Toxic effects of maternal cadmium exposure on the metabolism and transport system of amino acids in the maternal livers.

Fetal growth restriction (FGR) is one of the most common obstetric diseases, and affects approximately 10 % of all pregnancies worldwide. Maternal cadmium (Cd) exposure is one of the factors that may increase the risk of the development of FGR. However, its underlying mechanisms remain largely unknown. In this study, using Cd-treated mice as an experimental model, we analyzed the levels of some nutrients in the circulation and the fetal livers by biochemical assays; the expression patterns of several key genes involved in the nutrient uptake and transport, and the metabolic changes in the maternal livers were also examined by quantitative real-time PCR and gas chromatography-time of flight-mass spectrometry method. Our results showed that, the Cd treatment specifically reduced the levels of total amino acids in the peripheral circulation and the fetal livers. Concomitantly, Cd upregulated the expressions of three amino acid transport genes (SNAT4, SNAT7 and ASCT1) in the maternal livers. The metabolic profiling of maternal livers also revealed that, several amino acids and their derivatives were also increased in response to the Cd treatment. Further bioinformatics analysis indicated that the experimental treatment activated the metabolic pathways, including the alanine, aspartate and glutamate metabolism, valine, leucine and isoleucine biosynthesis, arginine and proline metabolism. These findings suggest that maternal Cd exposure activate the amino acid metabolism and increase the amino acid uptake in the maternal liver, which reduces the supply of amino acids to the fetus via the circulation. We suspect that this underlies the Cd-evoked FGR.

Efficacy of metoprolol combined with torasemide in elderly patients with degenerative valvular heart disease and heart failure and its influence on NT-proBNP levels.

Objective: To investigate the efficacy of metoprolol combined with torasemide in elderly patients with degenerative valvular heart disease (DVHD) and heart failure and its influence on N-terminal pro-B-type natriuretic peptide (NT-proBNP) concentrations. Methods: The records of 129 DVHD patients ≥60 years old with heart failure diagnosed and treated in our hospital from January 2020 to February 2022 were retrospectively selected. According to the treatment records, 62 patients received metoprolol treatment (Control-group), and 67 patients received metoprolol combined with torasemide treatment (Observation-group). The changes in cardiac function, NT-proBNP and inflammatory factor concentrations and clinical efficacy were analyzed and compared between the two groups before and after treatment. Results: After treatment, left ventricular ejection fraction (LVEF), left ventricular end-diastolic diameter (LVEDD) and the mitral ratio of peak early to late diastolic filling velocity (E/A) were lower, with a greater decrease in the Observation-group compared to the Control-group (P<0.05). After treatment, NT-proBNP and interleukin-1beta (IL-1ß), tumor necrosis factor-alpha (TNF-α), interleukin 6 (IL-6) concentrations were lower in both groups, with a greater decrease in the Observation-group compared to the Control-group (P<0.05). The total clinical efficacy of the Observation-group was significantly higher than the Control-group (P<0.05). There was no significant difference in the total incidence of adverse drug reactions between the two groups (P>0.05). Conclusion: Metoprolol combined with torasemide has a significant therapeutic effect on DVHD patients with heart failure. This drug combination improved cardiac function, reduced NT-proBNP concentrations and has good safety.

The efficacy of negative pressure wound therapy after hepatopancreatobiliary surgery: A systematic review and meta-analysis.

Objective: To evaluate the comparative influence of NPT and standard surgical dressing administration on incidence risk for surgical site infections, complications, and hospital re-admission after hepatopancreatobiliary surgery. Methods: Five databases were systematically searched according to PRISMA guidelines. These databases included Web of Science, MEDLINE, CENTRAL, EMBASE, and Scopus for eligible studies published prior to March 2021. With eligible studies, we conducted a random-effects meta-analysis to evaluate comparative outcomes such as superficial surgical infection, deep surgical infection, seroma incidence, hematoma incidence, and hospital re-admission in patients receiving NPT or standard surgical dressings after hepatopancreatobiliary surgery. Results: The search strategy yielded 963 studies, with six studies meeting inclusion criteria. Odds of superficial surgical site infection (OR: 1.58), deep surgical site infection (1.43), seroma complication (1.64), hematoma complication (0.40) were insignificantly different between patients receiving NPT and standard surgical dressing. The odds of hospital re-admission rate (2.37), however, were elevated in patients receiving standard surgical dressing relative to those receiving NPT. Conclusion: This meta-analysis shows that NPT usage slightly reduces risk of hospital readmission as compared to standard surgical dressing. We did not observe any significant effect of NPT on superficial, deep surgical infections, seroma, and haematoma outcomes following hepatopancreatobiliary surgery. These findings may aid clinicians in stratifying risk and selecting treatment strategy in patients undergoing hepatopancreatobiliary surgery.

