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1.
Chinese Journal of Pathophysiology ; (12): 1608-1613, 2016.
Article in Chinese | WPRIM | ID: wpr-498739

ABSTRACT

AIM: To explore whether necroptosis contributes to the high glucose (HG)-induced damage in hu-man umbilical vein endothelial cells (HUVECs).METHODS: The protein levels of receptor-interacting protein 3 (RIP3) and cleaved caspase-3 were detected by Western blot.The intracellular levels of reactive oxygen species (ROS) were deter-mined by DCFH-DA staining followed by photofluorography.Mitochondrial membrane potential (MMP) was measured by rhodamine 123 staining followed by photofluorography.RESULTS: Treatment of HUVECs with HG at different concentra-tions (10, 20 and 40 mmol/L glucose) for 24 h gradually enhanced the expression levels of RIP3.Treatment of HUVECs with HG (40 mmol/L glucose) for different time (3 h, 6 h, 9 h, 12 h and 24 h) also up-regulated the expression levels of RIP3, peaking at 9 h.Pretreatment of HUVECs with 20 μmol/L Z-VAD-FMK (an inhibitor of caspase) for 30 min before exposure to HG enhanced the expression level of RIP3.Pretreatment of HUVECs with 100 μmol/L necrostatin-1 (an inhi-bitor of necroptosis) for 1 h before exposure to HG alleviated the HG-induced injuries, such as a decrease in cell viability, an increase in ROS generation and dissipation of MMP, but up-regulated the protein level of cleaved caspase-3.CON- CLUSION: Necroptosis mediates HG-induced injury in HUVECs.There is a negative interacting between necroptosis and apoptosis.

2.
Chinese Journal of Pathophysiology ; (12): 1161-1166, 2016.
Article in Chinese | WPRIM | ID: wpr-496562

ABSTRACT

AIM: To explore whether exogenous hydrogen sulfide (H2S) depresses high glucose (HG)-in-duced injury by modulating the Janus kinase/signal transducer and activator of transcription ( JAK/STAT) pathway in hu-man umbilical vein endothelial cells (HUVECs).METHODS:The protein levels of JAK2, STAT3 and cleaved caspase-3 were determined by Western blot.The cell viability was measured by CCK-8 assay.Mitochondrial membrane potential ( MMP) was detected by rhodamine 123 staining followed by photofluorography.The intracellular level of reactive oxygen species (ROS) was analyzed by DCFH-DA staining followed by photofluorography.The activity of superoxide dismutase (SOD) was also measured.RESULTS:Pretreatment of the HUVECs with 400 μmol/L NaHS (a donor of H2S) for 30 min prior to exposure to 40 mmol/L glucose ( HG) markedly attenuated HG-induced upregulation of the phosphorylation of JAK2 and STAT3.Pretreatment with 400μmol/L NaHS for 30 min or with 20μmol/L AG490 (inhibitor of the JAK/STAT pathway) for 30 min attenuated the injury of HUVECs induced by HG, as indicated by the increases in cell viability and SOD activity, and decreases in the protein level of cleaved caspase-3, ROS generation and dissipation of MMP.CONCLU-SION:Exogenous H2 S protects HUVECs against HG-induced injury by inhibiting JAK/STAT pathway.

3.
Article in Chinese | WPRIM | ID: wpr-329256

ABSTRACT

<p><b>OBJECTIVE</b>To observe the therapeutic effect and safety of vildagliptin combined with insulin aspart injection in elderly patients with type 2 diabetes.</p><p><b>METHODS</b>Sixty-six elderly patients with type 2 diabetes who had poor blood glucose control with insulin aspart injection were divided into two groups to have additional Vildagliptin (50 mg, twice daily, n=36, observation group) or Acarbose (50 mg, three times a day, n=30, control group). Blood glucose (including FBG and 2hPG), HbA1C, fasting c-peptide, postprandial c-peptide, BMI and GFR were observed after 12 weeks.</p><p><b>RESULTS</b>In the observation group, FBG, 2hPG and HbA1C decreased significantly (P<0.05), fasting and postprandial c-peptide increased (P<0.05), and BMI and GFR showed no obvious changes (P>0.05). In the control group, 2hPG and HbA1C were significant lowered (P<0.05) but FBG, fasting and postprandial c-peptide, BMI or GFR showed no changes (P>0.05). Compared with those in the control group, FBG in the observation group showed a significant reduction (P<0.05), but no significant differences were found in 2hPG, HbA1C, BMI or GFR (P>0.05). No hypoglycemia occurred in the two groups during the treatment.</p><p><b>CONCLUSION</b>Vildagliptin with insulin aapart injection has equivalent effect with Acarbose combined with insulin aspart injection in decreasing 2hPG and HbA1C without increasing the body weight or the risk to hypoglycemia or causing lowered GFR. Vildagliptin has better effect in decreasing FBG and improving the function of the islet cells.</p>


Subject(s)
Aged , Humans , Adamantane , Therapeutic Uses , Blood Glucose , Diabetes Mellitus, Type 2 , Drug Therapy , Glycated Hemoglobin , Metabolism , Hypoglycemic Agents , Therapeutic Uses , Injections , Insulin Aspart , Therapeutic Uses , Nitriles , Therapeutic Uses , Pyrrolidines , Therapeutic Uses
4.
Article in Chinese | WPRIM | ID: wpr-315482

ABSTRACT

<p><b>OBJECTIVE</b>To observe the effect of zoledronic acid on bone mineral density (BMD) and bone metabolic markers in elderly patients with primary osteoporosis.</p><p><b>METHODS</b>Forty-eight elderly patients with osteoporosis were randomly assigned to zoledronic acid group (n=23) to receive treatment with 5 mg zoledronic acid once a year and the control group (n=25). In both groups, the patients were given Vitamin D3 and caltrate on a daily basis for a year. The bone mineral density (BMD) and bone metabolic markers were observed after the treatment.</p><p><b>RESULTS</b>Compared with the control group, zoledronic acid group had significantly higher L1-4, neck, Inter and Ward's BMD (P<0.05) with reduced B-NTX (P<0.05). The N-MID and CT showed no significant differences between the two groups (P<0.05).</p><p><b>CONCLUSION</b>Zoledronic acid administration once a year can increase BMD and lower the serum bone turnover metabolism, and can be used in the treatment of primary osteoporosis in elderly patients.</p>


Subject(s)
Aged , Aged, 80 and over , Female , Humans , Male , Bone Density , Bone Density Conservation Agents , Therapeutic Uses , Diphosphonates , Therapeutic Uses , Imidazoles , Therapeutic Uses , Osteoporosis , Drug Therapy , Metabolism , Treatment Outcome
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