Liu T.-Q.,Fudan University |
Liu T.-Q.,Nanjing Medical College |
Luo W.-L.,Fudan University |
Tan X.,Fudan University |
And 9 more authors.
Oxidative Medicine and Cellular Longevity | Year: 2014
Contrast-induced acute kidney injury (CI-AKI) is a serious complication in patients after administration of iodinated contrast media. Proper animal models of CI-AKI can help understand the mechanisms involved and prevent the disorder. We used the 5/6-nephrectomized (NE) rat to develop a CI-AKI model and to evaluate differences in the toxic effects on the kidney between iohexol and iodixanol. We found that six weeks after ablative surgery was the preferred time to induce CI-AKI. We compared multiple pretreatment plans and found that dehydration for 48 hours before iodixanol (320, 10 mL/kg) administration was optimal to induce CI-AKI in the 5/6 NE rats. Compared with iodixanol, iohexol induced a significantly greater reduction in renal function, severe renal tissue damage, intrarenal hypoxia, and apoptotic tubular cells. Iohexol and iodixanol resulted in similarly marked increases in levels of inflammation and oxidative stress. In summary, the 5/6 NE rat combined with dehydration for 48 hours is a useful pretreatment to establish a novel and reliable CI-AKI model. Iohexol induced more severe CI-AKI than iodixanol in this model. © 2014 Tong-qiang Liu et al.
Zhou J.-Y.,Soochow University of China |
Li X.-Q.,Nanjing Medical College |
Xu X.-T.,Soochow University of China |
Wang L.-L.,Soochow University of China |
And 2 more authors.
Tumor | Year: 2010
Objective: To investigate the inhibitory effects of celecoxib, a selective cyclooxygenase 2 (COX-2) inhibitor, on the proliferation and migration of human glioblastoma SHG-44 cells in vitro. Methods: The human glioblastoma cell lines SHG-44 were treated with different concentrations of celecoxib (30, 50, 100, and 150 μmol/L) for 24 and 48 h. The cells without celecoxib treatment were as control group. Cell morphologic changes were observed using optical microscopy. MTT assay was performed to determine the effects of celecoxib on the proliferation of SHG-44 cells. The migration ability of SHG-44 cells was measured using wound healing assay. The content of matrix metalloproteinase 2 (MMP-2) in the culture supernatant was detected with ELISA. Results: Celecoxib inhibited the growth of SHG-44 cells in concentration-and time-dependent manners. The migration ability of SHG-44 cells in celecoxib treated group was decreased compared with control group. The decreasing degree was more significant with the increase of the concentration of celecoxib. ELISA found that the level of MMP-2 in the supernatant of celecoxib-treated cells was significantly decreased compared with that of control group (P < 0.05). Conclusion: Celecoxib inhibits the proliferation and migration of human glioblastoma cell lines SHG-44 in a concentration-and time-dependent manner in vitro. Celecoxib may inhibit the migration ability of the human glioblastoma cell lines SHG-44 by suppressing MMP-2 secretion.
Shao J.,Nanjing Medical College |
Yao Y.,Nanjing Medical College |
Sun W.,Suzhou Municipal Hospital |
Wang R.,Nanjing Medical College
Zhonghua Shiyan Yanke Zazhi/Chinese Journal of Experimental Ophthalmology | Year: 2016
Background: Diabetic retinopathy (DR) is a common microvascular complications of the retina, retinal vascular smooth muscle cells of large conductance calcium-activated potassium channels (BK) is a major factor in regulating vasomotor and hemodynamic. Currently, functional changes of BK channel in retinal artery smooth muscle cells (RASMCs) and its role in DR were rarely reported. Objective: This study was to investigate the early vascular damage mechanisms in DR by detecting the changes of BK channels current, calcium concentration and open probability (NP0) of BK channel with different calcium concentration in RASMCs of normal and diabetic rats. Method: Fifty SPF SD 8-12 weeks old rats were randomly divided into normal control group and diabetic model group. Forty diabetic rats was intraperitoneally injected with 60 mg/kg streptozotocin to form type 1 diabetic model, 10 rats (the normal control group) were injected sodium citrate solution with the same manner. Fluorescent probe was applied to detect calcium concentration in rat RASMCs; RASMCs were isolated by using enzyme digestion, and BK-channel electric currents and calcium concentrations in the RASMCs were measured by whole-cell patch clamp technique and fluorescence assay, respectively. The NP0 of BK channel was measured by single patch clamp technique. Results: Diabetic models were successfully established in 36 rats with the success rate 90%. When stimulation voltage is greater than 60 mV, the current density of BK channel in RASMCs of diabetic model group decreased; when stimulating voltage was 100 mV, the BK channel currents of RASMCs in the normal control group and diabetic model group were (100±23) PA/PF and (50±7) PA/PF, the difference was statistically significant (t=19.80, P<0.05). After adding specific BK channel blocker African scorpion toxin 100 nmol, the BK channel current in the normal control group significantly reduced, and that in the diabetes model group was not significantly changed; the calcium ion concentrations in RASMCs were (123±11) nmol/L and (255±10) nmol/L in the normal control group and diabetic model group, the difference was statistically significant (t=32.50, P<0.05). When stimulation voltage was 60 mV, with increasing calcium ion concentration, the NP0 of BK channel increased (F=15.28, P<0.05). Conclusions: The electric current and NP0 of BK-channel are obviously reduced and the calcium concentration is evidently elevated in RASMCs of diabetic rats, suggesting that the abnormal of BK-channel is probably one of the important causes of retinal artery abnormal contraction in diabetic rats. Copyright © 2016 by the Chinese Medical Association.
Che X.-L.,Nanjing Medical College |
Li J.,Nanjing Medical College |
He J.-D.,Nanjing Medical College |
Cao W.-K.,Nanjing Medical College |
Deng Z.-K.,Nanjing Medical College
Tumor | Year: 2011
Objective: To investigate the effects of Kanglaite Injection combined with oxaliplatin on the proliferation and apoptosis of SW480 cells. Methods: The cell counting kit-8 (CCK-8) assay was used to examine the growth inhibition rates of SW480 cells treated with various concentrations of Kanglaite Injection or oxaliplatin alone or in combination. The apoptosis and cell cycle were examined by flow cytometry (FCM). The expression level of cell apoptosis-associated protein Bcl-2 was examined by immunocytochemistry and Western blotting. Results: The proliferation of SW480 cells was inhibited by Kanglaite Injection or oxaliplatin, and the synergistic effect of proliferation inhibition was observed when Kanglaite Injection and oxaliplatin were administered together (P<0.05). The cell cycle was blocked at G2/M phase (P<0.05). The apoptosis rate of SW480 cells treated with Kanglaite Injection combined with oxaliplatin was significantly higher than those treated with Kanglaite Injection or oxaliplatin alone [(23.30±3.04)%, (7.50±0.85)% and (9.00±2.14)%, respectively; P<0.05]. The immunocytochemistry and Western blotting methods revealed that the Kanglaite Injection could significantly enhance the inhibitory efficacy of Bcl-2 expression in SW480 cells treated with oxaliplatin (P±0.05). Conclusion: The cell proliferation inhibition and the apoptosis of SW480 cells can be synergistically enhanced by the treatment of Kanglaite Injection combined with oxaliplatin. Copyright@2009-2010 Tumor All rights reserved.