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1.
BMC Endocr Disord ; 23(1): 189, 2023 Sep 04.
Artículo en Inglés | MEDLINE | ID: mdl-37667210

RESUMEN

OBJECTIVE: The objective was to analyze the relationship between serum 25-hydroxy-vitamin D (25(OH)D) level and albuminuiria in middle-aged and older patients with type 2 diabetes of Gansu Province. METHODS: Data pertaining to 380 in-patients with type 2 diabetes were collected. Subjects were classified groups based on gender,age,25(OH)D,BMI and UACR.Serum 25(OH)D and other clinical characteristics among various UACR groups were compared.The relationship between albuminuiria and 25(OH)D was analyzed. RESULTS: Out of the 380 subjects, 83.4%were classified as vitamin D deficiency, 14.5%were classified as vitamin D insufficiency, while 2.1% were classified as vitamin D sufficiency. Among the participants,41% had albuminuria (microalbuminuria,28.7%;macroalbuminuria,12.3%).The prevalence of 25(OH)D deficiency in the albuminuria group(84.6%) was significantly higher than that in the normoalbuminuria group(82.6%)(Mann-Whitney U test:Z = -3.86,P = 0.000); patients with macroalbuminuria had the highest prevalence of 25(OH)D deficiency (91.5%; P < 0.01 versus normoalbuminuria).A binary logistic analysis demonstrated that 25(OH)D were protective factors for albuminuria. CONCLUSIONS: The prevalence of vitamin D deficiency in patients with albuminuria was overtly higher than that in patients without albuminuria among middle-aged and older adults with type 2 diabetes.


Asunto(s)
Diabetes Mellitus Tipo 2 , Deficiencia de Vitamina D , Persona de Mediana Edad , Humanos , Anciano , Adulto , Diabetes Mellitus Tipo 2/complicaciones , Diabetes Mellitus Tipo 2/epidemiología , Albuminuria/epidemiología , Pueblos del Este de Asia , Vitamina D , Calcifediol , Deficiencia de Vitamina D/complicaciones , Deficiencia de Vitamina D/epidemiología
2.
Environ Technol ; 43(15): 2380-2390, 2022 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-33487132

RESUMEN

Degradation of neonicotinoid insecticide dinotefuran (DIN) in dielectric barrier discharge (DBD) non-thermal plasma combined with lanthanum-doped titanium dioxide (La-TiO2) system was investigated. A La-TiO2 catalyst was prepared by the sol-gel method and characterized by SEM, XRD, and DRS. The effects of various factors (initial concentration, initial pH, input power, and addition of metal ions) on the removal rate of DIN were evaluated. The results indicated that when the initial concentration, input power, initial pH, and Fe2+ catalyst ions were 100 mg/L, 150 W, 10.5 and 50 mg/L, respectively, the DIN degradation efficiency was improved to 99.0% by coupling 10 wt% La-TiO2 at 180 min. La-TiO2 showed excellent catalytic performance on DIN degradation in a DBD system. The removal rate decreased with the presence of H2O2 and a scavenger, manifesting that HO∙ plays an imperative role in the degradation process. Furthermore, intermediate products were analyzed by MS and the possible degradation pathway of DIN was proposed.


Asunto(s)
Peróxido de Hidrógeno , Lantano/química , Titanio , Catálisis , Guanidinas , Peróxido de Hidrógeno/química , Neonicotinoides , Nitrocompuestos , Titanio/química
3.
J Diabetes Res ; 2016: 9741483, 2016.
Artículo en Inglés | MEDLINE | ID: mdl-27579327

RESUMEN

We found in the present study that treatment with ox-LDL decreased the cell viability and the content of nitric oxide (NO) and the activity of nitric oxide synthase (NOS) as well as eNOS mRNA expression, while increasing the mRNA expression and content of endothelin-1 (ET-1) in human umbilical vein endothelial cells (HUVECs). However, endomorphins EM1/EM2 increased the cell viability and the content of NO and the activity of NOS as well as eNOS mRNA expression, while decreasing the mRNA expression and content of ET-1 compared with ox-LDL alone. Meanwhile, the expressions of JNK and p-JNK were enhanced by ox-LDL while being suppressed by EM1/EM2. The results suggested that EM1 and EM2 can correct the endothelial cell dysfunction induced by ox-LDL and the protective effect may be achieved by affecting the JNK pathway.