Phenolic Compounds from Clinopodium chinense (Benth.) O. Kuntze and Their Inhibitory Effects on α-Glucosidase and Vascular Endothelial Cells Injury.

Following an in vitro bioactivity-guided fractionation procedure, 14 compounds including eight flavonoids and six phenylpropanoids were isolated and identified from the AcOEt fraction of Clinopodium chinense (Benth.) O. Kuntze. All constituents were tested for α-glucosidase and high glucose-induced injury in human umbilical vein endothelial cells (HUVECs) inhibitory activities. All constituents exhibited varying degrees α-glucosidase inhibitory activity and protective activity on HUVECs. Among them, luteolin (2), eriodictyol (5), ethyl rosmarinate (13), and clinopodic acids B (14) were proved to be potent α-glucosidase inhibitors with IC50 value ranging from 0.6 to 2.0 µm. Additionally, luteolin (2), naringenin (4), eriodictyol (5), ethyl (2R)-3-(3, 4-dihydroxyphenyl)-2-hydroxypropanate (9), caffeic acid (11), ethyl rosmarinate (13), and clinopodic acids B (14) significantly ameliorate HUVECs injury induced by high glucose with an approximate EC50 value of 3 - 36 µm. These results suggest that the 14 bioactive constituents were responsible for hypoglycemic and protective vascular endothelium effect of C. chinense (Benth.) O. Kuntze and their structure-activity relationship was also analyzed briefly. Eriodictyol, luteolin, ethyl rosmarinate, and clinopodic acids B were the potential lead compounds of antidiabetic drugs.

[Expression of vascular endothelial growth factor and microvessel density in different brain regions in aged rats].

OBJECTIVE: To observe the distribution of vascular endothelial growth factor (VEGF) and microvessel density (MVD) in different brain regions in aged rats and determine the role of VEGF and MVD in the aging process of the nervous system. METHODS: We observed the expression of VEGF and MVD in different parts of rat brain in the 3- month group and 30-month group with immunohistochemical technique. RESULTS: Compared with the 3-month group, the 30-month group showed fewer VEGF-positive cells and MVD in the brain (P<0.01), and the number varied significantly in different brain regions (P<0.01). The motor cortex region contained more VEGF-positive cells and MVD than the hippocampus and cerebellum. CONCLUSION: VEGF-positive cells and MVD are decreased in every brain region of aged rats, and the motor cortex region contains more positive cells, suggesting exogenous VEGF may enhance the formation of microvessels and delay the aging of the nervous system.

C1q/tumor necrosis factor-related protein-9 exerts antioxidant and anti-inflammatory effects on oxygen-glucose deprivation/reoxygenation-stimulated neurons by modulating the Akt-GSK-3ß-Nrf2 cascade via AdipoR1.

C1q/tumor necrosis factor-related protein-9 (CTRP9) is linked to diverse pathological conditions via the effects on cell apoptosis, inflammatory response, and oxidative stress. However, its functional relevance in ischemic brain injury is not well determined. The present work aimed to evaluate the role of CTRP9 in ischemia/reperfusion-associated neuronal injury using an in vitro model. The cultured cortical neurons were subjected to oxygen-glucose deprivation/reoxygenation (OGD/R) to simulate ischemia/reperfusion in vitro. CTRP9 level was lowered in cultured neurons exposed to OGD/R. Neurons with overexpressed CTRP9 were resistant to OGD/R-elicited injuries, including neuronal apoptosis, oxidative stress, and pro-inflammatory response. Mechanism research revealed that CTRP9 could boost the activation of the nuclear factor erythroid 2-related factor (Nrf2) pathway associated with modulation of the Akt-glycogen synthase kinase-3ß (GSK-3ß) axis. CTRP9 regulated the transduction of the Akt-GSK-3ß-Nrf2 cascade via adiponectin receptor 1 (AdipoR1). Restraining Nrf2 could diminish CTRP9-mediated neuroprotective effects in OGD/R-injured neurons. Altogether, these results confirmed that CTRP9 exerts a protective effect on OGD/R-injured neurons by modulating Akt-GSK-3ß-Nrf2 cascade via AdipoR1. This work suggests a possible link between CTRP9 and ischemic brain injury.

