| Objective: The present study examined the effect of serum uric acid onmodulating coronary local inflammation by activating the NLRP3inflammsome.Methods:46patients undergong coronary angiography were dividedinto CHD group (23cases) and normal group (23cases). Treated or withouttreated atorvastatin, CHD group and normal group were further divided intotwo subgroups respectively, included CHD non-atorvastatin group (9cases),CHD atorvastatin group (14cases), normal non-atorvastatin group(18cases),normal atorvastatin group (5cases). The NLRP3,ASC and caspase-1mRNAexpression of coronary blood monocylcs were measured using real-timequantitative polymerase chain reaction (RT-qPCR). The serum levels of IL-1βand IL-18were examined using enzyme linked immunosorbent assay(ELISA).Results:1.SUA level was significantly higher in the CHD group than inthe normal group [(362.23±85.15) μmol/L vs.(298.87±59.65) μmol/L; P＜0.05]; mRNA expression of NLRP3and ASC were down-regulated in theCHD group compared with the normal group, but level of caspase-1wasup-regulated [NLRP3,(0.82±0.53) vs.(1.12±0.52), P＜0.05; ASC,(0.85±0.43) vs.(1.05±0.21), P＜0.05; caspase-1,(1.48±0.64) vs.(1.05±0.41), P＜0.05]; Serum levels of IL-1β and IL-18were increasd in the CHD groupthan in the normal group [IL-1β,(4.52±1.94) pg/ml vs.(3.52±1.21) pg/ml,P＜0.05; IL-18,(176.08±48.20) pg/ml vs.(128.03±65.91) pg/ml, P＜0.05]. 2.mRNA expression of NLRP3inflammasome were higher in the CHDnon-atorvastatin group than in the CHD atorvastatin group [NLRP3,(1.44±0.15) vs.(0.41±0.08), P<0.05; ASC,(1.30±0.33) vs.(0.56±0.14), P<0.05;caspase-1,(2.14±0.45) vs.(1.05±0.28), P<0.05], and serum levels ofSUA,IL-1β and IL-18were higher in the CHD non-atorvastatin group than inthe CHD atorvastatin group [SUA,(441.29±70.95) μmol/L vs.(311.41±45.44) μmol/L, P<0.05; IL-1β,(5.55±2.21) pg/ml vs.(3.85±1.61) pg/ml,P<0.05; IL-18,(209.19±45.04) pg/ml vs.(154.80±37.91) pg/ml, P<0.05];mRNA expression of NLRP3inflammasome were higher in the CHDnon-atorvastatin group than in the normal non-atorvastatin group [NLRP3,(1.44±0.15) vs.(1.12±0.50), P<0.05; ASC,(1.30±0.33) vs.(1.05±0.21),P<0.05; caspase-1,(2.14±0.45) vs.(1.05±0.44), P<0.05], and serum levelsof SUA,IL-1β and IL-18were higher in the CHD non-atorvastatin group thanin the normal non-atorvastatin group [SUA,(441.29±70.95) μmol/L vs.(300.13±48.11) μmol/L, P<0.05; IL-1β,(5.55±2.21) pg/ml vs.(3.54±0.99)pg/ml, P<0.05; IL-18,(209.19±45.04) pg/ml vs.(128.61±62.24) pg/ml,P<0.05]; mRNA expression of NLRP3inflammasome were higher in theCHD non-atorvastatin group than in the normal atorvastatin group [NLRP3,(1.44±0.15) vs.(1.11±0.62), P<0.05; ASC,(1.30±0.33) vs.(1.06±0.22),P<0.05; caspase-1,(2.14±0.45) vs.(1.04±0.28), P<0.05], and serum levelsof SUA,IL-1β and IL-18were higher in the CHD non-atorvastatin group thanin the normal atorvastatin group [SUA,(441.29±70.95) μmol/L vs.(294.34±98.48) μmol/L, P<0.05; IL-1β,(5.55±2.21) pg/ml vs.(3.45±1.96) pg/ml,P<0.05; IL-18,(209.19±45.04) pg/ml vs.(125.97±86.18) pg/ml, P<0.05];mRNA expression of NLRP3and ASC were lower in the CHD atorvastatingroup than in the normal atorvastatin group [NLRP3,(0.41±0.08) vs. (1.11±0.62), P<0.05; ASC,(0.56±0.14) vs.(1.06±0.22), P<0.05], and therewere no significant differences in levels of caspase-1,SUA,IL-1β and IL-18between the CHD atorvastatin group and the normal atorvastatin group[caspase-1mRNA,(1.05±0.28) vs.(1.04±0.28); SUA,(311.41±45.44)umol/L vs.(294.34±98.48) umol/L; IL-1β,(3.85±1.61) pg/ml vs.(3.45±1.96) pg/ml; IL-18,(154.80±37.91) pg/ml vs.(125.97±86.18) pg/ml;all not significant]; mRNA expression of NLRP3and ASC were lower in theCHD atorvastatin group than in the normal non-atorvastatin group [NLRP3,(0.41±0.08) vs.(1.12±0.50), P<0.05; ASC,(0.56±0.14) vs.(1.05±0.21),P<0.05], and there were no significant differences in levels of caspase-1,SUA,IL-1β and IL-18between the CHD atorvastatin group and the normalnon-atorvastatin group [caspase-1mRNA,(1.05±0.28) vs.(1.05±0.44);SUA,(311.41±45.44) μmol/L vs.(300.13±48.11) μmol/L; IL-1β,(3.85±1.61) pg/ml vs.(3.54±0.99) pg/ml; IL-18,(154.80±37.91) pg/ml vs.(128.61±62.24) pg/ml; all not significant]; There were no significantdifferences in levels of NLRP3inflammasome,SUA,IL-1β and IL-18betweenthe normal non-atorvastatin group and the normal atorvastatin group [NLRP3mRNA,(1.12±0.50) vs.(1.11±0.62); ASC mRNA,(1.05±0.21) vs.(1.06±0.22); caspase-1mRNA,(1.05±0.44) vs.(1.04±0.28); SUA,(300.13±48.11) μmol/L vs.(294.34±98.48) μmol/L; IL-1β,(3.54±0.99) pg/ml vs.(3.45±1.96) pg/ml; IL-18,(128.61±62.24) pg/ml vs.(125.97±86.18)pg/ml; all not significant]; mRNA expression of NLRP3inflamasome weresignificantly positively correlated with SUA in the CHD atorvastatin group(NLRP3compared with SUA, r=0.65and P=0.011; ASC compared with SUA,r=0.63and P=0.017; caspase-1compared with SUA, r=0.60and P=0.024).Conclusion: Our study finds that levels of SUA,NLRP3inflammasome, IL-1β and IL-18are significant differences between the CHD patients andnormal group. It suggests that SUA and NLRP3inflammasome play a role incoronary local inflammatory reaction. SUA maybe modulate coronary localinflammatory reaction by activating the inflammasome directly or indirectly. |
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