Asunto(s)
Supervivencia Celular/efectos de los fármacos , Células Endoteliales de la Vena Umbilical Humana/efectos de los fármacos , Lipoproteínas LDL/farmacología , Endotelina-1/metabolismo , Células Endoteliales de la Vena Umbilical Humana/metabolismo , Humanos , Óxido Nítrico/metabolismo , Óxido Nítrico Sintasa/metabolismo , Fosforilación/efectos de los fármacos , Transducción de Señal/efectos de los fármacos
4.
Environ Toxicol Pharmacol ; 42: 231-6, 2016 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-26896612

RESUMEN

Diabetes mellitus can cause a wide variety of vascular complications and is one of the major risk factors for Non Alcoholic Fatty Liver Disease (NAFLD). The present study was designed investigate the expression of laminin (LN) in human liver sinusoidal endothelial cells (HLSECs) induced by high glucose and the role of reactive oxygen species (ROS) and integrin αvß3 in the regulation of LN expression. HLSECs were cultured and treated with media containing 25 mM glucose in the presence or absence of N-acetylcysteine (NAC) or clone LM609. The level of intracellular ROS of HLSECs was measured with 2',7' dichloro-fluorescein diacetate (DCFH-DA) probe. Expression of integrin αvß3 was measured using RT-PCR and Western blot. Expression of LN was testified by immunofluorescence assay. Compared with that in control group, ROS level and the expression of integrin αvß3 and LN increased in high glucose group. Compared with that in high glucose group, antioxidant NAC inhibited the expression of integrin αvß3, NAC and the anti-body for blocking integrin αvß3 (clone LM609) down-regulated the expression of LN. However, the above parameters did not differ between control and mannitol groups. High glucose up-regulates expression of LN in HLSECs through ROS/integrin αvß3 pathway.


Asunto(s)
Células Endoteliales/fisiología , Glucosa/metabolismo , Integrina alfaVbeta3/metabolismo , Laminina/metabolismo , Hígado/fisiología , Especies Reactivas de Oxígeno/metabolismo , Acetilcisteína , Células Cultivadas , Fluoresceínas , Humanos
5.
Eur J Intern Med ; 23(3): 287-92, 2012 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-22385890

RESUMEN

BACKGROUND: Diabetes mellitus can cause a wide variety of vascular complications and it is one of the major risk factors for cardiovascular diseases (CVD). High glucose can induce vascular endothelial cell apoptosis. In this study, we investigated the effect of radix hedysari polysaccharide (HPS) on the depression of apoptosis of human umbilical vein endothelial cells (HUVECs) induced by high glucose. METHODS: HUVECs were treated with media containing 30 mM glucose in the presence or absence of vitamin C or HPS. The level of intracellular reactive oxygen species (ROS) and apoptosis of HUVECs was measured with flow cytometry. Expression of c-Jun NH(2)-terminal kinase (JNK) and caspase-3 were testified by real-time quantitative RT-PCR and immunofluorescence. RESULTS: High glucose was capable of eliciting the overexpression of JNK during the treatment procedure. Moreover, we found that the caspase-3 became overexpressed in apoptosis induced by high glucose; HPS could inhibit apoptosis under high glucose and suppress the generation of ROS and the overexpression of JNK and caspase-3. The effect of HPS on ROS quenching, inhibition of JNK and caspase-3 overexpression at the concentration of 100 µg/ml was similar to that of vitamin C at the concentration of 100 µM. CONCLUSION: The findings of the present study may suggest that HPS play a protection role on HUVECs against apoptosis induced by high glucose.


Asunto(s)
Apoptosis/efectos de los fármacos , Medicamentos Herbarios Chinos/farmacología , Células Endoteliales/citología , Células Endoteliales/efectos de los fármacos , Glucosa/toxicidad , Apoptosis/fisiología , Astragalus propinquus , Caspasa 3/genética , Caspasa 3/metabolismo , Citoprotección/efectos de los fármacos , Interacciones Farmacológicas , Células Endoteliales/metabolismo , Células Endoteliales de la Vena Umbilical Humana , Humanos , Proteínas Quinasas JNK Activadas por Mitógenos/metabolismo , ARN Mensajero/metabolismo , Especies Reactivas de Oxígeno/metabolismo
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