[Effects of valsartan on aortic angiotensin converting enzyme 2 expression after aortic balloon injury in rats].

OBJECTIVE: To investigate the process and mechanism of neointimal formation, the level of angiotensin II and angiotensin (1-7), the expression of angiotensin converting enzyme 2(ACE2), angiotensin II type 1 receptor (AT(1)R), extracellular signal regulated kinase (ERK) and the effects of valsartan on them after aortic balloon injury in rats. METHODS: Aortic endothelial denudation of rats was induced by 2F balloon catheter. Thirty-six rats were randomly allocated into three groups: Group 1 (n = 12): controls; Group 2 (n = 12): aortic balloon injury; Group 3 (n = 12): valsartan (20 mg×kg(-1)×d(-1)) given from 1 day before injury to 14 and 28 days after aortic injury. The expression of ACE2 and AT1, the level of P-ERK, AngII, Ang(1-7) and intimal thickening were investigated by RT-PCR technique, immunohistochemistry, Western blot, radioimmunological method, enzyme linked immunosorbent assay (ELISA) and HE stain, respectively. RESULTS: (1) The proliferation of vascular smooth muscle cells (VSMC) and the intimal thickening were evidenced at day 14 and 28 after aortic balloon injury. (2) The mRNA and protein expressions of ACE2 decreased significantly, but AT(1)R mRNA and protein expression increased significantly at day 14 and 28 after balloon injury. (3) The level of AngII and p-ERK increased and Ang(1-7) reduced after balloon injury. (4) Valsartan not only attenuated the proliferation of VSMC and the intimal thickening but also upregulated the expression of ACE2 and the level of Ang(1-7) and downregulated the expression of AT(1)R and the level of AngII, p-ERK in this model. CONCLUSION: Intimal thickening after balloon injury is linked with reduced expression of ACE2.Valsartan can inhibit the intimal thickening possibly by upregulating ACE2 and Ang(1-7) and downregulating AT(1) in this model.

[Association between plasma adiponectin and small, dense low density lipoprotein in patients with coronary artery disease].

OBJECTIVE: To observe the association between adiponectin and small dense low-density lipoprotein (sLDL-c) in coronary artery disease (CAD) patients. Furthermore, we sought to determine the association between single nucleotide polymorphisms (SNP) rs1501299 (+276G/T), rs266729 (-11365C/G) and the incidence of CAD. METHODS: Consecutive subjects with chest discomfort were examined by coronary angiography and divided into non-CAD [n = 250, 147 male, mean age (60.26 ± 7.52) years] and CAD [n = 267, 153 male, mean age (60.79 ± 9.63) years] groups. Blood samples were collected from all participants following an overnight fasting for at least 12 hours. Plasma adiponectin levels were measured by competitive enzyme-linked immunosorbent assay (ELISA). The serum levels of sLDL-C and oxidized low-density lipoprotein (ox-LDL) were determined by ELISA. Genotypes in rs1501299 and rs266729 of the adiponectin were determined by polymerase chain reaction (PCR). RESULTS: 1. The adiponectin levels were significantly lower [(306.17 ± 74.52) mg/L vs. (321.78 ± 86.28) mg/L], whereas sLDL-C and ox-LDL levels were significantly higher [(276.30 ± 45.55) ng/L vs. (249.00 ± 32.02) ng/L and (545.06 ± 115.46) µg/L vs. (497.74 ± 106.09) µg/L, P < 0.05] in CAD group than non-CAD group. 2. Adiponectin level was negatively associated with sLDL-C, whereas sLDL-C positively correlated with ox-LDL in all subjects. 3. Genotype distribution and allele frequencies of rs1501299 and rs266729 were similar between CAD and non-CAD subjects and not related to the serum levels of adiponectin, sLDL-C and ox-LDL. CONCLUSIONS: Reduced adiponectin and increased sLDL-C were independent risk factors for coronary artery disease. Genetic polymorphisms in rs1501299 and rs266729 were not linked with coronary artery disease.

Effects of roleplay simulation on improving quality management of nursing service.

