mRNA expressions of IL-6, TNF-α, and IL-10 were determined by real-time PCR. Results Compared with vehicle or AAV-GFP groups, GDF11 and AAV-GDF11 groups presented improved endothelium-dependent vasodilatation, decreased levels of blood inflammatory factors, blood lipid, reduced plaque on face area sections[Vehicle group : GDF11 group:(31. 23 ± 3. 12)% vs (17. 18 ± 2. 17) %;AAV-GFP group : AAV-GDF11 group:(38.01±4.43)% vs(14.54±2.86)%,P<0.05]andcrosssections[Vehiclegroup :GDF11 group:(19. 87 ± 2. 11)% vs (10. 32 ± 1. 47)%;AAV-GFP group : AAV-GDF11 group:(23. 02 ± 2. 76)%vs (9.06±1.63)%, P<0. 05]. There were less macrophages and T lymphocytes infiltration in plaques and lower mRNA expressions of inflammatory factors at aortic wall. Conclusion GDF11 reduces the area of atherosclerotic lesion in ApoE-/-mice, which may be involved in endothelial protection, such as to reduce inflammatory reaction, and to change cellular composition in plaques.
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Objective: To explore the effect of irisin on atherosclerosis with possible mechanisms in diabetes mellitus (DM) mice. Methods: A total of 30 ApoE-/- mice were randomly divided into 2 groups: Control group, the mice received citrate buffer solution for modeling control,n=10. DM group, the mice received streptozotocin injection for DM modeling,n=20; the DM group was further divided into 2 subgroups as DM control (DM-C) group, the mice received normal saline injection for 12 weeks and DM + irisin group, the diabetic mice received irisin injection for 12 weeks.n=10 in each subgroup. With 4 weeks of irisin intervention, the endothelium-dependent vasodilatation was detected. With 12 weeks of intervention, the blood levels of tumor necrosis factor-α (TNF-α), high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6) and oxidized low-density lipoprotein (ox-LDL) were examined by ELISA, the plaque areas in aortic en face and cross sections were measured by Oil red O or HE staining, the macrophages/T lymphocytes inifltration in plaques were detected with immunohistochemistry, and the mRNA expressions of IL-6, IL-10, TNF-α were determined by RT-PCR. Results: Compared with DM-C group, DM + irisin group presented improved endothelium-dependent vasodilatation, decreased levels of blood inlfammatory factors, reduced plaque on face area sections (22.57 ± 2.17) % vs (35.09 ± 2.38) % and cross sections (19.36 ± 1.85) % vs (25.53 ± 7.87) %,P < 0.05, less macrophages (30.5 ± 2.79) % vs (41.34 ± 9.13) % T and lymphocytes infiltration (28.11 ± 4.24) % vs (35.79 ± 9.11) % in plaques and lower mRNA expressions of inflammatory factors(IL-6: 1.76 ± 0.50 vs 3.78 ± 1.15; TNF-α: 1.05 ± 0.30 vs 2.11 ± 0.48; ICAM-1: 1.96 ± 0.69 vs 2.71 ± 0.72; VCAM-1: 0.87 ± 0.21vs 1.45±0.25; MCP-1: 1.34 ± 0.34 vs 1.77 ± 0.55) at aortic wall, P<0.05.Conclusion: Irisin may improve atherosclerosis condition in ApoE-/- DM mice, the endothelial protection and antiinflammatoryreaction were the important mechanisms. Irisin has the potential for preventing/treating atherosclerosis.
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Four-week-old male Sprague-Dawley rats were rendered diabetic by intraperitoneal injection of streptozotocin (STZ) after feeding high-fat-diet for 8 weeks,and divided into diabetes group and tumor necrosis factorrelated apoptosis ligand(TRAIL) group.Normal rats severed as a control group.Treatment with TRAIL lasted for 3 months.Total cholesterol,triglycerides,low-density lipoprotein-cholesterol,blood glucose,and insulin levels were decreased in TRAIL group,as compared with diabetes group.Area of atherosclerotic lesion in TRAIL group [(23.8 ± 5.7) ％] was significantly smaller than that in diabetes group [(47.6 ± 7.8) ％].It suggested that TRAIL may reduce the area of atherosclerotic lesion in diabetic rats.
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Objective To explore the effect and mechanism of osteoprotegerin on apoptosis in human umbilical vein endothelial cells(HUVECs) induced by triiodothyronine(T3) with different concentrations.Methods HUVECs were cultured in control group (0 nmol/L T3),low-concentration group (0.1 nmol/L T3),physiologicalconcentration group(1 nmol/L T3),high-concentration group(10 nmol/L T3) with OPG for 48 h.The cell apoptosis was measured by cytometry and Hoechst 33258.The expressions of p-IκKβ,lκKβ,p-TSC2,TSC2,p-S6K,S6K,p-AKT,AKT,Bcl-2,and Bax were analyzed by Western blot.Results (1) After OPG pretreatment and being cultured in control group、low-concentration group and high-concentration group,the HUVEC apoptosis was decreased significantly(P＜0.05) as compared with groups without OPG pretreatment.There was no difference in physiological concentration group before and after intervention of OPG.(2) The expression of p-IκKβ,p-S6K,and Bax in other groups were higher than those in physiological concentration group ; however,the expressions of p-TSC2,p-AKT,and Bcl-2 were lower than those in physiological concentration group(P＜0.05).After OPG pretreatment in control group,low-concentration group,and high-concentration group,the expressions of p-IκKβ,p-S6K,and Bax decreased significantly (P＜0.05)and the expression of p-TSC2,p-AKT,and Bcl-2 increased significantly (P＜ 0.05) ; there were no differences in the expressions of p-IκKβ,p-S6K,p-TSC2,p-AKT,Bcl-2,and Bax in physiological concentration group before and after intervention of OPG.Conclusions Low and high concentrations of T3 increase apoptosis of HUVECs by way of activation of IκKβ/mTOR pathway.Osteoprotegerin is able to protect HUVECs from apoptosis induced by low and high concentration of T3 via the way of inhibiting the IκKβ/mTOR pathway.
