Association between high sensitivity C-reactive protein and contrast induced acute kidney injury in patients with acute coronary syndrome undergoing percutaneous coronary intervention: impact of atorvastatin / 中华心血管病杂志

<p><b>OBJECTIVE</b>To observe the association between preprocedural high sensitivity C-reactive protein (hs-CRP) level and incidence of contrast induced acute kidney injury (CI-AKI) in acute coronary syndrome (ACS) patients undergoing percutaneous coronary intervention (PCI) and the impact of atorvastatin pretreatment on CI-AKI.</p><p><b>METHODS</b>According to the level of preprocedural hs-CRP, 270 ACS patients were divided into three groups: high hs-CRP group (hs-CRP ≥ 3 mg/L, n = 176), moderate hs-CRP group (hs-CRP 1-3 mg/L, n = 60) and normal hs-CRP group (hs-CRP < 1 mg/L, n = 34). According to the dosage of preprocedural atorvastatin, the high hs-CRP group was further divided into 10 mg group (n = 49), 20 mg group (n = 66) and 40 mg group (n = 61). Serum creatinine (Scr), blood urea nitrogen (BUN), cystatin C (Cys C), hs-CRP were measured at before and 24 hours, 48 hours after PCI. CCr and GFR were calculated according to Scr and Cys C. Risk factors for CI-AKI were determined by multivariate logistic regression analysis.</p><p><b>RESULTS</b>(1) Cys C was significantly increased and GFR after PCI significantly reduced in high and moderate hs-CRP groups compared with normal hs-CRP group (P < 0.05). (2) Incidence of CI-AKI was 43.18%, 38.33%, 20.59% in high, moderate and normal hs-CRP groups, respectively (P < 0.05). (3) In high hs-CRP group, postprocedural GFR was significantly higher while postprocedural Cys C and hs-CRP were significantly lower in 40 mg statin subgroup than 10 mg and 20 mg statin subgroups (P < 0.05), similar trends were documented when comparing 20 mg statin subgroup with 10 mg statin subgroup (P < 0.05). (4) Multivariate logistic regression analysis showed that pretreatment with high dose atorvastatin was a protective factor for post CI-AKI (20 mg atorvastatin: OR = 0.15, 95%CI 0.06 - 0.33, P = 0.001; 40 mg atorvastatin: OR = 0.10, 95%CI 0.04 - 0.23, P = 0.001), while high levels of preprocedural hs-CRP (OR = 2.06, 95%CI 1.01 - 4.23, P = 0.048), diabetes mellitus (OR = 10.71, 95%CI 5.29 - 21.70, P = 0.001), advanced age (OR = 2.64, 95%CI 1.05 - 6.63, P = 0.038) and renal failure (OR = 5.14, 95%CI 1.13 - 23.39, P = 0.034) were independent risk factors of CI-AKI.</p><p><b>CONCLUSION</b>High hs-CRP level is linked with the development of CI-AKI in ACS patients undergoing PCI and pretreatment with 40 mg atorvastatin is associated with lower incidence CI-AKI, possibly by reducing the postprocedural inflammation responses.</p>

Inhibitory effect of p16, p53 transfection on leukemic cell lines K562 and HL-60 / 中国实验血液学杂志

This study was purposed to construct a vector containing human suppressor gene p53 and p16, and to investigate their expression and effect on K562 and HL-60 cells. pBudCE4.1-53-16 is a vector designed for simultaneous expression of human suppressor gene p53 and p16 in mammalian cell line. After transfection into K562 cells with lipofectamine(TM) 2000, the expression of p53 and p16 genes was detected by Western blot and immunocytochemical method. The growth curve, apoptosis, cell cycle were assayed by CCK-8 and flow cytometry. The results showed that the recombinant plasmid pBudCE4.1-53-16 was constructed successfully and were verified by PCR and restriction analysis. The expression of P53 and P16 protein could be detected after transfection into leukemia cells (K562 and HL-60) for 48 hours. As compared with control group, the cell proliferation in experimental group was inhibited, the cells were arrested in G0 phase and apoptotic cells increased (p<0.001). It is concluded that the recombinant plasmid pBudCE4.1-53-16 has been established. p16 and p53 in the recombinant plasmid pBudCE4.1-53-16 synchronously express in leukemic cells after transfection in vitro for 2 days and results in reduced proliferation, G0 arrest and apoptosis increase.

Arresting effect of p16 and dll4 transfection on cell cycle of K562 cells / 中国实验血液学杂志

This study was purposed to investigate the expression and role of eukaryotic expression vector containing p16, dll4 genes in leukemia K562 cells. A vector pBudCE4.1-16-dll4 containing wild type p16cDNA and dll4cDNA was designed and constructed, then this vector was transfected into leukemia K562 cells by using lipofectamine 2000. The expression of p16 and dll4 genes was detected by Western blot, the cell growth curve and cell cycle were determined by CCK-8 kit and flow cytometry respectively. The results showed that the recombinant plasmid pBudCE4.1-16-dll4 was constructed and transfected into K562 cells in vitro successfully. The expression of exogenous P16 and Dll4 proteins could be detected in K562 cells. After transfection for 48 hours, the K562 cells were arrested in G(1) phase, the cell count increased in G(0)/G(1) phase and reduced in S phase, the cell proliferation decreased as compared with control. It is concluded that the p16 and dll4 genes can simultaneously express in K562 cells transfected with recombinant plasmid pBudCE4.1-16-dll4 in vitro which results in G(0)/G(1) arrest and reduces cell proliferation.