OBJECTIVE: To observe the feasibility of roleplay simulation in improving the quality management of nursing services. METHOD: In this retrospective study, 80 nursing staff were enrolled as the study subjects from January 2019 to December 2020. They were divided into a study group (n=40, trained in roleplay simulation) and a control group (n=40, trained in conventional nursing skills) according to different training methods. The self-efficacy and quality of nursing services of the staff in the two groups were assessed retrospectively. Spearman's correlation analysis was conducted to analyze the relationship between the self-efficacy score and nursing service. RESULTS: After training, the self-efficacy scores of the nursing staff in the study group were higher than those in the control group (P<0.05). After training, the nursing staff in the study group had significantly higher service quality scores than those in the control group (P<0.05). Spearman's analysis showed that the self-efficacy scores were positively correlated with the quality of nursing scores (r=0.7091, P<0.0001). After training, the scores of the condition assessment of the nursing staff in the study group was higher than those in the control group (P<0.05). CONCLUSION: Roleplay simulation for nursing staff is helpful to improve the quality of nursing and the ability to deal with emergencies. This can be related to the improvement of self-efficacy in nursing staffs.

Ginsenoside Rg3 attenuates angiotensin II-induced myocardial hypertrophy through repressing NLRP3 inflammasome and oxidative stress via modulating SIRT1/NF-κB pathway.

BACKGROUND: Ginsenoside Rg3 (Rg3), one of the most potent components extracted from the roots of the traditional Chinese herb Panax ginseng, has prominent roles in anti-tumor and anti-inflammation. However, the applications of Rg3 against myocardial hypertrophy are not fully revealed. METHODS: Transverse aortic constriction (TAC) was adopted to build the myocardial hypertrophy model in rats. The in vitro model of myocardial hypertrophy was induced by angiotensin II (Ang II) in the human cardiomyocyte cell line AC16 and HCM, which were then treated with different doses of Rg3. The levels of myocardial hypertrophy markers (ANP, BNP, and ß-MHC) were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Western blot (WB) was conducted to verify the expressions of myocardial fibrosis-associated proteins (MyHc, Collagen Ⅰ, and TGF-ß1) and oxidative stress (OS) proteins (HO-1 and Nrf2). The markers of fibrosis, hypertrophy, NLRP3 inflammasome and OS in cardiomyocytes were evaluated by qRT-PCR, western blot (WB), enzyme-linked immunosorbent assay (ELISA), and cellular immunofluorescence, respectively. Furthermore, pharmacological intervention on sirtuin-1 (SIRT1) was performed to clarify the function of SIRT1 in Rg3-mediated effects. RESULTS: Rg3 dose-dependently attenuated the Ang II-induced myocardial hypertrophy and fibrosis. What's more, Rg3 markedly inhibited NLRP3-ASC-Caspase1 inflammasome and OS (reflected by SOD, MDA, HO-1, and Nrf2) in cardiomyocytes treated with Ang II. Mechanistically, Rg3 attenuated NF-κB activation and promoted SIRT1 expression. Inhibiting SIRT1 (by AGK2) mostly reversed Rg3-mediated effects against Ang II-induced myocardial hypertrophy and fibrosis. In the TAC rat model, administration of Rg3 mitigated myocardial hypertrophy and fibrosis through pressing overproduced inflammation and OS. CONCLUSION: Rg3 prevents Ang II-induced myocardial hypertrophy via inactivating NLRP3 inflammasome and oxidative stress by modulating the SIRT1/NF-κB pathway.

[Expression of vascular endothelial growth factor and microvessel density in hippocampus of rats with aging].

OBJECTIVE: To investigate the expression of vascular endothelial growth factor (VEGF) and microvessel density (MVD) in hippocampus of rats with aging. METHODS: Paraffin sections of brain tissue of rats at the age of 3, 18, 24, 30 months were stained by immunohistochemistry, the expression of VEGF and MVD was quantitatively analyzed. RESULTS: Innunohistochemical staining showed that the VEGF-positive cells were mainly pyramidal neuron in hippocampus; the intensity of VEGF-positivity in neuron cells was decreased with the aging (P<0.05). The MVD in hippocampus was also decreased with the aging of rats (P<0.05). CONCLUSION: Increasing VEGF contents and improving blood circulation in brain tissue may prevent or treat vascular dementia and cerebrovascular diseases.

[Expression of GLUT 3 in different brain regions of aged rats].