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Objective To explore the effect and its mechism of osteoprotegerin (OPG) on human umbilical vein endothelial cells(HUVECs) induced by high glucose.Methods (1) The cultured HUVECs were treated with normal glucose(5.5 mmol/L),high glucose(33 mmol/L),high glucose + OPG(0.5,1,and 2 μg/ml)as well as mannitol(5.5 mmol/L glucose+27.5 mmol/L mannitol) for 48 h,respectively.Flow cytometry assay and Hoechst 33258 staining were used to detect the cell apoptosis.The expression levels of Bcl-2 and Bax protein were measured by western blot analysis.(2) The cultured HUVECs were treated with normal glucose,high glucose,high glucose + OPG (2 μg/ml OPG),high glucose + rapamycin(10 ng/ml rapamycin) as well as high glucose + rapamycin + OPG for 24h,respectively.The expression levels of S6K,p-S6K,4EBP1 and p-4EBP1 protein were measured by western blot analysis.(3)The cultured HUVECs were treated with normal glucose,high glucose,high glucose + OPG(2 μg/ml)for 24 h,respectively.The expression levels of tuberin and p-tuberin protein were measured by western blot analysis.Results (1) Compared with normal glucose group,the apoptosis of HUVECs and the expression level of Bax was dramatically increased,and the expression of Bcl-2 was decreased significantly in high glucose group (P＜0.05).The apoptosis of HUVECs and the expression level of Bax in high glucose + OPG group was significantly lower than that in high glucose group,which was still higher than that in normal glucose group (P＜ 0.05).and the expression of Bcl-2 in high glucose + OPG group was significantly higher than that in high glucose group,which was still lower than that in normal glucose group (P＜0.05).There was no statistically difference between hyperosmolar control group and normal glucose group.(2) Compared with normal glucose group,the expression levels of p-S6K and p-4EBP1 were increased markedly in high glucose group(P＜0.05).The expression levels of p-S6K and p-4EBP1 in high glucose + OPG group were significantly lower than that in high glucose group,which were still higher than that in normal glucose group(P＜0.05).No significant difference was found between high glucose + OPG group and high glucose + rapamycin group.(3) Compared with normal glucose group,the expression level of p-tuberin was increased markedly in high glucose group (P ＜ 0.05).The expression level of p-tuberin in high glucose + OPG group was significantly lower than that in high glucose group,which was still higher than that in normal glucose group (P ＜0.05).Conclusions It suggests that the protective effect and mechanism of OPG on HUVECs cultured with high glucose may be association with tuberin/mTORC1 pathway.
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Objective To investigate the circadian change of autonomic nervous system in hyperthyroidism (HT) patients. Methods Recording 24 h dynamic electrocardiography from 33 HT patients( HT group) and 35 controls (control group). The cardiac autonomic nervous function was evaluated by the time domain and frequency domain analysis of heart rate variability( HRV). Results Comparing with control group, the SDNN, SDANN, ASDNN and rMSSD were significantly lower in HT group[ (82.3 ± 29.0)ms vs. (139.4±40.2 ) ms, ( 75.0 ± 27.4) ms vs. ( 130.3 ± 43.9) ms, (29.9 ± 14.9 ) ms vs. (57.3 ± 14.4) ms,( 19.8 ± 10.9 ) ms vs. (29.5 ± 9.4) ms ] (P ＜ 0.01 or ＜ 0.05 ), the long term total power (TP), high frequency (HF), low frequency (LF) and very low frequency (VLF) were significantly lower in HT group [ (566.1±573.2) ms2/Hz vs. ( 1894.2 ± 984.3)ms2/Hz, (68.1 ± 88.9 ) ms2/Hz vs. (232.7 ± 155.5 ) ms2/Hz, ( 127.4 ±163.0) ms2/Hz vs. (551.3 ± 390.6) ms2/Hz, (330.3 ± 300.6) ms2/Hz vs. (1073.2 ± 570.2) ms2/Hz] (P ＜0.01 ). Comparing with control group, short term VLF was higher in HT group during most time in 24 hours (P＜ 0.05 ). Short term LF was higher in HT group mainly in day time (P＜ 0.05 ). Short term HF was higher in HT group occasionally in the whole day (P＜0.05). Short term LF/HF didn't show significant difference between HT group and control group at most time points (P＞0.05).Conclusion In HT patients, cardiac chronotropic property is impaired, sympathetic activity increases in whole day, vagal activity increases correspondently but the increase in day is more marked than that in night.
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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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In order to characterize the effects of 17β-estradiol (17β-E2) on the expression of IL-6,IL-11 and NF-κB in the human MG-63 osteoblast-likecell line, the expression of IL-6 was detected by RT-PCR, Northern blot and Western blot. The expression of IL-11 was determined by RT-PCR, and NF-κB by Western blot. The results showed that 17β-E2 down-regulated the expression of IL-6 mRNA and protein, IL-11 mRNA and NF-κB protein in MG-63 cells. It was suggested that the expression of NF-κB, IL-6 and IL-11 in MG-63 cells could be suppressed by 17β-E2, and this might lend support to estrogen replacement therapy in postmenopausal women.
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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