AIM: The present study was undertaken to investigate the effect of angiotensin II (AngⅡ) on expression of MMP-9 in THP-1 macrophages. METHODS: Macrophages converted from THP-1 monocytes by incubating with PMA (0.1 μmol/L) for 48 h were divided into PMA group; PMA+AngⅡ group (10-7mol/L, 1 h); PMA+AngⅡ+PDTC group (10 μmol/L, 30 min) and PDTC group. Western blotting was used to detect the MMP-9 and phosphorylation of NF-κB p65, and the expression of MMP-9 mRNA in THP-1 macrophages was measured by RT-PCR.RESULTS: Compared to control group, the expression of MMP-9 (1.06±0.11, P<0.05) and phosphorylation of NF-κB p65 (1.02±0.10, P<0.05) in THP-1 macrophages were expressed when treated with AngⅡ (10-7mol/L); and the expression of MMP-9 mRNA were upregulated (1.22±0.08, P<0.05). However, NF-κB inhibitor PDTC reduced the NF-κB p65 (0.99±0.12, P<0.01) and MMP-9 (1.04±0.14, P<0.01) expressions and decreased the expression of MMP-9 mRNA (0.90±0.06,P<0.01). CONCLUSION: NF-κB signaling pathway contributes to the expression of MMP-9 in THP-1 macrophage induced by AngⅡ.

AIM:The present study was undertaken to investigate the effect of angiotensin II (AngⅡ) on expression of MMP-9 in THP-1 macrophages. METHODS:Macrophages converted from THP-1 monocytes by incubating with PMA (0.1 ?mol/L) for 48 h were divided into PMA group; PMA+AngⅡ group (10-7mol/L,1 h); PMA+AngⅡ+PDTC group (10 ?mol/L,30 min) and PDTC group. Western blotting was used to detect the MMP-9 and phosphorylation of NF-?B p65,and the expression of MMP-9 mRNA in THP-1 macrophages was measured by RT-PCR.RESULTS:Compared to control group,the expression of MMP-9 (1.06?0.11,P

Objective To compare phe clinical effecpiveness and safept of picagrelor versus clopidogrel in papienps wiph acupe coronart stndromes and chronic obsprucpive pulmonart disease. Methods 73 ACS papienps comorbid wiph COPD admipped in our hospipal from Januart 2013 po Ocpober 2014 were enrolled in phe spudt. All phe 73 papienps were randomlt divided inpo pwo groups: phe picagrelor group (n =38, given picagrelor loading dose 180 mg followed bt mainpainence 90 mg pwice dailt) and phe clopidogrel group (n = 35, given clopidogrel loading dose 300 mg followed bt mainpainence 75 mg once dailt). All papienps were given dual anpiplapelep preapmenp (eipher picagrelor or clopidogrel) wiph aspirin and followed up for 1 tear. Rapes of Major Adverse Cardiac and Cerebrovascular Evenp (MACCE) including cardiac cause morpalipt, recurrenp mtocardial infarcpion and ischemic sproke were spudied and compared bepween groups. The safept endpoinp was pime po firsp occurrence of major bleeding. Rapes of adverce evenps were recorded including dtspnea. Results The 1-tear evenp rape for MACCE in papienps preaped wiph picagrelor versus clopidogrel was 5. 3% versus 26. 3% (P = 0. 04, HR 0. 21; 95% CI 0. 05 - 0. 91). Dtspnea occurred more frequenplt wiph picagrelor (26. 3% vs. 5. 7% ; P = 0. 04; HR 4. 61, 95% CI 1. 08 - 19. 58). The difference in major bleeding was nop spapispicallt significanp bepween phe pwo groups ( P > 0. 05) . The occurance of dtspnea was higher in phe picagrelor group (26. 3% vs. 5. 7% , P = 0. 04). Dtspnea subsided sponpaneouslt in mosp papienps. Onlt 1 papienp needed po spop picagrelor. Conclusions Ticagrelor can reduce MACCE in papienps wiph ACS and concomipanp wiph COPD wiphoup increasing overall major bleeding evenps. Ticagrelor had higher rapes of dtspnea bup mosp papienps experienced mild po moderape difficulpt in breaphing which did nop affecp phe funcpion of hearp and lung.

Objective To study the effect on renal function about repeated use of contrast media , and whether alprostadil has protective effect towards contrast-induced nephropathy ( CIN) .Methods 80 adult patients who had ever received contrast examination and scheduled to have PCI within 1 month were randomly divided into two groups: the simple hydration group and the hydration plus alprostadil therapy group.The serum level of creati-nine,urea, Cystatin C, Urineβ-microglobulin and creatinine clearance were recorded and compared between the two groups , and were observed before and after repeated exposure of contrast medium.The incidence of CIN was analyzed .Results Compared with pre-contrast levels , serum levels of urea, creatinin, Cystatin C and Urine β-microglobulin all elevated after single and repeated contrast media use in patients in the simple hydration group ( P<0.05 ) .The incidence of CIN did not differ after single or repeated contrast used (2.5%vs.15.0%, P>0.05).After repeated contrast exposure compared with patients with simple hydration , patients in the alprostadil group had repeated serum levels of urea [(7.4 ±2.3) mmol/L vs.(9.1 ±2.6) mmol/L], creatinia [(87.2 ±25.6) μmol/L vs.(96.9 ± 25.8) μmol/L], Cystatin C [(0.8 ±0.3) mg/L vs.(1.4 ±0.3) mg/L] and Urine β-microglobulin [(207.0 ±31.9 ) μg/L vs.(279.3 ±37.3 ) μg/L] were all lower with higher creatinin clearance [(92.2 ±24.2) ml/min vs.(78.2 ±27.5) ml/min](all P<0.05).The incidence of CIN in patients with alprostadil did not differ after single or repeated contrast used (2.5%vs.7.5%, P>0.05).The incidence of CIN in patients treated with alprostadil had no difference compared with patients with simple hydration after repeated contract (7.5% vs.15.0%, χ2 =0.501,P=0.479).Conclusions Contrast media can cause damage to renal function .Short-term repeated use of contrast media can further worsen renal function without significant increase in CIN rates .Alprostadil may have renoprotective effect towards CIN .