Transplantation of mesenchymal stem cells transfected with hepatocyte growth factor gene improves heart function in rats with heart failure / 中国应用生理学杂志

<p><b>AIM</b>To investigate the effects of hepatocyte growth factor gene transfected MSCs transplantation on cardiac function and fibrosis in rats heart failure model induced by adriamycin.</p><p><b>METHODS</b>MSCs were isolated from SD rats by density gradient centrifugation, purified, and transfected with Ad-hHGF. ELISA were used to detect the protein expression of hHGF in these MSCs. Forty SD rats underwent intraperitoneal injection with adriamycin to induce heart failure model. 8 healthy rats served as control, 24 survival rats were randomly divided into 3 groups (n = 8): Rats in Ad-hHGF transfected MSCs group were injected with Ad-hHGF transfected MSCs 2 weeks after the establishment of the model, rats in MSC group injected with suspension of MSCs only, and model group was injected with cold culture fluid. Heart function was evaluated by a physiological recorder 4 weeks after cell transplantation. Myocardial cell morphology and interstitial collagen were studied by electron microscope and were stained by Sirus red. TGF-beta1 was detected by immunohistochemical method.</p><p><b>RESULTS</b>(1) MSCs could be transfected efficiently by Ad-hHGF, manifested by a higher level of expression in vitro, persisting 14 days at least. (2) Four weeks after the cells transplantion, cardiac necrosis in MSC-hHGF rats was improved when compared with those in the MSCs (P < 0.05) and Model group (P < 0.01). The heart function of the MSC-hHGF rats was greatly improved with an significant increase in LVSP and + dp/dt(max), although LVEDP still highter than that of normal rats. (3) MSC-Ad-hHGF decreased Myocardial collagen content and the level of TGFbeta1 compaired with MSCs transplanted rats (P < 0.01).</p><p><b>CONCLUSION</b>Transplantation of HGF gene transfected MSCs improved heart function, decreased myocardial collagen and the level of TGFbeta1.</p>

Atorvastatin attenuated contrast induced renal function damage / 中华心血管病杂志

<p><b>OBJECTIVE</b>To study the effects of atorvastatin on contrast induced renal function change and plasma hsCRP in patients undergoing coronary angiography.</p><p><b>METHODS</b>120 patients who underwent coronary angiography were randomized to receive atorvastatin (20 mg/qn, n = 60) or no atorvastatin (n = 60) treatment 2 to 3 days before coronary angiography. Urinary alpha1-MG, TRF and mALB were checked for evidence of tubular or glomerular damage at start, 1 day and 2 days after the administration of a radiocontrast agent. Serum creatinine, BUN, cystatin C and hsCRP levels were also assessed at the same time. Ccr and GFR were calculated according to Cockcroft-Gault and GFR (ml/min) = 74.835/Cys C(1.333) formulas basing on serum creatinine or cystatin C concentration.</p><p><b>RESULTS</b>(1) In control group, comparison with the value before coronary angiography, urinary alpha1-MG, TRF and mALB or serum cystatin C and hsCRP significantly increased at day 1 after angiography (P < 0.01). In comparison to the levels at day 1 after angiography, urinary alpha1-MG, TRF, mALB, serum cystatin C significantly decreased at day 2 after angiography (P < 0.01), but alpha1-MG, cystatin C still exceeded the values before coronary angiography, TRF and mALB levels at day 2 after angiography had no significant change compared to baseline (P > 0.05), hsCRP level at day 2 after angiography had no significant change compared to that at day 1 after angiography (P > 0.05) too. (2) In comparison with the value before coronary angiography in atorvastatin-treated group, the levels of urinary alpha1-MG, TRF and mALB or serum cystatin C at day 1 and day 2 after angiography had no significant change compared to baseline (P > 0.05).Serum hsCRP significantly increased at day 1 after angiography compared to baseline (P < 0.01), but it had no significant change compared to day 2 after angiography (P > 0.05). (3) To compare to the atorvastatin-treated group, the values of urinary alpha1-MG, TRF and mALB or Cys C and hsCRP significantly increased at day 1 after angiography in control group (P < 0.01), the values of urinary alpha1-MG, cystatin C and hsCRP still significantly increased at day 2 (P < 0.01)too, but those of TRF and mALB had no significantly change at day 1 or day 2 after angiography between the two groups (P > 0.05). There was no significant change in BUN, Cr, Ccr levels before and after angiography between the two groups.</p><p><b>CONCLUSIONS</b>Low dose contrast induces light renal function damage. Pretreatment with atorvastatin 20 mg/qn for 2 to 3 days could significantly reduce procedural inflammatory reaction, attenuate urinary protein and the effect of degrading GFR in coronary angiography patients.</p>