OBJECTIVE: To examine the distribution of glucose transport 3 (GLUT 3) in different brain regions of aged rats and to investigate its role in ageing process of the nervous system. METHODS: The GLUT 3 expression in different brain regions was examined with immunohistochemical method in rats aged 3, 18 and 30 months, respectively. RESULTS: The number of GLUT 3-positive cells varied in the different brain regions in rats of all age groups (P<0.01); the CA1 region contained the greatest number of positive cells,and fewer in the motor cortex and cerebellum. The number of GLUT 3-positive cells was reduced in the brain of aged rats (P<0.01); and the neural cells in 4 different brain regions presented with large cell body and loose alignment. CONCLUSION: The expression of GLUT 3 decreased in aged rats, which suggests that GLUT 3 may be involved in the ageing process of nervous system.

Apigenin and naringenin regulate glucose and lipid metabolism, and ameliorate vascular dysfunction in type 2 diabetic rats.

Vascular endothelial dysfunction is regarded as the initial step of vascular complications in diabetes mellitus. This study investigated the amelioration of apigenin and naringenin in type 2 diabetic (T2D) rats induced by high-fat diet and streptozotocin and explored the underlying mechanism. Apigenin or naringenin was intragastrically administered at 50 or 100mg/kg once a day for 6 weeks. Biochemical parameters including blood glucose, glycated serum protein, serum lipid, insulin, superoxide dismutase (SOD), malonaldehyde and intercellular adhesion molecule-1 (ICAM-1) were measured. Vascular reactivity in isolated thoracic aortic rings was examined. Pathological features of the thoracic aorta were further observed through optical microscopy and transmission electron microscopy. Lastly, we evaluated their effects on insulin resistance of palmitic acid (PA)-induced endothelial cells. Compared with diabetic control group, apigenin and naringenin significantly decreased the levels of blood glucose, serum lipid, malonaldehyde, ICAM-1 and insulin resistance index, increased SOD activity and improved impaired glucose tolerance. Apigenin and naringenin restored phenylephrine-mediated contractions and acetylcholine or insulin-induced relaxations in aortic tissues. Furthermore, pathological damage in the thoracic aorta of apigenin and naringenin groups was more remissive than diabetic control group. In vitro, apigenin and naringenin inhibited NF-κB activation and ICAM-1 mRNA expression in PA-treated endothelial cells and improved nitric oxide production in the presence of insulin. In conclusion, both apigenin and naringenin can ameliorate glucose and lipid metabolism, as well as endothelial dysfunction in T2D rats at least in part by down-regulating oxidative stress and inflammation. In general, apigenin showed greater potency than naringenin equivalent.

Apigenin and naringenin ameliorate PKCßII-associated endothelial dysfunction via regulating ROS/caspase-3 and NO pathway in endothelial cells exposed to high glucose.

Endothelial dysfunction is a key event in the progression of atherosclerosis with diabetes. Increasing cell apoptosis may lead to endothelial dysfunction. Apigenin and naringenin are two kinds of widely used flavones. In the present study, we investigated whether and how apigenin and naringenin reduced endothelial dysfunction induced by high glucose in endothelial cells. We showed that apigenin and naringenin protected against endothelial dysfunction via inhibiting phosphorylation of protein kinase C ßII (PKCßII) expression and downstream reactive oxygen species (ROS) production in endothelial cells exposed to high glucose. Furthermore, we demonstrated that apigenin and naringenin reduced high glucose-increased apoptosis, Bax expression, caspase-3 activity and phosphorylation of NF-κB in endothelial cells. Moreover, apigenin and naringenin effectively restored high glucose-reduced Bcl-2 expression and Akt phosphorylation. Importantly, apigenin and naringenin significantly increased NO production in endothelial cells subjected to high glucose challenge. Consistently, high glucose stimulation impaired acetylcholine (ACh)-mediated vasodilation in the rat aorta, apigenin and naringenin treatment restored the impaired endothelium-dependent vasodilation via dramatically increasing eNOS activity and nitric oxide (NO) level. Taken together, our results manifest that apigenin and naringenin can ameliorate endothelial dysfunction via regulating ROS/caspase-3 and NO pathway.

[Analysis of washing efficiency and change in lead speciation in lead-contaminated soil of a battery factory].

Lead-contaminated soil with different pollution load in a lead battery factory in the southwest of China was chosen as the research object, the lead content and speciation were analyzed, and different washing agents were screened. The lead washing efficiency and lead speciation were analyzed under different pH conditions, and the soil of different particle size was washed using different duration to determine the best washing time. The results showed that the soil of sites A and B in the factory was severely contaminated, the lead concentration reaching 15,703.22 mg x kg(-1) and 1747.78 mg x kg(-1), respectively, and the proportion of the active-state lead was relatively high, while the residue state accounted for only 17.32%, 11.64%, 14.6% and 10.2%. EDTA and hydrochloric acid showed the best extraction effect in the 5 washing agents tested, which included EDTA, hydrochloric acid, citric acid, rhamnolipid and SDS. Cleaning under acidic conditions could not only effectively extract the total amount of lead but also effectively reduce the environmental risk of active-state lead. pH 4-7 was suggested as the most appropriate condition. The cleaning effect of coarse sand and fine sand was good, while for washing powder clay, it is better to improve the process, with the optimal washing time determined as 240 min.

Effects of rosuvastatin on expression of angiotensin-converting enzyme 2 after vascular balloon injury in rats.

OBJECTIVE: To investigate the effects and mechanisms of rosuvastatin on angiotensin -converting enzyme 2 (ACE2) in the process of neointimal formation after vascular balloon injury in rats, and to explore the effects of ACE2 and rosuvastatin in restenosis. METHODS: Thirty-six Wistar rats were randomly allocated into three groups: control group (n = 12), surgery group (n = 12), and statin group (n = 12). Aortic endothelial denudation of rats was performed using 2F balloon catheters. At days 14 and 28 after injury, aortic arteries were harvested to examine the following. Intimal thickening was examined by hematoxylin and eosin staining. We measured angiotensin II (Ang II) and angiotensin 1-7 (Ang-[1-7]) levels by a radioimmunological method or enzyme-linked immunosorbent assay. Protein and mRNA expression of ACE2 and Ang II type 1 receptor (AT1) were investigated by immunohistochemistry, Western blots, and Reverse transcriptase-polymerase chain reaction (RT-PCR). We measured changes in proliferating cell nuclear antigen (PCNA) by immunohistochemistry. The level of phosphorylated extracellular signal regulated kinase 1/2 (P-ERK1/2) was evaluated by Western blotting. RESULTS: Proliferation of vascular smooth muscle cells (VSMC) and intimal thickening were higher at day 14 after vascular balloon injury in the surgery group compared with the control group. Proliferation of VSMC was decreased by day 28 after injury, while intimal thickening continued. With rosuvastatin treatment, the extent of VSMC proliferation and intimal thickening was reduced at day 14 and 28 after injury. Ang II and P-ERK levels were significantly increased, Ang-(1-7) levels were significantly decreased, mRNA and protein expressions of ACE2 were significantly decreased, and AT1 expression was significantly increased at days 14 and 28 after vascular balloon injury in the surgery group compared with the control group. PCNA expression was higher in the surgery group than in the control group, and it was significantly decreased after being given rosuvastatin. Expression of ACE2 mRNA and protein, and Ang-(1-7) levels were significantly increased, while AT1 expression and levels of Ang II and P-ERK were significantly decreased in the statin group compared with the surgery group. CONCLUSIONS: Expression of ACE2 mRNA and protein is decreased in the process of intimal thickening after balloon injury. The inhibitory effect of rosuvastatin on intimal thickening is related to upregulation of ACE2, an increase in Ang-(1-7), downregulation of AT1, and activation of the P-ERK pathway.

[Expression of glucose transporter-3 in the cerebral cortex of aging rats].

OBJECTIVE: To observe the changes in the expression of glucose transporter-3 (GLUT3) in the cerebral cortex of rats during aging and investigate the role of GLUT3 in the aging process of the nervous system. METHODS: The cerebral tissues were collected from rats of 3, 18, 24, and 30 months old (10 in each age group), and the expression of GLUT3 in the cerebral cortex was detected by immunohistochemistry. RESULTS: Under optical microscope, GLUT3-positive cells were found in every group. Within the age range of 3 to 8 months, GLUT3-positive cells increased significantly with age (P<0.01), but at 24-30 months of age, the number of GLUT3-positive cells reduced significant with age (P<0.01). CONCLUSION: The expression changes of GLUT3 ir the cerebral cortex of rats during aging indicate that GLUT3 plays an important role in the maturation and aging of the nervous system.